Unique_ID	Origin_ID	Name	Sequence	Length	Treatment_Type	Category	Clinical_Stage	Indications	Target	serial_number	has_non_natural_amino_acids	is_cyclic	has_modification	molecular_weight	chemical_formula	isoelectric_point	hydrophobicity	melting_point	half_life	description	pharmacodynamics	mechanism_of_action	toxicity	metabolic_pathway	absorption_rate	apparent_volume_of_distribution	clearance_rate	patent_number	patent_publication_date	expiry_date	drug_interactions	specific_indications	chemical_name	dosage_form	physical_form	route_of_administration	recommended_dosage	contraindications	side_effects	useful_links
FPDB21340	Th1001	Lepirudin	LVYTDCTESGQNLCLCEGSNVCGQGNKCILGSDGEKNQCVTGEGTPKPQSHNDGDFEEIPEEYLQ	65	Antithrombins & Fibrinolytic Agents	Antithrombins  and Fibrinolytic Agents	Ia	For the treatment of heparin-induced thrombocytopenia.	Prothrombin	1001				6963.425	C287H440N80O110S6	4.04	-0.777	65	Approximately 1.3 h	Lepirudin is identical to natural hirudin except for substitution of leucine for isoleucine at the N-terminal end of the molecule and the absence of a sulfate group on the tyrosine at position 63. It is produced via yeast cells.	Lepirudin is used to break up clots and to reduce thrombocytopenia. It binds to thrombin and prevents thrombus or clot formation. It is a highly potent, selective, and essentially irreversible inhibitor of thrombin and clot-bond thrombin. Lepirudin requires no cofactor for its anticoagulant action. Lepirudin is a recombinant form of hirudin, an endogenous anticoagulant found in medicinal leeches.	Lepirudin forms a stable non-covalent complex with alpha-thrombin, thereby abolishing its ability to cleave fibrinogen and initiate the clotting cascade. The inhibition of thrombin prevents the blood clotting cascade.	In case of overdose (eg, suggested by excessively high aPTT values) the risk of bleeding is increased.	Lepirudin is thought to be metabolized by release of amino acids via catabolic hydrolysis of the parent drug. However, conclusive data are not available. About 48% of the administration dose is excreted in the urine which consists of unchanged drug (35%)	Bioavailability is 100% following injection.	12200 ml [Healthy young subjects (n = 18, age 18-60 years)]	9840 ml/h [Healthy 18-60 yrs]	CA1339104	1997-07-29 00:00:00	2014-07-29 00:00:00	Ginkgo biloba = may increase bleed risk.	heparin-induced thrombocytopenia (HIT) and associated thromboembolic disease	[Leu1, Thr2]-63-desulfohirudin	Each vial of REFLUDAN contains 50000 ug lepirudin. Other ingre-dients are 40000 ug mannitol and sodium hydroxide for adjust-ment of pH to approximately 7	Sterile, white, freeze-dried powder	Intravenous infusion	Recommended dose is 400 ug/kg body weight (up to 110kg) slowly intravenously (eg, over 15 to 0.005556 h) as a bolus dose, and can be followed by 150 ug/kg body weight (up to 110kg)/hour as a continuous Intravenous infusion for 2 to 240 h or longer if CL.	Hypersensitivity		http://www.drugs.com/pro/refludan.html
FPDB21341	Th1006	Bivalirudin	FPRPGGGGNGDFEEIPEEYL	20	Antithrombins & Fibrinolytic Agents	Antithrombins	Ia	For treatment of heparin-induced thrombocytopenia and for the prevention of thrombosis. Bivalirudin is indicated for use in patients undergoing percutaneous coronary intervention (PCI), in patients at moderate to high risk acute coronary syndromes due to unstable angina or non-ST segment elevation in whom a PCI is planned.	Prothrombin	1032				2180.2853	C98H138N24O33	3.91	-0.985		Normal renal function: 0.42 h (in normal conditions)	Bivalirudin is a synthetic 20 residue peptide which acts as a thrombin inhibitor. Once bound to the active site of the inhibitor, thrombin cannot activate fibrinogen into fibrin which is a crucial step in the formation of thrombus. As it can cause blood stagnation, it is important to monitor changes in hematocrit, activated partial thromboplastin time, international normalized ratio and blood pressure. It is administered intravenously.	Bivalirudin directly and reversibly inhibits thrombin by specifically binding to both the catalytic site and the anion-binding exosite of circulating and clot-bound thrombin.  The action of bivalirudin is reversible as thrombin will slowly cleave the thrombin-bivalirudin bond which recovers the active site of thrombin.	Inhibits the action of thrombin by binding to both its catalytic site and to its anion-binding exosite. Thrombin, a serine proteinase that plays a central role in the thrombotic process, acts to cleave fibrinogen into fibrin monomers and activate Factor XIII to Factor XIIIa, allowing fibrin to develop a covalently cross-linked framework which stabilizes the thrombus; thrombin also activates Factors V and VIII, promoting further thrombin generation, and activates platelets, stimulating aggregation and granule release.	Based on a study by Gleason et al., the no observed adverse effect level (NOAEL) for bivalirudin administered to rats via Intravenous infusion over a 24-hour period, was 2000000 ug/kg/24 h.	80% proteolytic cleavage	Bivalirudin exhibits linear pharmacokinetics. The mean steady state concentration is 12.3 ± 1.7 ug/ml after administration of an intravenous bolus of 1000 ug/kg followd by a 2500 ug/kg/hr Intravenous infusion given over 4 h.	200 ml/kg	204 ml/h/kg [Normal renal function]	US7582727	2009-01-27 00:00:00	2029-01-27 00:00:00	Deferasirox, Anticoagulants increase the risk for gastrointestinal ulceration/irritation and/or GI bleeding. If these two agents must be used, patients need to be closely monitored for signs and symptoms of GI toxicity.	It is used for thinning the blood in patients with unstable angina who are undergoing percutaneous transluminal coronary angioplasty (PTCA) and in patients undergoing percutaneous coronary intervention (PCI).	D-phenylalanyl-L-prolyl-L-arginyl-L-prolyl-glycylglycyl-glycyl-glycyl-L-asparagyl-glycyl-L-aspartyl-L-phenylalanyl-L-glutamyl-L-glutamyl-L-isoleucyl-L-prolyl-L-glutamyl-L-glutamyl-L-tyrosyl-L-leucine trifluoroacetate (salt) hydrate	Each vial contains 250000 ug bivalirudin, 125000 ug mannitol, and sodium hydroxide to adjust the pH to 5-6 (equivalent of approximately 12500 ug sodium). When reconstituted with Sterile Water for Injection, the product yields a clear to opalescent, colorless to	Supplied in single-use vials as a white lyophilized cake	Intravenous infusion	Intravenous (IV) bolus dose of 750 ug/kg, followed by an infusion of 1750 ug/kg/h for the duration of the PCI/PTCA procedure.	Allergic and have major active bleeding	Anxiety; back, stomach, or pelvic pain; headache; nausea; nervousness; pain at the injection site; trouble sleeping; upset stomach; vomiting. And severe side effect may include  Severe allergic reactions (rash; hives; itching; difficulty breathing.	http://reference.medscape.com/drug/angiomax-angiox-bivalirudin-342137
FPDB21342	Th1007	Leuprolide	PHWSYLLR	8	Antineoplastic Agents	Antineoplastic Agents	IIa	To treat prostate cancer, endometriosis, uterine fibroids and premature puberty.	Gonadotropin-releasing hormone receptor	1038				1209.3983	C59H84N16O12		0.1		Approximately 3 h	Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease).	Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer.	Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion.	Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a	Primarily degraded by peptidase (instead of cytochrome P450 enzymes).	Bioavailability by subcutaneous administration is comparable to that by intravenous administration.	27000 ml [intravenous bolus administration to healthy male volunteers]	Excretion in urine, 8340 ml/h [healthy male receiving a 1-mg IV bolus]					Eligard is used to treat the symptoms of prostate cancer in men.	5-oxo-L-prolyl-L-histidyl-L-tryptophyl-L-seryl-L-tyrosyl-D-leucyl-L-arginyl-N-ethyl-L-prolinamide acetate	ELIGARD is prefilled and supplied in two separate, sterile syringes whose contents are mixed immediately prior to administration. The two syringes are joined and the single dose product is mixed until it is homogenous. One syringe contains the ATRIGEL De	Suspension	Subcutaneous Injection	7500 ug-1 injection/month, 22500 ug-1 injection per 2190 h, 30000 ug-1 injection per 2920 h, 45000 ug- 1 injection every 4380 h.	Hypersensitivity and pregnancy	Rare pain or unusual sensations in your back; numbness, weakness, or tingly feeling in your legs or feet; muscle weakness or loss of use;  loss of bowel or bladder control; or liver problems - nausea, upper stomach pain, itching, tired feeling, loss of apetite.	http://www.freepatentsonline.com/EP1790656.html# RxMed:http://www.rxmed.com/b.main/b2.pharmaceutical/b2.1.monographs/CPS-%20Monographs/CPS-%20(General%20Monographs-%20000 ml)/LUPRON%20DEPOT.html
FPDB21343	Th1014	Salmon Calcitonin	CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP	32	Bone Density Conservation Agents	Bone Density Conservation Agents	Ib	Used for the treatment of post-menopausal osteoporosis.	Calcitonin receptor	1098				3431.853	C145H240N44O48S2	8.86	-0.537		0.83-1.33 h	Synthetic peptide of 32 residues, formulated as a nasal spray.	Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney.	Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of  calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway.	It is devoid of embryotoxic, teratogenic and mutagenic potential.	Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule.	Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively).		Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney.	US6440392	2001-02-02 00:00:00	2021-02-02 00:00:00	Eskalith (lithium)	To treat Paget's disease of bone		Each mL of sterile solution contains calcitonin salmon 200 IU. Nonmedicinal ingredients include acetic acid, phenol, sodium acetate, sodium chloride, sodium hydroxide and water for injection.	Solution	Subcutaneous or intramuSubcutaneousular Injection	Based on body weight and injected every 12 h	Allergy	Feeling light-headed, fainting; or muscle stiffness.	http://www.drugs.com/sfx/calcimar-side-effects.html
FPDB21344	Th1018	Secretin	HSDGTFTSELSRLRDSARLQRLLQGLV	27	Diagnostic Agents	Diagnostic Agents	IV	For diagnosis of pancreatic exocrine dysfunction and gastrinoma	Secretin receptor	1129				3056.4	C130H219N43O42	9.45	-0.463			This drug is the synthetic form of natural secretin.  It is prepared using solid phase peptide synthesis.  Secretin is a peptide hormone produced in the S cells of the duodenum. Its main effect is to regulate the pH of the small  intestine contents through the control of gastric acid secretion and buffering with bicarbonate. It was the first hormone to be discovered.	Secretin is a hormone produced in the S cells of the duodenum in response to low local pH. It stimulates the secretion of bicarbonate from bicarbonate producing organs(liver, pancreas, Brunner's glands) when the pH drops below a set value. This helps neutralize the gastric acid entering the duodenum from the stomach. It also inhibits acid secretion from the stomach by reducing gastrin release from the G cells of the stomach.	Secretin binds to the secretin receptor found on the lining of S cells in the duodenum and G cells in the stomach. Binding leads to the secrection of bicarbonate or the reduction of the secretion of gastrin. Properly functioning organs (duodenum, pancreas and stomach) should be responsive to this hormone.									Clidinium. Anticholinergic agents such as secretin may diminish the stimulatory effect of secretin. Avoid using drugs with substantial anticholinergic effects in patients receiving secretin whenever possible. If such agents must be used in combina	Testing for stimulation of pancreatic secretions, including bicarbonate, to aid in the diagnosis of pancreatic exocrine dysfunction.	H-His-Ser-Asp-Gly-Thr-Phe-Thr-Ser-Glu-Leu-Ser-Arg-Leu-Arg-Asp-Ser- Ala-Arg-Leu-Gln-Arg-Leu-Leu-Gln-Gly-Leu-Val-NH2		Lyophilized white powder	Intravenous infusion		Allergy	Abdominal discomfort, Nausea, Mild bradycardia (reduced heart rate), Decreased blood pressure and Diaphoresis (profuse perspiration)	http://www.medilexicon.com/drugs/secreflo.php
FPDB21345	Th1067	Daptomycin	WNDTGKDADGSEY	13	Antibiotics	Antibiotic (Lipopeptide class).	IIa	For the treatment of complicated skin and skin structure infections caused by susceptible strains of Gram-positive microorganisms.	Bacterial cell membrane disruption	1409				1620.6706	C72H101N17O26	3.84	-3.1		168 h	Daptomycin is a lipopeptide antibiotic that kills susceptible gram positive bacteria by disrupting their membrane potential. It is a naturally-occurring compound found in the soil bacterium <i>Streptomyces roseosporus</i>. Antibiotics are used in the treatment of infections caused by bacteria. They work by killing bacteria or preventing their growth. Daptomycin will not work for colds, flu, or other virus infections. It was approved in September 2003 for the treatment of complicated skin and soft tissue infections. It has a safety profile similar to other agents commonly administered to treat gram-positive infections.	Daptomycin is a 13 member amino acid cyclic lipopeptide antibiotic active against Gram-positive bacteria only. It has proven in vitro activity against enterococci (including glycopeptide-resistant Enterococci (GRE)), staphylococci (including methicillin-resistant <i>Staphylococcus aureus</i>), streptococci and corynebacteria. Daptomycin is derived from the fermentation product of Streptomyces roseosporus. 
	Daptomycin appears to bind or insert into the outer membrane of gram positive bacteria. The binding and integration of daptomycin into the cell membrane is calcium dependent. Calcium ions cause a conformational change in daptomycin, augmenting its amphipathicity (hydrophilic head group and hydrophobic tail group), leading to incorporation into the cell membrane.
 This binding causes rapid depolarisation, resulting in a loss of membrane potential leading to inhibition of protein, DNA and RNA synthesis, which results in bacterial cell death. The bactericidal activity of daptomycin is concentration-dependent. There is in vitro evidence of synergy with β-lactam antibiotics.	Primary toxicityMuscle toxicity (myopathy, rhabdomyolysis) – monitor CPK levels.	Minor amounts of three oxidative metabolites and one unidentified compound have been detected in urine. The site of metabolism has not been identified.	administered intravenously (IV).	100 ml/Kg [healthy adult subjects]	enal excretion (~80% unchanged).	US6468967	2003-09-25 00:00:00	2023-09-25 00:00:00	HMG-CoA reductase inhibitors (statins): Increased risk of myopathy.	Complicated skin and skin structure infections (cSSSI),  Staphylococcus aureus bloodstream infections (bacteremia), including those with right-sided infective endocarditis, caused by methicillin-susceptible and methicillin-resistant isolates	N-decanoyl-L-tryptophyl-Dasparaginyl-L-aspartyl-L-threonylglycyl-L-ornithyl-L-aspartyl-D-alanyl-L-aspartylglycyl-Dseryl-threo-3-methyl-L-glutamyl-3-anthraniloyl-L-alanine ε1-lactone	CUBICIN contains 500000 ug of daptomycin and reconstituted with 0.9% sodium chloride injection. The only inactive ingredient is sodium hydroxide, which is used in minimal quantities for pH adjustment.	CUBICIN is a Sterile, preservative-free, pale yellow to light brown, lyophilized cake containing approx 500000 ug of daptomycin	Intravenous (Intravenous) Injection	CUBICIN 4000 ug/kg should be administered intravenously in 0.9% sodium chloride injection once every 24 h for 7 to 336 h. Staphylococcus aureus Bloodstream Infections (Bacteremia) - CUBICIN 6000 ug/kg should be administered intravenously in 0.9% sodium chloride injection once every 24 h for 2 to 6 weeks.	CUBICIN is contraindicated in patients with known hypersensitivity to daptomycin	fatigue, weakness, rigors, flushing, hypersensitivity, leukocytosis, thrombocytopenia, thrombocytosis, eosinophilia, increased International Normalized Ratio (INR), supraventricular arrhythmia, eczema, abdominal distension, stomatitis, jaundice, increased serum lactate dehydrogenase, hypomagnesemia, increased serum bicarbonate, electrolyte disturbance, myalgia, muscle cramps, muscle weakness, arthralgia, vertigo, mental status change, paresthesia, taste disturbance, eye irritation	http://www.rxlist.com/cubicin-drug.htm http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a7975871-46a6-4e9b-a8b5-38bfcb465f0e
FPDB21346	Th1156	Abarelix	Ac-D-Nal-D-Phe(p-Cl)-D-Pal-Ser-N-Me-Tyr-D-Asn-Leu-Lys(iPr)-Pro-D-Ala-NH₂	48	Hormonal Agents	Anti-Testosterone Agents	IIIc	For palliative treatment of advanced prostate cancer.	Gonadotropin-releasing hormone receptor	1664				1416.063	C72H95ClN14O14	7.5-8.5	0.5	>200	316.8 ± 76.8 h	Synthetic decapeptide antagonist to gonadotropin releasing hormone (GnRH). It is marketed by Praecis Pharmaceuticals as Plenaxis. Praecis announced in June 2006 that it was voluntarily withdrawing the drug from the market.	Used in the palliative treatment of advanced prostate cancer. Abarelix is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis	Abarelix binds to the gonadotropin releasing hormone receptor and acts as a potent inhibitor of gonadotropin secretion	The maximum tolerated dose of abarelix has not been determined. The maximum dose used in clinical studies was 150000 ug. There have been no reports of accidental overdose with abarelix.	In vitro hepatocyte (rat, monkey, human) studies and in vivo studies in rats and monkeys showed that the major metabolites of abarelix were formed via hydrolysis of peptide bonds. No significant oxidative or conjugated metabolites of abarelix were found either in vitro or in vivo.	Following IM administration of 100000 ug, abarelix is absorbed slowly with a mean peak concentration of 0.0434 ug/ml observed approximately 72 h after the injection	Not well characterized (acts locally at mucosal surfaces).	*Mechanism**: Degraded locally by oral enzymes; immune-mediated clearance.  Half-life**: Not applicable (immune tolerance effects persist post-treatment)	US5968895	1996-12-11 00:00:00	2013-12-11 00:00:00	Tacrolimus, Thiothixene, Toremifene, Trimipramine, Voriconazole, Vorinostat, Ziprasidone, Zuclopenthixol- All above drugs cause Additive QTc Prolongation and increases the risk of severe ventricular arrythmias	Plenaxis is indicated for the palliative treatment of men with advanced symptomatic prostate cancer, in whom LHRH agonist therapy is not appropriate and who refuse surgical castration, and have one or more of the following: (1) risk of neurological compromise due to metastases, (2) ureteral or bladder outlet obstruction due to local encroachment or metastatic disease, or (3) severe bone pain from skeletal metastases persisting on narcotic analgesia.	Abarelix is chemically described as acetyl-D-β-naphthylalanyl-D-4-chlorophenylalanyl- D-3-pyridylalanyl-L-seryl-L-N-methyl-tyrosyl-D-asparagyl-L-leucyl-L-N(ε)-isopropyllysyl- L-prolyl-D-alanyl-amide.	The single-dose vial contains 113000 ug of anhydrous free base abarelix peptide (net) supplied in an abarelix CMC complex. This complex also contains 19.1 to 31000 ug of CMC. After the vial is reconstituted with 2.2 ml of 0.9% sodium chloride injection	Abarelix for injectable suspension is supplied as a white to off-white sterile dry powder	Intramuscular Injection	The recommended dose of Plenaxis is 100000 ug administered intramuscularly to the buttock on Day 1, 15, 29 (week 4) and every 4 weeks thereafter.	Plenaxis is not indicated in women or pediatric patients. In addition, Plenaxis may cause fetal harm if administered to a pregnant woman.	Diarrhea, Dizziness, Flushing of Skin, Headache, Constipation, Sleep Disturbance	http://www.rxlist.com/plenaxis-drug.htm
FPDB21347	Th1175	Desirudin	VVYTDCTESGQNLCLCEGSNVCGQGNKCILGSDGEKNQCVTGEGTPKPQSHNDGDFEEIPEEYLQ	65	Unclassified		Ib	Preventing blood clots in patients having hip replacement surgery. It may also be used for other conditions as determined by your doctor. Desirudin is a thrombin inhibitor. It works by blocking the activity of thrombin, which helps to prevent the formation of blood clots.	Thrombin	1725				6963.52	C287H440N80O110 S6	4.04	-0.771		Mean terminal elimination half-life of 2 to 3 h	Desirudin is a direct, highly selective thrombin inhibitor. Reversibly binds to the active thrombin site of free and clot-associated thrombin. Inhibits fibrin formation, activation of coagulation factors V, VII, and XIII, and thrombin-induced platelet aggregation resulting in a dose-dependent prolongation of the activated partial thromboplastin time (aPTT).	The pharmacodynamic effect of desirudin on proteolytic activity of thrombin was assessed as an increase in aPTT. A mean peak aPTT prolongation of about 1.38 times baseline value (range 0.58 to 3.41) was observed following subcutaneous b.i.d. injections of 15000 ug desirudin. Thrombin time (TT) frequently exceeds 0.055556 h even at low plasma concentrations of desirudin, which renders this test unsuitable for routine monitoring of Iprivask therapy. At therapeutic serum concentrations, desirudin has no effect on other enzymes of the hemostatic system such as factors IXa, Xa, kallikrein, plasmin, tissue plasminogen activator, or activated protein C. In addition, it does not display any effect on other serine proteases, such as the digestive enzymes trypsin, chymotrypsin, or on complement activation by the classical or alternative pathways.	Desirudin is a direct inhibitor of free circulating and clot-bound thrombin. The anticoagulant properties of desirudin are demonstrated by its ability to prolong the clotting time of human plasma. One molecule of desirudin binds to one molecule of thrombin and thereby blocks the thrombogenic activity of thrombin. As a result, all thrombin-dependent coagulation assays are affected. Activated partial thromboplastin time (aPTT) is a measure of the anticoagulant activity of desirudin and increases in a dose-dependent fashion.	No toxic effects were observed in rats receiving desirudin at doses up to 100000 ug/kg.	Human and animal data suggest that desirudin is primarily eliminated and metabolized by the kidney. The total urinary excretion of unchanged desirudin amounts to 40 to 50% of the administered dose. Metabolites lacking one or two C-terminal amino acids constitute a minor proportion of the material recovered from urine ( < 7%).	The absorption of desirudin is complete when subcutaneously administered at doses of 300 ug/kg or 500 ug/kg. Following subcutaneous administration of single doses of 0.1 to 750 ug/kg, plasma concentrations of desirudin increased to a maximum level (C max ) between 1 and 3 h. Both C max and area-under-the-curve (AUC) values are dose proportional.	Desirudin is distributed in the extracellular space with a volume of distribution at steady state of 250 ml/kg, independent of the dose.	Total clearance of desirudin is approximately 1.5 to 162 ml/h/kg following either subcutaneous or intravenous administration and is independent of dose.	US2021132088A1	43034		Abciximab may increase the anticoagulant activities of Desirudin; Acenocoumarol may increase the anticoagulant activities of Desirudin; Acetylsalicylic acid may increase the anticoagulant activities of Desirudin; Alteplase may increase the anticoagulant activities of Desirudin; Anistreplase may increase the anticoagulant activities of Desirudin; Apixaban may increase the anticoagulant activities of Desirudin; Chlorotrianisene may decrease the anticoagulant activities of Desirudin; Citric Acid may increase the anticoagulant activities of Desirudin; The risk or severity of adverse effects can be increased when Desirudin is combined with Collagenase; Dabigatran etexilate may increase the anticoagulant activities of Desirudin.						Initial Dosage: In patients undergoing hip replacement surgery, the recommended dose of Iprivask is 15000 ug every 12 h administered by subcutaneous injection with the initial dose given up to 5 to 0.25 h prior to surgery, but after induction of regional block anesthesia, if used	Iprivask is contraindicated in patients with known hypersensitivity to natural or recombinant hirudins due to risk of anaphylaxis, and in patients with active bleeding and/or irreversible coagulation disorders due to risk of hemorrhage.	Spinal/Epidural Hematoma; Hemorrhagic Events; Increased Risk of Bleeding with Renal Impairment; Antibodies/Re-exposure.	http://www.rxlist.com/iprivask-drug.htm; https://www.drugs.com/cdi/desirudin.html DOI:10.1160/TH07-01-0033  https://worldwide.espacenet.com/patent/search?q=pn%3DUS2021132088A1  https://go.drugbank.com/drugs/DB00099
FPDB21348	Th1184	Human calcitonin	MDHYDSQQTNDYMQPEEDWDRDLLLDPAWEKQQRKTFTAWCNSHLRKAGTQIENIEEDFRDGLKLMLLLEVISGERLAKPERGKMRVHKISNVNKALDFIASKGVKLVSIGAEEIVDGNVKMTLGMIWTIILRFAIQDISVEETSAKEGLLLWCQRKTAPYKNVNIQNFHISWKDGLGFCALIHRHRPELIDYGKLRKDDPLTNLNTAFDVAEKYLDIPKMLDAEDIVGTARPDEKAIMTYVSSFYHAFSGAQKAETAANRICKVLAVNQENEQLMEDYEKLASDLLEWIRRTIPWLENRVPENTMHAMQQKLEDFRDYRRLHKPPKVQEKCQLEINFNTLQTKLRLSNRPAFMPSEGRMVSDINNAWGCLEQVEKGYEEWLLNEIRRLERLDHLAEKFRQKASIHEAWTDGKEAMLRQKDYETATLSEIKALLKKHEAFESDLAAHQDRVEQIAAIAQELNELDYYDSPSVNARCQKICDQWDNLGALTQKRREALERTEKLLETIDQLYLEYAKRAAPFNNWMEGAMEDLQDTFIVHTIEEIQGLTTAHEQFKATLPDADKERLAILGIHNEVSKIVQTYHVNMAGTNPYTTITPQEINGKWDHVRQLVPRRDQALTEEHARQQHNERLRKQFGAQANVIGPWIQTKMEEIGRISIEMHGTLEDQLSHLRQYEKSIVNYKPKIDQLEGDHQLIQEALIFDNKHTNYTMEHIRVGWEQLLTTIARTINEVENQILTRDAKGISQEQMNEFRASFNHFDRDHSGTLGPEEFKACLISLGYDIGNDPQGEAEFARIMSIVDPNRLGVVTFQAFIDFMSRETADTDTADQVMASFKILAGDKNYITMDELRRELPPDQAEYCIARMAPYTGPDSVPGALDYMSFSTALYGESDL	892	Unclassified		Ib	Human calcitonin is indicated for the treatment of Paget's disease in the cases where the use of salmon calcitonin may provoke the generation of high-titer of antibodies.3 Paget's disease is a metabolic bone disorder characterized by focal areas of increased and disorganized bone turnover coupled with an increased bone formation. The majority of the cases are asymptomatic but some clinical manifestations include pain, bone deformity and some complications such as pathological fractures and deafness.4 The increased activity in bone is associated with a rise in serum level of alkaline phosphatase and the increased urinary excretion of hydroxyproline which is a product of bone breakdown.2		1765				3417.9	C151H226N40O45S3				Intravenous administration of human calcitonin presents a half-life in the range of 0.17-0.63 h	Calcitonin is a 32-amino acid linear polypeptide hormone that is produced in humans primarily by the parafollicular cells (also known as C-cells) of the thyroid, and in many other animals in the ultimobranchial body. It acts to reduce blood calcium (Ca2+), opposing the effects of parathyroid hormone (PTH). It has been found in fish, reptiles, birds, and mammals. Its importance in humans has not been as well established as its importance in other animals, as its function is usually not significant in the regulation of normal calcium homeostasis. Calcitonin was extracted from the Ultimobranchial glands (thyroid-like glands) of fish, particularly salmon. Salmon calcitonin resembles human calcitonin, but is more active. At present, it is produced either by recombinant DNA technology or by chemical peptide synthesis. The pharmacological properties of the synthetic and recombinant peptides have been demonstrated to be qualitatively and quantitatively equivalent.	Administration of human calcitonin has shown to increase bone calcium content and reduce the levels of serum calcium and serum phosphorus. This calcium inhibition leads to decreases in urinary calcium, magnesium and urine hydroxyproline. Some reports indicate a calcitonin-driven reduction of phosphate plasma concentration which is thought to be related to increased excretion of phosphate. Calcitonin can increase excretion of calcium, phosphate, and sodium. It also is proven to induce the appearance of normal lamellar bone against the diseased trabeculae and a striking decrease in the number of osteoclasts. Bone pain tends to be relieved within a few weeks, and it does not present an important effect on normal bone.3 It is important to point out that human calcitonin is less active than the salmon calcitonin. This characteristic happens because of a high tendency to aggregate, and thus, human calcitonin is used just in cases where the usage of salmon calcitonin generated the formation of antibodies.5 For this reason, the use of human calcitonin is only indicated when there is the appearance of a high-titer of antibodies anti-salmon calcitonin because these antibodies are suggested to cause a relapse.	Calcitonin inhibits osteoclast-mediated bone resorption through the regulation of the number and activity of osteoclasts.1 The action of human calcitonin on osteoclasts is due to a disruption of cytoskeletal organization, by the distraction of actin rings, and due to a disappearance of the cellular polarity of osteoclasts. At the subcellular level, calcitonin is suggested to perform its activity by the modulation of the cAMP-PKA signaling pathway.6		The kidneys account for two-thirds of the metabolism of calcitonin and generate low molecular weight forms. At a subcellular level, it has been observed the metabolic activity of N-acetyl-beta-glucosaminidase, alanyl aminopeptidase, and phosphoglucomutase.1			The metabolic clearance rate is in the range of 360-540 ml/h.kg while the secretion rate is 0.059 ug/dl.kg for men and 0.022 ug/dl.kg for women.9 The total renal clearance of human calcitonin is 117.6 ml/h. The renal clearance exceeds the glomerular filtration rate which indicates a filtration-independent removal	KR100284038*	36874											Human calcitonin: Uses, Interactions, Mechanism of Action | DrugBank Online
FPDB21349	Th1234	Protamine sulfate	PRRRRSSSRPVRRRRRPRVSRRRRRRGGRRRR	32	Heparin Antagonists	Heparin Antagonists, Hematologic Agents	Ib	Protamine sulfate is usually administered to reverse the large dose of heparin administered during certain surgeries, especially heart surgery.		1846				4249.98	C167H319N95O37	12.15 (Salmon Protamine)	2.13	219.8°C (Sulfate Crystals)	Without heparin in healthy individuals: Median 0.123333 h. With heparin: Median 0.075 h.	Protamine sulfate is a drug that reverses the anticoagulant effects of heparin by binding to it. It was originally isolated from the sperm of salmon and other species of fish but is now produced primarily through recombinant biotechnology. Protamine sulfate was approved for medical use in the United States in 1969. Protamine sulfate (protamine (protamines) s) occurs as fine white or off-white amorphous or crystalline powder. It is sparingly soluble in water. The pH is between 6 and 7. The cationic hydrogenated protamine at a pH of 6.8 to 7.1 reacts with anionic heparin at a pH of 5.0 to 7.5 to form an inactive complex.	Protamine sulphate 1% demonstrates activity neutralising anticoagulant properties of heparin, creating the complex heparin/protamine. Activity of protamine (towards heparin) takes place within five minutes after intravenous injection of the preparation.	It is a highly cationic peptide that binds to either heparin or low molecular weight heparin (LMWH) to form a stable ion pair, which does not have anticoagulant activity. The ionic complex is then removed and broken down by the reticuloendothelial system. In large doses, protamine sulfate may also have an independent—however weak—anticoagulant effect.	Administration of protamine sulfate intravenously could result in severe drop in blood pressure, dyspnea, bradycardia, pulmonary hypertension and anaphylaxis. Systemic hypertension, nausea, vomiting and lassitude were also reported. Overdosage of this drug may theoretically result in hemorrhage.	Metabolic fate of the protamine-heparin complex has not been elucidated; however, protamine-heparin complex may be partially metabolized or attacked by fibrinolysin, freeing heparin.	After IV adminsteration, protamine sulfate takes less than 0.083333 h. to neutralize heparin.	12300 ml	Clearance is: 132000 ml/h	US10684286	2020-06-16 00:00:00	2037-06-16 00:00:00		Protamine Sulfate (protamine (protamines) s) Injection, USP is indicated in the treatment of heparin overdosage.		Protamine sulfate 10000 ug, sodium chloride 9000 ug and Water for Injection q.s. Sulfuric acid and/or dibasic sodium phosphate (heptahydrate) may have been added for pH adjustment.	off-white amorphous or crystalline powder	Intravenous	Protamine Sulfate (protamine (protamines) s) Injection,USP should be given by very slow intravenous injection in doses not to exceed 50000 ug of protamine sulfate (protamine (protamines) s) in any 10-minute period	Protamine sulfate (protamine (protamines) s) is contraindicated in patients who have shown previous intolerance to the drug.	Intravenous injections of protamine (protamines) may cause a sudden fall in blood pressure, bradycardia, pulmonary hypertension, dyspnea, or transitory flushing and a feeling of warmth. There have been reports of anaphylaxis that resulted in respiratory embarrassment	http://www.rxlist.com/protamine-drug.htm
FPDB21350	Th1027	Insulin Regular	A-chain:GIVEQCCTSICSLYQLENYCN B-chain:FVNQHLCGSHLVEALYLVCGERGFFYTPKT	63	Antidiabetic Agents	Antidiabetic Agents	Ia	Indicated as an adjunct to diet and exercise to improve glycemic control in adults and children with type 1 and type 2 diabetes mellitus.	Insulin receptor,Insulin-like growth factor 1 receptor,Retinoblastoma-associated protein,Cathepsin D,Insulin-degrading enzyme,Neuroendocrine convertase 2,Carboxypeptidase E,Neuroendocrine convertase 1,Protein NOV homolog,Low-density lipoprotein receptor-r	1205				5808	C257H383N65O77S6	5.39	0.218	81		Insulin regular is a 51 residue peptide hormone, composed of two amino acid chains covalently linked by disulfide bonds. The structure is identical to native human insulin. Recombinant insulin is synthesized by recombinant DNA techncology. Inserting the human insulin gene into the Escherichia coli bacteria or Saccharomyces cerevisiae produces insulin for human use.	Insulin regular is a short-acting insulin. When subcutaneously administered, the onset of action (as evidenced by a decrease in glucose level) occurs 0.5 h post-dose. Maximal effect occurs between 1.5 and 3.5 h post-dose. The glucose-lowering effect occurs 8 h post-dose. Compared to other rapid-acting insulin analogs, insulin regular has a slower onset of action and longer duration of action.	The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty  acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism.	Hypoglycemia is caused due to insulin toxicity.	Predominantly cleared by metabolic degradation via a receptor-mediated process.	Generally well absorbed.	150 ml/kg					Liraglutide's coadministration may increase the risk of hypoglycemia. A lower dose of the antidiabetic agent may be needed.	Treating diabetes mellitus.Used for the treatment of patients with diabetes mellitus, for the control of hyperglycemia		It contains human insulin (rDNA origin) 100 units/mL, glycerin 16000 ug/ml and metacresol 2500 ug/ml, endogenous zinc (approximately 15 ug/100 units) and water for injection. The pH is 7.0 to 7.8. Sodiumhydroxide and/or hydrochloric acid may be added durin，It contains human insulin (rDNA origin) 100 units/mL, glycerol 16000 ug/ml, metacresol 3000 ug/ml, zinc chloride approximately 7 ug/ml and water for injection. The pH is adjusted to 7.4. Hydrochloric acid 2N or sodium hydroxide 2N may be added to adjust pH. No	Sterile, clear, aqueous, and colorless solution	SubcutSubcutaneous and Intravenous infusionaneous Injection in the abdominal wall, the thigh, the gluteal region or in the upper arm and Intravenous administration of Humulin R (insulin (human recombinant)) U-100 is possible under medical supervision.	Humulin R (insulin (human recombinant)) U-100, when used subcutaneously, is usually given three or more times daily before meals. The average range of total daily insulin requirement for maintenance therapy in insulin-treated patients without severe insulin resistance lies between 0.5 and 1 unit/kg/day. The injection of Novolin R (recombinant dna origin) should be followed by a meal within approximately 0.5 h of administration The average range of total daily insulin requirement for maintenance therapy in insulin-treated patients lies between 0.5 and 1.0 IU/kg.	During episodes of hypoglycemia and in patients hypersensitive to humulin R.During episodes of hypoglycemia and in patients with hypersensitivity to Novolin R	Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; wheezing; muscle pain; changes in vision; chills; confusion; dizziness; drowsiness; fainting; fast or irregular heartbeat; headache; loss of apetite.Hypoglycemia, or low blood sugar, is the most common side effect. Symptoms include headache, hunger, dizziness, sweating, irritability, trouble concentrating, rapid breathing, fast heartbeat, fainting, or seizure (severe hypoglycemia can be fatal).	http://www.drugs.com/cdi/humulin-r.html
FPDB21351	Th1035|||P01275	Glucagon recombinant|||Human GCG	HSQGTFTSDYSKYLDSRRAQDFVQWLMNT	29	Antidiabetic Agents	Hypoglycemic Agents	IV|||Endogenous hormones (non-drug)	Used to treat severe hypoglycemia, also used in gastrointestinal imaging.|||Endogenous glycemic regulation	Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor|||GCG receptors	1252				3767.1|||3482.79	C165H249N49O51S1|||C153H225N43O49S	9.52|||7.4	-1.197|||-0.5		0.05-0.1 h	Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons.|||Endogenous glycemic regulation	Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract.|||GLP-1R (EC50, nM)：NA；GCGR (EC50, nM)：NA; GIPR (EC50, nM)：0.106.	Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion|||Activates GCG receptors → CAMP→ promotes hepatic glycogen production		Hepatic/renal metabolism		250 ml/kg	810 ml/h/kg [Adults with IV 1000 ug]				Walfarin- Glucagon may increase the anticoagulant effect of warfarin (Coumadin) and other anticoagulants causing an increase in the slow clotting of blood and a greater risk of developing an episode of bleeding.Indomethacin (Indocin, Indocin-SR) reduces the effect of glucagon.	GlucaGen is used to treat severe hypoglycemic (low blood sugar) reactions which may occur in patients with diabetes mellitus treated with insulin. It is also used as a diagniostic aid. GlucaGen is indicated for use during radiologic examinations to tempor，Glucagon is used to increase the blood glucose level in severe hypoglycemia (low blood glucose). Glucagon is a glucose-elevating drug	glucagon	The reconstituted solution contains glucagon as hydrochloride 1000 ug/ml (1 unit/mL) and lactose monohydrate (107000 ug). GlucaGen is supplied at pH 2.5-3.5 and is soluble in water.Glucagon is available as an emergency kit. The kit contains freeze-dried glucagon as a powder for injection 1 ml syringe of diluent. The powder contains 1000 ug (1 unit) of glucagon and 49000 ug of lactose. The diluent contains 12000 ug/ml of glycerine, water for	Sterile, lyophilized white powder，Powder|||Glucose-dependent insulinotropic polypeptide	Subcutaneous, intramuSubcutaneousular, or Intravenous infusion，Subcutaneously or intramuSubcutaneousularly Injection	Inject 1 ml (adults and children, weighing more than 55 lbs (25 kg)) or 0.5 ml (children weighing less than 55 lbs (25 kg)) subcutaneously, intramuscularly, or intravenously. If the weight is not known: children younger than 6 years should be given a 0.5 ，Adults and children weighing 44 pounds or more should receive 1000 ug (1 unit) of glucagon	Hypersensitivity，Pheochromocytoma，Insulinoma，Allergy	Severe side effects are very rare, although nausea and vomiting may occur occasionally especially with doses above 1000 ug or with rapid injection (less than 1 minute). You may also have rapid heart beat for a short while. Nausea and vomiting may occur occasionally after injection of glucagon, but this may be a symptom of the hypoglycemia for which glucagon is being given. Rare allergic-type reactions may occur with glucagon including itching, respiratory distress, or low blood pressure.	http://www.novonordisk.co.in/documents/article_page/document/Glucagen.asp|||https://m.chem960.com/offer/1219580/
FPDB21352	Th1040	Insulin Lispro	A chain:GIVEQCCTSICSLYQLENYCN;B chain:FVNQHLCGSHLVEALYLVCGERGFFYTKPT	63	Antidiabetic Agents	Hypoglycemic Agents，Antidiabetic Agents	Ia	To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump.	Insulin receptor,Insulin-like growth factor 1 receptor	1275				5808	C257H387N65O76S6	5.39	0.218	81	On subcutaneous administration = 1 h	Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996.	Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 0.166667-0.25 h. Its activity peaks 1 h following subcutaneous injection and its duration of action is 4-5 h. Compared to regular human insulin, insulin lispro  has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis.	Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic  to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties.	Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat	Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process.	Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 0.5-1.5 h after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft	When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 720 ml/kg, respectively).	Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 1260 ml/h/kg and 576 ml/h/kg respectively.	US5474978，US5514646，CA2151564，CA2151560	1994-06-16 00:00:00	2014-06-16 00:00:00	The beta-blocker, acebutolol, atenolol, bisoprolol, carvedilol, may decrease symptoms of hypoglycemia.Concomitant therapy with drugs like Dextropropoxyphene, Pentoxifylline, Pramlintide, Fluoxetine, Fenofibrate and Disopyramide that may increase the blood-glucose-lowering effect of insulin lispro ，Concomitant therapy with ACE inhibitors like Enalapril and Ramipril may increase the blood-glucose-lowering effect of insulin lispro and thus the chance of hypoglycemia should be monitored closely.Concomitant therapy with diuretics like Hydrochlorothiazide  may reduce the blood-glucose-lowering effect of insulin lispro.Concomitant therapy with somatostatin analogs like Octreotide may increase the blood-glucose-lowering effect of insulin lispro and thus the chance of hypoglycemia should be monitored closely.The beta-blocker, esmolol, may decrease symptoms of hypoglycemia.Concomitant therapy with sympathomimetic agents like Epinephrine may reduce the blood-glucose-lowering effect of insulin lispro.	Humalog is used to treat type 1 diabetes in adults. It is usually given together with another long-acting insulin. Humalog is also used together with oral medications to treat type 2 diabetes in adults.Insulin lispro is used to treat type 1 diabetes in adults. It is usually given together with another long-acting insulin. Insulin lispro is also used together with oral medication to treat type 2 diabetes in adults.		Each milliliter of HUMALOG contains insulin lispro 100 units, 16000 ug glycerin, 1880 ug dibasic sodium phosphate, 3150 ug Metacresol, zinc oxide content adjusted to provide 19.7 ug zinc ion, trace amounts of phenol, and Water for Injection. Insulin lispro	Sterile, aqueous, clear, and colorless solution，Solution	Subcutaneous and Intravenous infusion，Subcutaneous injection	The total daily insulin requirement may vary and is usually between 0.5 to 1 unit/kg/day. Insulin requirements may be altered during stress, major illness, or with changes in exercise, meal patterns, or coadministered drugs. Usual maintenance range is 0.5-1 unit/kg/day in divided doses; nonobese may require 0.4-0.6 unit/kg/day; obese may require 0.8-1.2 units/kg/day.Insulin lispro can be administered intravenously under medical supervision at concentrations from 0.1 unit/mL to 1 unit/mL in infusion systems containing 0.9% sodium chloride. Blood glucose and potassium levels should be closely monitored to avoid hypoglycemia.	During episodes of hypoglycemia in patients who are hypersensitive to HUMALOG or to any of its excipients.	Low blood sugar--headache, hunger, weakness, sweating, confusion, irritability, dizziness, fast heart rate, or feeling jittery.Low blood sugar is the most common side effect. There are many causes of low blood sugar, including taking too much Humalog. Severe life-threatening allergic reactions (whole-body reactions) can happen.Reactions at the injection site (local allergic reaction.	http://pi.lilly.com/us/humalog-pen-pi.pdf
FPDB21353	Th1041	Insulin Glargine	A-chain:GIVEQCCTSICSLYQLENYCG;B-chain:FVNQHLCGSHLVEALYLVCGERGFFYTPKTRR	65	Antidiabetic Agents	Hypoglycemic Agents，Antidiabetic Agents	Ia	To treat Type 1 or 2 diabetes mellitus in patients over 17 years old who require a long-acting (basal) insulin for the control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for glycemic control.	Insulin receptor,Insulin-like growth factor 1 receptor	1283				6063	C267H404N72O78S6	6.88	0.098	81	Not reported in humans; 30 h in mammalian reticulocytes.	Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12). It is an analogue of human insulin made by replacing the asparagine residue at position A21 of the A-chain with glycine and adding two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4. Small amounts of insulin glargine are slowly released from microprecipitates giving the drug a long duration of action (up to 24 h) and no pronounced peak concentration.	Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 0.166667-0.25 h. Its activity peaks 1 h following subcutaneous injection and its duration of action is 4-5 h. Compared to regular human insulin, insulin lispro  has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis.	Insulin glargine binds to the insulin receptor, a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 h with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body.	Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat	Partly metabolized to two active metabolites with similar in vitro activity to insulin: A21-Gly-insulin and A21-Gly-des-B30-Thr-insulin.	Due to the modifications in the A and B chain, the isoelectric point shifts towards a neutral pH and insulin glargine is more stable in acidic conditions than regular insulin. As insulin glargine is less soluble at neutral pH, once injected, forms micro-p			US7476652，US6100376，CA1339044	1/23/2004	1/23/2024	Somatropin may antagonize the hypoglycemic effect of insulin glargine. Monitor for changes in fasting and postprandial blood sugars.The beta-blocker, Timolol, Sotalol, Propranolol, Practolol, Acebutolol, Atenolol, Betaxolol, Bevantolol, Bisoprolol, Carteolol, Carvedilol, Esmolol	Its used to improve glycemic control in adults and children with type 1 diabetes mellitus and in adults with type 2 diabetes mellitus.Its used to reduce high blood sugar in adults, adolescents and children of 6 years or above with diabetes mellitus.It works by helping your body to use sugar properly. This lowers the amount of glucose in the blood, which helps to treat diabetes.	21A-Gly-30Ba-L-Arg-30Bb-L-Arg-human insulin	LANTUS consists of insulin glargine dissolved in a clear aqueous fluid. Each milliliter of LANTUS contains 100 Units (3637.8 ug) insulin glargine. The 10 ml vial presentation contains the following inactive ingredients per mL: 30 ug zinc, 2700 ug m-cresol	Solution	Subcutaneous Injection	LANTUS may be administered at any time during the day. LANTUS should be administered subcutaneously once a day at the same time every day. The dose of LANTUS must be individualized based on clinical response.Patients need one injection of Lantus every day, at the same time of the day. In children, only evening injection has been studied.OptiSet delivers insulin in increments of 2 units up to a maximum single dose of 40 units. The dosage may vary from person tto person.	Hypersensitivity	Low blood sugar (headache, hunger, weakness, sweating, confusion, irritability, dizziness, fast heart rate, or feeling jittery). Sign of insulin allergy include itching skin rash over the entire body, wheezing, trouble breathing, fast heart rate, sweating.Hypoglycemia, skin changes at the injection site, allergic reactions, large-scale skin reactions (rash and itching all over the body), severe swelling of skin or mucous membranes (angio-oedema), shortness of breath, a fall in blood pressure with rapid headache.Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); changes in vision; chills; confusion; dizziness; drowsiness; fainting; fast heartbeat; fast, shallow breathing.	http://www.lantus.com
FPDB21354	Th1052	Eptifibatide	Mpr-Har-Gly-Asp-Trp-Pro-Cys-NH2.	23	Platelet Aggregation Inhibitors	Platelet Aggregation Inhibitors		For treatment of myocardial infarction and acute coronary syndrome.	Lutropin-choriogonadotropic hormone receptor,Follicle-stimulating hormone receptor	1363				831.962	C35H49N11O9S2		-2.3		Mean terminal half-life 29 ± 6 h (initial half-life is 4.5± 0.5 h)	Synthetic cyclic hexapeptide that binds to platelet receptor glycoprotein and inhibits platelet aggregation.	Eptifibatide is an anti-coagulant that selectively blocks the platelet glycoprotein IIb/IIIa receptor. Eptifibatide is a cyclic heptapeptide derived from a protein found in the venom of the southeastern pygmy rattlesnake (Sistrurus miliarus barbouri). It belongs to the class of the so called arginin-glycin-aspartat-mimetics and reversibly binds to platelets.	Eptifibatide inhibits platelet aggregation by reversibly binding to the platelet receptor glycoprotein (GP) IIb/IIIa of human platelets, thus preventing the binding of fibrinogen, von Willebrand factor, and other adhesive ligands. Inhibition of platelet aggregation occurs in a dose- and concentration-dependent manner.	Eptifibatide was not lethal to rats, rabbits, or monkeys when administered by continuous Intravenous infusion for 1.5 h at a total dose of 45000 ug/kg (about 2 to 5 times the recommended maximum daily human dose on a body surface area basis).	No major metabolites have been detected in human plasma. Deamidated eptifibatide and other, more polar metabolites have been detected in urine.	The mean absolute bioavailability following a single subcutaneous injection to healthy female volunteers is about 40%.		55 ml/kg/h [patients with coronary artery disease]，56 ml/kg/h [patients with coronary artery disease]	US6706681，US5767251	2005-03-17 00:00:00	2025-03-17 00:00:00		Acute Coronary Syndrome (ACS), Percutaneous Coronary Intervention (PCI)	N6-(aminoiminomethyl)-N2-(3-mercapto-1-oxopropyl)-Llysylglycyl-L-α-aspartyl-L-tryptophyl-L-prolyl-L-cysteinamide, cyclic (1→6)-disulfide.	Each 10-mL vial contains 2000 ug/ml of INTEGRILIN and each 100-mL vial contains either 750 ug/ml of INTEGRILIN or 2000 ug/ml of INTEGRILIN. Each vial of either size also contains 5250 ug/ml citric acid and sodium hydroxide to adjust the pH to 5.35.	INTEGRILIN Injection is a clear, colorless, Sterile, non-pyrogenic solution  of Eptifibatide	Injection Solution for Intravenous Use	Dosage in Acute Coronary Syndrome (ACS): 180 ug/kg intravenous (IV) bolus as soon as possible after diagnosis, followed by continuous infusion of 2 ug/kg/min Dosage in 180 ug/kg IV bolus immediately before PCI followed by continuous infusion of 2 ug/kg/min and a second bolus of 180 ug/kg (given 0.166667 h after the first bolus).	1. Severe hypertension (systolic blood pressure > 200 mm Hg or diastolic blood pressure > 110 mm Hg) not adequately controlled onantihypertensive therapy.  2. History of stroke within 720 h or any history of hemorrhagic stroke. 3. Current or planned administration of another parenteral GP IIb/IIIa inhibitor. 4.Hypersensitivity to INTEGRILIN or any component of the product (hypersensitivity reactions that occurred included anaphylaxis and urticaria).	Bleeding, Intracranial Hemorrhage and Stroke, Immunogenicity/Thrombocytopenia.	Guojie Ho, Antoinette Paone, Luciano Forni, Catherine De Tollenaere, Brice Bonnet, Christine Devijver, “Processes for preparing eptifibatide.” U.S. Patent US20060036071, issued February 16, 2006.
FPDB21355	Th1056	Vasopressin	CYFQNCPRG	9	Antidiuretic Agents	Antidiuretic Agents	Ib	For the treatment of enuresis, polyuria, diabetes insipidus, polydipsia and oesophageal varices with bleeding	Vasopressin V2 receptor,Vasopressin V1a receptor,Vasopressin V1b receptor	1375				1050.215	C43H67N15O12S2		-4.9		0.166667-0.333333 h	Antidiuretic hormone, also known as vasopressin, is a nine amino acid peptide secreted from the posterior pituitary. Antidiuretic hormone binds to receptors in the distal or collecting tubules of the kidney and promotes reabsorbtion of water back into the circulation.	Vasopressin is an antidiuretic hormone indicated for the prevention and treatment of postoperative abdominal distention, in abdominal roentgenography to dispel interfering gas shadows, and in diabetes insipidus. Vasopressin can cause contraction of smooth muscle of the gastrointestinal tract and of all parts of the vascular bed, especially the capillaries, small arterioles and venules. It has less effect on the smooth musculature of the large veins. Vasopressin may also be used to control bleeding in some forms of von Willebrand disease and to treat extreme cases of bed wetting in children. It may also play a role in memory formation although the mechanism is unknown.	Vasopressin acts on three different receptors, vasopressin receptor V1a (which initiates vasoconstriction, liver gluconeogenesis, platelet aggregation and release of factor VIII), vasopressin receptor V1b (which mediates corticotrophin secretion from the pituitary) and vasopressin receptor V2 which controls free water reabsorption in the renal medullar. The binding of vasopressin to the V2 receptor activates adenylate cyclase which causes the release of aquaporin 2 channels into the cells lining the renal medullar duct. This allows water to be reabsorbed down an osmotic gradient so the urine is more concentrated.		The majority of a dose of vasopressin is metabolized and rapidly destroyed in the liver and kidneys.								Vasopressin is indicated for prevention and treatment of postoperative abdominal distention, in abdominal roentgenography to dispel interfering gas shadows, and in diabetes insipidus.		Vasopressin 20 units, Sodium Chloride 9000 ug, Chlorobutanol 0.5% (as a preservative), Water for Injection q.s. pH (range 2.5 - 4.5) adjusted with Acetic Acid.	Vasopressin Injection, USP is a Sterile, aqueous solution of synthetic vasopressin (8-L-arginine vasopressin) of the posterior pituitary gland	intramuSubcutaneousular or Subcutaneous use	For Abdominal Distention, Abdominal Roentgenography, Diabetes Insipidus: Ten units of vassopressin (0.5 ml) will usually elicit full physiologic response in adult patients.	Anaphylaxis or hypersensitivity to the drug or its components.	anaphylaxia (cardiac arrest), circumoral pallor, arrhythmias, decreased cardiac output, angina, myocardial ischemia, peripheral vasoconstruction and gangrene, nausea, vomiting, tremor, vertigo, bronchial constriction	http://www.rxlist.com/pitressin-drug.ht http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=812240e4-fc28-46c2-92f3-1ba4e029645a
FPDB21356	Th1060	Insulin, porcine	A chain: GIVEQCCTSICSLYQLENYCN; B chain: FVNQHLCGSHLVEALYLVCGERGFFYTPKT	63	Antidiabetic Agents	Hypoglycemic Agents	Ia	For the treatment of type I and II diabetes mellitus.	Interferon alpha/beta receptor 2,Interferon alpha/beta receptor 1，Hyaluronan,Transforming growth factor beta-1	1382				5795.6	C257H387N65O76S6	5.39	0.298			Insulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure.	Insulin is used in the treatment of type I and type II diabetes. The primary activity of insulin is the regulation of glucose metabolism. In muscle and other tissues (except the brain), insulin causes rapid transport of glucose and amino acids intracellularly. It also promotes anabolism, and inhibits protein catabolism. In the liver, insulin promotes the uptake and storage of glucose in the form of glycogen, inhibits gluconeogenesis, and promotes the conversion of excess glucose into fat.	Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism.		Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process.								vetsulin (porcine insulin zinc suspension) is indicated for the reduction of hyperglycemia and hyperglycemia-associated clinical signs in dogs and cats with diabetes mellitus		purified porcine insulin 40 IU (35% amorphous and 65% crystalline), Zinc (as chloride) 80 ug, Sodium acetate trihydrate 1360 ug, Sodium chloride 7000 ug, Methylparaben (preservative) 1000 ug, pH is adjusted with hydrochloric acid and/or sodium hydroxide.	Vetsulin is supplied as a sterile injectable suspension in multidose vials containing 10 ml of 40 IU/mL porcine insulin zinc suspension. Vials are supplied in cartons of one, 10 ml vial.	Subcutaneous Injection	In dogs: The initial recommended vetsulin dose is 0.5 IU insulin/kg body weight. Initially, this dose should be given once daily concurrently with, or right after a meal; In Cats:The initial recommended dose in cats is 1 to 2 IU per injection. The injections should be given twice daily at approximately 12 h intervals.	Dogs and cats known to have a systemic allergy to pork or pork products should not be treated with vetsulin. vetsulin is contraindicated during periods of hypoglycemia.	In dogs: Clinical signs of hypoglycemia were generally mild in nature (described as weakness, lethargy, stumbling, falling down, and/or depression, hematuria, vomiting, diarrhea, pancreatitis, non-specific hepatopathy/pancreatitis, development of cataracts, and urinary tract infections.   In Cats: omiting, lethargy, diarrhea, decreased appetite/anorexia, pancreatitis, dermal events, respiratory disease, urinary tract disorder, renal disease, dehydration, weight loss, polydipsia, polyuria, behavioral change, and ocular discharge/conjunctivitis.	http://dailymed.nlm.nih.gov/dailymed/archives/fdaDrugInfo.cfm?archiveid=101642
FPDB21357	Th1077	Urofollitropin	Alpha chain:APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS Beta chain: NSCELTNITIAIEKEECRFCISINTTWCAGYCYTRDLVYKDPARPKIQKTCTFKELVYETVRVPGCAHHADSLYTYPVATQCHCGKCDSDSTDCTVRGLGPSYCSFGEMKE	222	Fertility Agents	Fertility Agents	Ib	For treatment of female infertility	Glutamate carboxypeptidase 2	1439				980.162	C42H65N11O12S2	7.5	-0.33	55	Circulation half life of 3-4 h, elimination half life of 35-40 h	Urofollitropin is a purified form of follicle-stimulating hormone (FSH) that is manufactured by extraction from human urine and then purified. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF).	Urofollitropin or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of urofollitropin is the primary hormone responsible for follicular recruitment and development.	FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells.			74%，174%，274%			US5767067	1999-06-17 00:00:00	2019-06-17 00:00:00		BRAVELLE (urofollitropin for injection, purified) is a gonadotropin indicated for Induction of ovulation in women who have previously received pituitary suppression – intramuscular and subcutaneous administration, Development of multiple follicles as part of an Assisted Reproductive Technology (ART) cycle in ovulatory women who have previously received pituitary suppression，Metrodin (urofollitropin for injection) and hCG given in a sequential manner are indicated for the stimulation of follicular development and the induction ofovulation in patients with polycystic ovary syndrome, and infertility, who have failed to respond or conceive following adequate clomiphene citrate therapy. Metrodin (urofollitropin for injection) and hCG may also be used to stimulate the development of multiple follicles in ovulatory patients undergoing Assisted Reproductive Technologies (ART) such as in vitro fertilization.FertinexTM (urofollitropin for injection, purified) and hCG given in a sequential manner are indicated for the stimulation of follicular recruitment and development and the induction of ovulation in patients with polycystic ovary syndrome and infertility, who have failed to respond or conceive following adequate clomiphene citrate therapy. Fertinex (urofollitropin) TM and hCG may also be used to stimulate the development of multiple follicles in ovulatory patients undergoing Assisted Reproductive Technologies (ART) such as in vitro fertilization.		Each vial of BRAVELLE contains 82.5 International Units (IU) of Follicle Stimulating Hormone (FSH) activity, 23000 ug Lactose Monohydrate, 5 ug Polysorbate 20, and Sodium Phosphate buffer (Sodium Phosphate dibasic, Heptahydrate and Phosphoric acid) for pH adjustments, which, when reconstituted with diluent, will deliver 75 International Units of FSH. BRAVELLE contains up to 2% luteinizing hormone (LH) activity based on bioassay. Human Chorionic Gonadotropin(hCG) is not detected in BRAVELLE. When stored at 3° to 25, up to 40% of the α-subunits may be oxidized.Each ampule of Metrodin (urofollitropin for injection) contains 75 or 150 IU of follicle-stimulating hormone (FSH) activity, in not more than 830 ug (75 IU) or 1660 ug (150 IU) of extract, plus 10000 ug lactose ，Each ampule of Fertinex (urofollitropin) TM contains either 75 IU or 150 IU of highly purified FSH and 10000 ug lactose. If required, pH is adjusted with 100000 uM hydrochloric acid and/or 100000 uM sodium hydroxide.	BRAVELLE is a sterile, lyophilized powder used after reconstitution with Sterile 0.9% Sodium Chloride Injection, USP，Metrodin (urofollitropin for injection) is a sterile, lypholized powder form contains an acidic, water soluble glycoprotein biologically standardized for FSH gonadotropin activity，Fertinex (urofollitropin) in asterile, lyophilized powder form contains an acidic, water soluble glycoprotein biologically standardized for FSH gonadotropin activity	IntramuSubcutaneousular and Subcutaneous administration ，IntramuSubcutaneousular Injection.Subcutaneous Injection.	Initial starting 150 International Units per day for 120 h, administered subcutaneously or intramuscularly in case of ovulation induction. In case of Assisted Reproductive Technology (ART) initial starting dose of the first cycle – 225 International Units per day for 120 h, administered subcutaneously.Initial starting 75 International Units per day for 120 h administered intramuscularly in polycystic ovary syndrome. In ART the dose is 150 IU per day.Initial starting 75 International Units per day for 120 h administered intramuscularly in polycystic ovary syndrome. In ART the dose is 150 IU per day.	RAVELLE is contraindicated in women who exhibits Prior hypersensitivity to BRAVELLE or urofollitropins, High levels of FSH indicating primary ovarian failure, Pregnancy, Presence of uncontrolled non-gonadal endocrinopathies, Sex hormone dependent tumors of the reproductive tract and accessory organ, Tumors of pituitary gland or hypothalamus, Abnormal uterine bleeding of undetermined origin, Ovarian cysts or enlargement of undetermined origin, not due to polycystic ovary syndrome.contraindicated in High levels of FSH indicating primary ovarian failure,  Uncontrolled thyroid or adrenal dysfunction, An organic intracranial lesion such as a pituitary tumor, The presence of any cause of infertility other than anovulation, as stated in the Indications unless they are candidates for Assisted Reproductive Technologies, Abnormal bleeding of undetermined origin, Ovarian cysts or enlargement of undetermined origin, Prior hypersensitivity to urofollitropin.contraindicated in High levels of FSH indicating primary ovarian failure,  Uncontrolled thyroid or adrenal dysfunction, An organic intracranial lesion such as a pituitary tumor, The presence of any cause of infertility other than anovulation, as stated in the Indications unless they are candidates for Assisted Reproductive Technologies, Abnormal bleeding of undetermined origin, Ovarian cysts or enlargement of undetermined origin, Prior hypersensitivity to urofollitropin.	The most common adverse reactions (≥5% incidence) in ovulation induction include: headache, hot flashes, OHSS, pain, and respiratory disorder. The most common adverse reactions (≥2% incidence) in ART include: abdominal cramps, abdominal fullness/enlargement, headache, nausea, OHSS, pain, pelvic pain, and post retrieval pain.Pulmonary and vascular complications,  Ovarian Hyperstimulation Syndrome,  Adnexal torsion,  Mild to moderate ovarian enlargement, Abdominal pain, Ovarian cysts, nausea, vomiting, diarrhea, abdominal cramps, bloating, Pain, rash, swelling, and/or irritation at the site of injection, Ectopic pregnancy, Congenital abnormalities, dry skin, body rash, hair loss, hives, Headache.Pulmonary and vascular complications,  Ovarian Hyperstimulation Syndrome,  Adnexal torsion,  Mild to moderate ovarian enlargement, Abdominal pain, Ovarian cysts, nausea, vomiting, diarrhea, abdominal cramps, bloating, Pain, rash, swelling, and/or irritation at the site of injection, Ectopic pregnancy, Congenital abnormalities, dry skin, body rash, hair loss, hives, Headache.	http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9bb87daf-d156-504e-adaf-4c21383f8d16 http://www.rxlist.com/bravelle-drug.htm
FPDB21358	Th1087	Oxytocin	CYIQNCPLG	9	Oxytocics & Labor Induction Agents	Oxytocics, Anti-tocolytic Agents and Labor Induction Agents	Ib	To assist in labor, elective labor induction, uterine contraction induction	Globotriaosylceramide，Interferon alpha/beta receptor 2,Interferon alpha/beta receptor 1	1460				1007.187	C43H66N12O12S2	5.51	-2.7		0.016667-0.1 h	9-residue cyclic peptide, synthetically prepared to avert possible contamination with vasopressin and small polypeptides	Used to induce labor or to enhance uterine contractions during labor. Uterine motility depends on the formation of the contractile protein actomyosin under the influence of the Ca2+-dependent phosphorylating enzyme myosin light-chain kinase. Oxytocin promotes contractions by increasing the intracellular Ca2+, which in turn activates myosins light chain kinase.. Oxytocin has specific receptors in the muscle llining of the uterus and the receptor concentration increases greatly during pregnancy, reaching a maximum in early labor at term.	Binds the oxytocin receptor which leads to an increase in intracellular calcium levels. The oxytocin-oxytocin receptor system plays an important role as an inducer of uterine contractions during parturition and of milk ejection.		hepatic oxytocinases								Induction or Stimulation of Labor, Control of Postpartum Uterine Bleeding, Treatment of Incomplete, Inevitable, or Elective Abortion			Pitocin (oxytocin injection, USP) is a sterile, clear, colorless aqueous solution of synthetic oxytocin, for Intravenous infusion or intramuscular injection. Pitocin is a nonapeptide found in pituitary extracts from mammals. It is standardized to contain 10 units of oxytocic hormone/mL and contains 0.5% Chlorobutanol, a chloroform derivative as a preservative, with the pH adjusted with acetic acid. Pitocin may contain up to 16% of total impurities. The hormone is prepared synthetically to avoid possible contamination with vasopressin (ADH) and other small polypeptides with biologic activity	Intravenous infusion	initial dose should be 0.5–1 mU/min (equal to 3–6 ml of the dilute oxytocin solution per hour). At 30–60 minute intervals the dose should be gradually increased in increments of 1–2 mU/min until the desired contraction pattern has been established.	Do NOT use Pitocin if: you are allergic to any ingredient in Pitocin; your birth canal is too small compared with the fetus's head; you have other complications that require medical intervention for birth; you have bacteria in the blood; you cannot have a child through vaginal delivery because of certain conditions (eg, genital herpes, cervical cancer)	Symptoms of overdose: Restlessness, shakiness, sleepiness, slow to respond, slurred speech, unconsciousness.	http://www.drugs.com/cdi/pitocin.html http://www.rxlist.com/pitocin-drug/indications-dosage.htm
FPDB21359	Th1088	Enfuvirtide	YTSLIHSLIEESQNQQEKNEQELLELDKWASLWNWF	36	HIV Fusion Inhibitors	HIV Fusion Inhibitors	IIa	Enfuvirtide is an antiretroviral drug used in combination therapy for the treatment of HIV-1/AIDS.	Oxytocin receptor,Oxytocin-neurophysin 1，Envelope glycoprotein	1462				4491.876	C204H301N51O64	4.3	-0.875		3.8 ± 0.6 h	36 residue, synthetically prepared peptide with N-terminal acetylation and C-terminal amidation.  It blocks the fusion of HIV-1 with CD4 cells.		Enfuvirtide binds to the first heptad-repeat (HR1) in the gp41 subunit of the viral envelope glycoprotein and prevents the conformational changes required for the fusion of viral and cellular membranes. It works by disrupting the HIV-1 molecular machinery at the final stage of fusion with the target cell, preventing uninfected cells from becoming infected. Enfuvirtide is a biomimetic peptide that was rationally designed to mimic components of the HIV-1 fusion machinery and displace them, preventing normal fusion.		Expected to undergo catabolism to its constituent amino acids, with subsequent recycling of the amino acids in the body pool.	After a 90000 ug single subcutaneous injection of Enfuvirtide into the abdomen in 12 HIV-1 infected subjects, the mean peak concentration is 4.59±1.5 ug/ml and the median time to peak concentration was 8 h (ranged from 3 to12 h).	5500 ± 1100 ml	24.8 ± 4.1 ml/h/kg [HIV-1 infected adult and pediatric subjects following a 90-mg single SC dose of enfuvirtide] 30.6 ± 10.6 ml/h/kg [Following 90-mg twice daily dosing of FUZEON SC in combination with other antiretroviral agents in HIV-1 infected subjects] 40 ± 17 ml/h/kg [pediatric patients in the presence of concomitant medications including antiretroviral agents receiving the 2000 ug/kg twice daily dose]	US6475491，US5464933，CA2224008	1999-06-08 00:00:00	2019-06-08 00:00:00		FUZEON in combination with other antiretroviral agents is indicated for the treatment of HIV-1 infection in treatment experienced patients with evidence of HIV-1 replication despite ongoing antiretroviral therapy.		Each single-use vial contains 108000 ug of enfuvirtide for the delivery of 90000 ug. Prior to subcutaneous administration, the contents of the vial are reconstituted with 1.1 ml of Sterile Water for Injection giving a volume of approximately 1.2 ml to provide the delivery of 1 ml of the solution. Each 1 ml of the reconstituted solution contains approximately 90000 ug of enfuvirtide with approximate amounts of the following excipients: 22550 ug of mannitol, 2390 ug of sodium carbonate (anhydrous), and sodium hydroxide and hydrochloric acid for pH adjustment as needed. The reconstituted solution has an approximate pH of 9.0	White to off-white, sterile, lyophilized powder. Each single-use vial contains 108000 ug of enfuvirtide for the delivery of 90000 ug. Prior to subcutaneous administration, the contents of the vial are reconstituted with 1.1 ml of Sterile Water for Injection giving a volume of approximately 1.2 ml to provide the delivery of 1 ml of the solution. Each 1 ml of the reconstituted solution contains approximately 90000 ug of enfuvirtide with approximate amounts of the following excipients: 22550 ug of mannitol, 2390 ug of sodium carbonate (anhydrous), and sodium hydroxide and hydrochloric acid for pH adjustment as needed. The reconstituted solution has an approximate pH of 9.0.	Subcutaneous	90000 ug (1 ml) twice daily injected subcutaneously into the upper arm, anterior thigh or abdomen. Each injection should be given at a site different from the preceding injection site, and only where there is no current injection site reaction from an earlier dose.	FUZEON is contraindicated in patients with known hypersensitivity to FUZEON or any of its components	fever, chills, chest congestion, cough with yellow or green mucus, stabbing chest pain, wheezing, feeling short of breath; signs of a new infection such as sore throat, flu symptoms, swollen glands, easy bruising or bleeding.	http://www.rxlist.com/fuzeon-drug.htm http://www.drugs.com/mtm/enfuvirtide.html
FPDB21360	Th1098	Exenatide	HGEGTFTSDLSKQMEEEAVRLFIEWLKNGGPSSGAPPPS	39	Antidiabetic Agents	Hypoglycemic Agents	Ib	Indicated as adjunctive therapy to improve glycemic control in patients with Type 2 diabetes mellitus who are taking metformin, a sulfonylurea, or a combination of both, but have not achieved adequate glycemic control.	Glucagon-like peptide 1 receptor	1478				4186.6	C184H282N50O60S				Mean terminal half-life is 2.4 h.	Derived from a compound found in the saliva of the Gila monster, a large lizard native to the southwestern United States. It is a functional analog of Glucagon-Like Peptide-1 (GLP-1) peptide.	Exenatide is an incretin mimetic, which has glucoregulatory effects. While it is has blood-sugar lowering actions alone, it can also be combined with other medications such as pioglitazone, metformin, sulfonylureas, and/or insulin to improve glucose control. The approved use of exenatide is with either sulfonylureas, metformin and thiazolinediones. The medication is injected twice per day using a pre-filled pen device. Typical human responses to exenatide plus eating include improvements in the initial rapid release of endogenous insulin, suppression of glucagon release by the pancreas, regulation of gastric empyting and reduced appetite; all behaviors more typical of individuals without blood sugar control problems. Exenatide is self-regulating in that in lowers blood sugar when levels are elevated but does not continue to lower blood sugar when levels return to normal, unlike with sulfonylureas or insulins.	Exenatide is a functional analog of the human incretin Glucagon-Like Peptide-1 (GLP-1). Incretins enhance glucose-dependent insulin secretion and exhibit other antihyperglycemic actions following their release into the circulation from the gut. The GLP-1 system increases insulin secretion only in the presence of elevated plasma glucose levels, avoiding inappropriately high insulin levels during fasting. The drug also moderates peak serum glucagon levels during hyperglycemic periods following meals, but does not interfere with glucagon release in response to hypoglycemia. Secondary effects of drug administration reduces the rate of gastric emptying and decreases food intake, mitigating the potential severity of hyperglycemic events after meals.	Effects of the overdoses included severe nausea, severe vomiting, and rapidly declining blood glucose concentrations.		Following subcutaneous administration to patients with type 2 diabetes, exenatide reaches median peak plasma concentrations in 2.1 h.	28300 ml	Apparent cl=9100 ml/h	US6872700，US5424286	2004-01-15 00:00:00	2024-01-15 00:00:00		BYETTA (exenatide injection) is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.BYDUREON is an extended-release formulation of exenatide, administered as an injection once every 168 h (weekly). BYDUREON is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus		BYETTA (exenatide injection) is supplied for SC injection as a sterile, preserved isotonic solution in a glass cartridge that has been assembled in a pen-injector (pen). Each milliliter (mL) contains 250 ug (ug) synthetic exenatide, 2200 ug metacresol as an antimicrobial preservative, mannitol as a tonicity-adjusting agent, and glacial acetic acid and sodium acetate trihydrate in water for injection as a buffering solution at pH 4.5. Two prefilled pens are available to deliver unit doses of 5 ug or 10 ug. Each prefilled pen will deliver 60 doses to provide for 720 h of twice daily administration (BID).Exenatide is incorporated in an extended-release microsphere formulation containing the 50:50 poly(D,L-lactide-co-glycolide) polymer (37200 ug per dose) along with sucrose (800 ug per dose). The powder must be suspended in the diluent prior to injection. The diluent for the BYDUREON vial is supplied in a prefilled syringe within each single-dose tray. The diluent for the BYDUREON Pen is contained within each single-dose pen. Each configuration contains sufficient diluent to deliver 0.65 ml. The diluent is a clear, colorless to pale-yellow solution composed of carboxymethylcellulose sodium (19000 ug), polysorbate 20 (630 ug), sodium phosphate monobasic monohydrate (610 ug), sodium phosphate dibasic heptahydrate (510 ug), sodium chloride (4100 ug), and water for injection. Sodium hydroxide may be added during manufacture of BYDUREON Pen for pH adjustment.	White to off-white powder that is available in a dosage strength of 2000 ug exenatide per vial or per pen		BYETTA (exenatide injection) should be initiated at 5 ug administered twice daily at any time within the 60-minute period before the morning and evening meals (or before the two main meals of the day, approximately 6 h or more apart). BYETTA (exenatide injection) should not be administered after a meal. Based on clinical response, the dose of BYETTA (exenatide injection) can be increased to 10 ug twice daily after 730 h of therapy. Initiation with 5 ug reduces the incidence and severity of gastrointestinal side effects. Use BYETTA (exenatide injection) only if it is clear, colorless and contains no particles.BYDUREON (2000 ug per dose) should be administered once every 168 h (weekly). The dose can be administered at any time of day, with or without meals.	BYETTA (exenatide injection) is not a substitute for insulin. BYETTA (exenatide injection) should not be used in patients with type 1 diabetes or for the treatment of diabetic ketoacidosis, as it would not be effective in these settings. The concurrent use of BYETTA (exenatide injection) with insulin has not been studied and cannot be recommended.Based on postmarketing data BYETTA (exenatide injection) has been associated with acute pancreatitis, including fatal and non-fatal hemorrhagic or necrotizing pancreatitis. BYETTA (exenatide injection) has not been studied in patients with a history of pancreatitis. It is unknown whether patients with a history of pancreatitis are at increased risk for pancreatitis while using BYETTA (exenatide injection) . Other antidiabetic therapies should be considered in patients with a history of pancreatitis.BYDUREON is not recommended as first-line therapy for patients who have inadequate glycemic control on diet and exercise. BYDUREON is not a substitute for insulin. BYDUREON should not be used in patients with type 1 diabetes or for the treatment of diabetic ketoacidosis, as it would not be effective in these settings. BYDUREON and BYETTA (exenatide) injection both contain the same active ingredient, exenatide, and therefore should not be used together. BYDUREON has not been studied in patients with a history of pancreatitis. It is unknown whether patients with a history of pancreatitis are at increased risk for pancreatitis while using BYDUREON. Other antidiabetic therapies should be considered in patients with a history of pancreatitis.	Severe allergic reactions include severe rash or itching, swelling of your face, lips, and throat that may cause difficulty breathing or swallowing, feeling faint or dizzy and very rapid heartbeat. Inflammation of the pancreas (pancreatitis) may happen, which may be severe and lead to death. Your risk for getting low blood sugar (hypoglycemia) is higher. Signs and symptoms of low blood sugar may include headache, drowsiness, weakness, dizziness, confusion, irritability, hunger, fast heartbeat, sweating, and feeling jittery.Possible thyroid tumors, including cancer, Allergic reaction Pancreatitis, Hypoglycemia	
FPDB21361	Th1100	Pramlintide	KCNTATCATQRLANFLVHSSNNFGPILPPTNVGSNTY	37	Unclassified		Ia	For the treatment of type 1 and type 2 diabetes mellitus as an adjunct to preprandial insulin therapy in patients without adequate glycemic control of insulin therapy.	Calcitonin receptor,Receptor activity-modifying protein 1,Receptor activity-modifying protein 2,Receptor activity-modifying protein 3	1482				3949.3896	C171H267N51O53S2				Approximately 0.8 h	New adjunct treatment for type I and type II diabetes. It  is developed by Amylin Pharmaceuticals. It is derived from amylin, a hormone released after meal, in a pattern similar to insulin. Diabetic patients are also deficient in amylin.	Pramlintide is a synthetic analog of amylin, a glucoregulatory hormone that is synthesized by pancreatic β-cells and released into the bloodstream, in a similar pattern as insulin, after a meal. Like insulin, amylin is deficient in individuals with diabetes. It is provided as an acetate salt. Pramlintide is a 37-amino acid polypeptide that differs structurally from human amylin by the replacement of alanine, serine, and serine at positions 25, 28, and 29 respectively with proline.	Pramlintide is an amlyinomimetic, a functional analog of the naturally occurring pancreatic hormone amylin. Amylin has activity in a number of gastrointestinal and glucodynamic systems, and by mimicking its activity, pramlintide acts to improve glycemic control through modulation of the rate of gastric emptying, prevention of post-prandial rise in glucagon levels, and by increasing sensations of satiety, thereby reducing caloric intake and potentiating weight loss. There appears to be at least three distinct receptor complexes that bind with high affinity to amylin. All three complexes contain the calcitonin receptor at the core, plus one of three Receptor activity-modifying proteins, RAMP1, RAMP2, or RAMP3.		Metabolized primarily by the kidneys.	The absolute bioavailability of a single subcutaneous dose of pramlintide is approximately 30 to 40%.			US5686411，US6610824	2003-03-17 00:00:00	2023-03-17 00:00:00		SYMLIN is indicated as an adjunctive treatment in patients with type 1 or type 2 diabetes who use mealtime insulin therapy and who have failed to achieve desired glucose control despite optimal insulin therapy.		The disposable multidose SymlinPen pen-injector contains 1000 ug/ml of pramlintide (as acetate). The formulation contains 2250 ug/ml of metacresol as a preservative, D-mannitol as a tonicity modifier, acetic acid, sodium acetate as pH modifiers, and water for injection. SYMLIN has a pH of approximately 4.0	Clear, isotonic, sterile solution for subcutaneous administration	Subcutaneous	Reduce mealtime insulin doses by 50%, then initiate SYMLIN at 15 ug subcutaneously, injecting immediately prior to each major meal. Increase the SYMLIN dose to the next increment (30, 45, or 60 ug) when no clinically significant nausea has occurred for at least 72 h. If significant nausea persists at the 45 or 60 ug dose level, the SYMLIN dose should be decreased to 30 ug. If the 30 ug dose is not tolerated, discontinuation of SYMLIN therapy should be considered.		Nausea, Anorexia, Vomiting, Arthralgia, Fatigue, Allergic Reaction, Dizziness	http://www.symlin.com/ http://www.rxlist.com/symlin-drug.htm http://www.drugs.com/pro/symlin.html http://diabetes.emedtv.com/symlin/symlin.html
FPDB21362	Th1103	Cosyntropin	ACTH(1-24)SYSMEHFRWGKPVGKKRRPVKVYP	28	Hormonal Agents	Hormones and Diagnostic Agents	IV	For use as a diagnostic agent in the screening of patients presumed to have adrenocortical insufficiency.	Adrenocorticotropic hormone receptor	1500				2933.437	C136H210N40O31S				0.25 h (IV adminstration)	A synthetic peptide identical to the 24-amino acid N-terminal segment  of adrenocorticotropic hormone. ACTH. This segment is similar in all species and responsible for biological activity.	Cosyntropin exhibits the full corticosteroidogenic activity of natural ACTH. Various studies have shown that the biologic activity of ACTH resides in the N- terminal portion of the molecule and that the 1-20 amino acid residue is the minimal sequence retaining full activity. Partial or complete loss of activity is noted with progressive shortening of the chain beyond 20 amino acid residue. For example, the decrement from 20 to 19 results in a 70% loss of potency. The pharmacologic profile of Cosyntropin is similar to that of purified natural ACTH. It has been established that 250 ug of Cosyntropin will stimulate the adrenal cortex maximally and to the same extent as 25 units of natural ACTH. Cosyntropin has less immunogenic activity than ACTH because the amino acid sequence having most of the antigenic activity of ACTH, i.e., amino acids 25-39, is not present in cosyntropin. The extra-adrenal effects which natural ACTH and Cosyntropin have in common include increased melanotropic activity, increased growth hormone secretion and an adipokinetic effect. These are considered to be without physiological or clinical significance.	Cosyntropin combines with a specific receptor in the adrenal cell plasma membrane and, in patients with normal adrenocortical function, stimulates the initial reaction involved in the synthesis of adrenal steroids (including cortisol, cortisone, weak androgenic substances, and a limited quantity of aldosterone) from cholesterol by increasing the quantity of the substrate within the mitochondria. Cosyntropin does not significantly increase plasma cortisol concentration in patients with primary or secondary adrenocortical insufficiency.			Rapidly absorbed following intramuscular administration.							CORTROSYN (cosyntropin) for Injection is intended for use as a diagnostic agent in the screening of patients presumed to have ad-renocortical insufficiency. Because of its rapid effect on the adrenal cortex it may be utilized to perform a 30-minute test of adrenal func-tion (plasma cortisol response) as an office or outpatient procedure, using only 2 venipuncture		Box of 10 vials of CORTROSYN (cosyntropin) for Injection 250 ug without antimicrobial preservatives		Intravenous, Intravenous infusion, Intramuscular	CORTROSYN (cosyntropin) for Injection may be administered intramuscularly or as a direct Intravenous infusion when used as a rapid screening test of adrenal function. It may also be given as an Intravenous infusion over a 4 to 8 h period to provide a greater stimulus to the adrenal glands. Doses of CORTROSYN (cosyntropin) 0.25 to 750 ug have been used in clinical studies and a maximal response noted with the smallest dose.	The only contraindication to CORTROSYN (cosyntropin) for Injec-tion is a history of a previous adverse reaction to it.	Since CORTROSYN (cosyntropin) for Injection is intended for diag-nostic and not therapeutic use. A rare hypersensitivity reaction usually associated with a pre-existing allergic disease and/or a previous reaction to natural ACTH is possible. Symptoms may include slight whealing with splotchy erythema at the injection site. The other effects such as  bradycardia, tachycardia, hypertension, peripheral edema.	
FPDB21363	Th1104	Corticotropin	SYSMEHFRWGKPVGKKRRPVKVYPDGAEDQLAEAFPLEF	39	Unclassified		IV	For use as a diagnostic agent in the screening of patients presumed to have adrenocortical insufficiency.		1501				4541.0658	C207H308N56O58S				0.25 h (IV adminstration)	Corticotropin (ACTH or adrenocorticotropic hormone) is a polypeptide hormone produced and secreted by the pituitary gland. It is an important player in the hypothalamic-pituitary-adrenal axis.	Corticotropin acts through the stimulation of cell surface ACTH receptors, which are primarily located on the adrenocortical cells. Corticotropin stimulates the cortex of the adrenal gland and boosts the synthesis of corticosteroids, mainly glucocorticoids but also sex steroids (androgens). Corticotropin is also related to the circadian rhythm in many organisms.	As a diagnostic aid (adrenocortical function), corticotropin combines with a specific receptor on the adrenal cell plasma membrane. In patients with normal adrenocortical function, it stimulates the initial reaction involved in the synthesis of adrenal steroids (including cortisol, cortisone, weak androgenic substances, and a limited quantity of aldosterone) from cholesterol by increasing the quantity of cholesterol within the mitochondria. Corticotropin does not significantly increase serum cortisol concentrations in patients with primary adrenocortical insufficiency (Addison's disease). The mechanism of action of corticotropin in the treatment of infantile myoclonic seizures is unknown.			Corticotropin is rapidly absorbed following intramuscular administration; the repository dosage form is slowly absorbed over approximately 8 to 16 h.							Infantile spasms, Multiple Sclerosis, Rheumatic Disorders such as Psoriatic arthritis, Rheumatoid arthritis, including juvenile rheumatoid arthritis (selected cases may require low-dose maintenance therapy), Ankylosing spondylitis, Collagen Diseases such as systemic lupus erythematosus, systemic dermatomyositis (polymyositis). Dermatologic Diseases Severe erythema multiforme, Stevens-Johnson syndrome. Allergic States, Serum sickness, Ophthalmic Diseases. Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa such as: keratitis, iritis, iridocyclitis, diffuse posterior uveitis and choroiditis, optic neuritis, chorioretinitis, anterior segment inflammation. Respiratory Diseases		Also contains 0.5% phenol, not more than 0.1% cysteine (added), sodium hydroxide and/or acetic acid to adjust pH and water for injection.			In the treatment of infantile spasms, H.P. Acthar Gel must be administered intramuscularly. The recommended regimen is a daily dose of 150 U/m² (divided into twice daily intramuscular injections of 75 U/m²) administered over a 2-week period. Dosing with H.P. Acthar Gel should then be gradually tapered over a 2-week period to avoid adrenal insufficiency. The following is one suggested tapering schedule: 30 U/m² in the morning for 72 h; 15 U/m² in the morning for 72 h; 10 U/m² in the morning for 72 h; and 10 U/m² every other morning for 6-days. The usual dose of H.P. Acthar Gel is 40-80 units given intramuscularly or subcutaneously every 24-72 h.	if you are allergic to corticotropin, or if you have adrenal insufficiency (Addison's disease), scleroderma, a fungal infection, herpes infection of the eyes, osteoporosis, a stomach ulcer, congestive heart failure, high blood pressure, recent surgery, or if you are allergic to pork then this medication is not be administered.	problems with your vision;swelling, rapid weight gain, feeling short of breath; severe depression, unusual thoughts or behavior, seizure (convulsions);bloody or tarry stools, coughing up blood; pancreatitis (severe pain in your upper stomach spreading to your back, nausea and vomiting, fast heart rate); low potassium (confusion, uneven heart rate, extreme thirst, increased urination, leg discomfort, muscle weakness or limp feeling); or dangerously high blood pressure (severe headache, blurred vision, buzzing in your ears, anxiety, confusion, chest pain, shortness of breath, uneven heartbeats, seizure).	http://www.acthar.com/ http://www.healthline.com/goldcontent/corticotropin http://www.drugs.com/cons/acthar.html http://www.rxlist.com/hp-acthar-gel-drug/indications-dosage.htm
FPDB21364	Th1106	Insulin detemir	A chainGIVEQCCTSICSLYQLENYCN B chain FVNQHLCGSHLVEALYLVCGERGFFYTPK	62	Antidiabetic Agents	Antidiabetic Agents	Ia	For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone.	Insulin receptor	1511				5916.9	C267H402N64O76S6				Adults (18-65 years) = 7.083333 ± 1.3 h	Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin.	Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 h and its duration of action is up to 24 h. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin.	Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism.&#13; Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action.	Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site.	As with natural insulin, all metabolites formed are inactive.	Maximum serum concentrations are reached 6 to 8 h following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%.	100 ml/kg	Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 60000 ml/h·kg	US5750497，US6011007，CA2171424	2003-05-17 00:00:00	2023-05-17 00:00:00		LEVEMIR is indicated to improve glycemic control in adults and children with diabetes mellitus.		Each milliliter of LEVEMIR contains 100 units (14200 ug/ml) insulin detemir, 65.4 meg  inc, 2060 ug m-cresol, 16000 ug glycerol, 1800 ug phenol, 890 ug disodium phosphate dihydrate, 1170 ug sodium chloride, and water for injection. Hydrochloric acid and/or sodium hydroxide may be added to adjust pH. LEVEMIR has a pH of approximately 7.4	Clear, colorless, aqueous, neutral Sterile solution	Subcutaneous	Patients who require twice-daily dosing can administer the evening dose with the evening meal, at bedtime, or 12 h after the morning dose. The dose of LEVEMIR must be individualized based on clinical response. Blood glucose monitoring is essential in all patients receiving insulin therapy.	LEVEMIR is not recommended for the treatment of diabetic ketoacidosis. Intravenous rapid-acting or short-acting insulin is the preferred treatment for this condition. LEVEMIR is contraindicated in patients with hypersensitivity to LEVEMIR or any of its excipients. Reactions have included anaphylaxis.	Hypoglycemia, upper respiratory tract infection, Headache, Pharyngitis, Influenza-like illness, Abdominal Pain	http://www.rxlist.com/levemir-drug.htm http://www.drugs.com/levemir.html http://www.webmd.com/drugs/2/drug-95095/levemir-subq/details http://www.levemir.com/considering-levemir/levemir-flextouch/
FPDB21365	Th1107	Insulin glulisine	A chainGIVEQCCTSICSLYQLENYCN B chainFVKQHLCGSHLVEALYLVCGERGFFYTPET	63	Antidiabetic Agents	Antidiabetic Agents	Ib	For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents.	Insulin receptor	1520				5823	C258H384N64O78S6				Elimination half life= 0.7 h (SC injection)	Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin.	Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 0.25 h. Its activity peaks 1 h following subcutaneous injection and its duration of action is 2-4 h.	Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action.	Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia.		Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 1 h (range of 0.666667 - 2 h); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection.	13000 ml		US6960561，US6221633	2007-01-26 00:00:00	2027-01-26 00:00:00		APIDRA is indicated to improve glycemic control in adults and children with diabetes mellitus.		Each milliliter of APIDRA contains 100 units (3490 ug) insulin glulisine, 3150 ug metacresol, 6000 ug tromethamine, 5000 ug sodium chloride, 10 ug polysorbate 20, and water for injection. APIDRA has a pH of approximately 7.3. The pH is adjusted by addition of aqueous solutions of hydrochloric acid and/or sodium hydroxide	Sterile, aqueous, clear, and colorless solution		APIDRA is a recombinant insulin analog that is equipotent to human insulin (i.e. one unit of APIDRA has the same glucose-lowering effect as one unit of regular human insulin) when given intravenously. When given subcutaneously, APIDRA has a more rapid onset of action and a shorter duration of action than regular human insulin. The dosage of APIDRA must be individualized. Blood glucose monitoring is essential in all patients receiving insulin therapy. The total daily insulin requirement may vary and is usually between 0.5 to 1 Unit/kg/day. Insulin requirements may be altered during stress, major illness, or with changes in exercise, meal patterns, or coadministered drugs.	APIDRA is contraindicated: during episodes of hypoglycemia, in patients who are hypersensitive to APIDRA or to any of its excipients When used in patients with known hypersensitivity to APIDRA or its excipients, patients may develop localized or generalized hypersensitivity reactions.	Hypoglycemia, Hypokalemia	http://www.rxlist.com/apidra-drug/side-effects-interactions.htm http://www.apidra.com/default.aspx http://www.drugs.com/pro/apidra.html
FPDB21366	Th1109	Nesiritide	SPKMVQGSGCFGRKMDRISSSSGLGCKVLRRH	32	Unclassified		Ib	For the intravenous treatment of patients with acutely decompensated congestive heart failure who have dyspnea at rest or with minimal activity.		1530				3464					Approx. 0.3 h	Recombinant, 32 amino acid human B-type natriuretic peptide, which is normally produced by the ventricular myocardium. Nesiritide is a medication used to treat acutely decompensated congestive heart failure with dyspnea at rest or with minimal exertion.	Nesiritide works to facilitate cardiovascular fluid homeostasis through counterregulation of the renin-angiotensin-aldoesterone system, stimulating cyclic guanosine monophosphate, leading to smooth muscle cell relaxation. In simpler terms, it promotes vasodilation, natriuresis, and diuresis.	Human BNP binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells, leading to increased intracellular concentrations of guanosine 3'5'-cyclic monophosphate (cGMP) and smooth muscle cell relaxation. Cyclic GMP serves as a second messenger to dilate veins and arteries. Nesiritide has been shown to relax isolated human arterial and venous tissue preparations that were precontracted with either endothelin-1 or the alpha-adrenergic agonist, phenylephrine. In human studies, nesiritide produced dose-dependent reductions in pulmonary capillary wedge pressure (PCWP) and systemic arterial pressure in patients with heart failure. In animals, nesiritide had no effects on cardiac contractility or on measures of cardiac electrophysiology such as atrial and ventricular effective refractory times or atrioventricular node conduction. Naturally occurring atrial natriuretic peptide (ANP), a related peptide, increases vascular permeability in animals and humans and may reduce intravascular volume. The effect of nesiritide on vascular permeability has not been studied.&#13;	No data are available with respect to overdosage in humans.  The expected reaction would be excessive hypotension, which should be treated with drug discontinuation or reduction and appropriate measures.	Nesiritide undergoes proteolytic cleavage of the peptide by endopeptidases, such as neutral endopeptidase, which are present on the vascular lumenal surface.	Administration of nesiritide exhibits biphasic disposition from the plasma.	190 ml/kg	552 ml/h/k [patients with congestive heart failure receiving IV infusion]					NATRECOR (nesiritide) is indicated for the treatment of patients with acutely decompensated heart failure who have dyspnea at rest or with minimal activity. In this population, the use of NATRECOR reduced pulmonary capillary wedge pressure and improved short term (3 h) symptoms of dyspnea.		NATRECOR is formulated as the citrate salt of rhBNP, and is provided in a sterile, single-use vial. Each 1500 ug vial contains a white- to off-white lyophilized powder for intravenous (IV) administration after reconstitution. The quantitative composition of the lyophilized drug per vial is: nesiritide 1580 ug, citric acid monohydrate 2100 ug, mannitol 20000 ug, and sodium citrate dihydrate 2940 ug	White- to off-white lyophilized powde	Intravenous	IV bolus of 2 ug/kg followed by a continuous infusion of 0.01 ug/kg/min	NATRECOR is contraindicated in patients with: Persistent systolic blood pressure < 100 mm Hg prior to therapy because of an increased risk of symptomatic hypotension  Known hypersensitivity to any of its components.	Hypotension	http://www.rxlist.com/natrecor-drug.htm https://en.wikipedia.org/wiki/Nesiritide http://dailymed.nlm.nih.gov/dailymed/archives/fdaDrugInfo.cfm?archiveid=13531 http://www.fda.gov/Safety/MedWatch/SafetyInformation/ucm169897.htm
FPDB21367	Th1110	Thymalfasin	SDAAVDTSSEITTKDLKEKKEVVEEAEN	28	Unclassified		Ib	Indicated as an adjuvant for influenza vaccine in elderly patients and as an adjuvant for both influenza and hepatitis B vaccines in chronic hemodialysis patients who failed to achieve adequate antibody titers from previous immunization.		1531				3108.2755	C129H215N33O55				Approx. 2 h	Chemically synthesized version identicle to human acetylated polypeptide , thymosin alpha 1. It is now approved in 35 developing countries for the treatment of Hepatitis B and C and in boosting immunity against other diseases.	Thymalfasin is a 28-amino acid polypeptide produced synthetically but originally isolated from thymosin fraction 5, a bovine thymus extract containing a number of immunologically active peptides. In vitro studies have shown that Thymalfasin can influence T-cell production and maturation, stimulate production of Th1 cytokines such as interferon-gamma and interleukin-2, and activate natural killer cell-mediated cytotoxicity.	The mechanism of action of thymalfasin is not completely understood but is thought to be related to its immunomodulating activities, centered primarily around augmentation of T-cell function. In various in vitro assays, thymosin alpha 1 has been shown to promote T-cell differentiation and maturation; for example, CD4+, CD8+, and CD3+ cells have all been shown to be increased. Thymosin alpha 1 has also been shown to increase production of IFN-g, IL-2, IL-3, and expression of IL-2 receptor following activation by mitogens or antigens, increase NK cell activity, increase production of migratory inhibitory factor (MIF), and increase antibody response to T-cell dependent antigens. Thymosin alpha 1 has also been shown to antagonize dexamethasone-induced apoptosis of thymocytes in vitro. In vivo administration of thymosin alpha 1 to animals immunosuppressed by chemotherapy, tumor burden, or irradiation showed that thymosin alpha 1 protects against cytotoxic damage to bone marrow, tumor progression and opportunistic infections, thereby increasing survival time and number of survivors. Many of the in vitro and in vivo effects of thymosin alpha 1 have been interpreted as influences on either differentiation of pluripotent stem cells to thymocytes or activation of thymocytes into activated T-cells. Thymalfasin also has been shown in vitro to upregulate expression of toll like receptors (TLR) including TLR2 and TLR9 in mouse and human dendritic cells, as well as activate NF-kB and JNK/P38/AP1 pathways. Thymalfasin's activation of dendritic cells provides another possible pathway explaining thymalfasin's immunomodulatory and antiviral effects.	There are no reported instances of deliberate or accidental overdosage in humans. Animal toxicology studies have shown no adverse reactions in single doses up to 20000 ug/kg and in repeated doses up to 6000 ug/kg/day for 13 weeks, which were the highest doses studied. The highest single dose tested in animals represents 800-times the clinical dose.		Rapidly absorbed with peak serum levels achieved at approximately 2 h.							ZADAXIN thymosin alpha 1 (thymalfasin) is indicated as a monotherapy or combination therapy with interferon for the treatment of chronic hepatitis B.		lyophilized preparation contains 1600 ug thymosin alpha 1, 50000 ug mannitol, and sodium phosphate buffer to adjust the pH to 6.8	N. A.	Subcutaneous	The recommend-ed dose of ZADAXIN (thymalfasin) for chronic hepatitis B when used as a monotherapy or in combination with interferon (at the labeled dose and schedule for interferon) is 1600 ug (900 ug/m2) administered subcutaneously twice a week for 6 to 8760 h. Patients weighing less than 40 kg should receive a ZADAXIN (thymalfasin) dose of 40 ug/kg.	ZADAXIN (thymalfasin) is contraindicated in patients with a history of hypersensitivity to thymosin alpha 1 or any component of the injection. Because ZADAXIN (thymalfasin) therapy appears to work by enhancing the immune system, it should be considered contraindicated in patients who are being deliberately immunosuppressed, such as organ transplant patients, unless the potential benefits of the therapy clearly outweigh the potential risks.	Adverse experiences have been infrequent and mild, consisting primarily of local discomfort at the injection site, and rare instances of erythema, transient muscle atrophy, polyarthralgia combined with hand edema, and rash.	http://www.sciclone.com/product-portfolio/zadaxin/ http://www.rxlist.com/zadaxin-drug.htm  http://www.drugs.com/international/zadaxin.html
FPDB21368	Th1113	Glatiramer acetate	EAYKAAEKAYAAKEAAKEAAKAKAEKKAAYAKAKAAKYEKKAKKAAAEYKKK	52	Unclassified		IIa	For reduction of the frequency of relapses in patients with Relapsing-Remitting Multiple Sclerosis.		1534				5000-9000	C254H422N70O72					Glatiramer acetate comprises acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000-9,000 daltons.  It is an immunomodulator, known to reduce the frequency of relapses in relapsing-remitting multiple sclerosis	Glatiramer acetate was originally designed to mimic a protein in myelin, called myelin basic protein, with the intention of inducing EAE (an animal model of MS). Quite to the contrary, it was found to suppress the disease and as a result came to be trialed in human MS. There is some evidence that Glatiramer acetate converts the body's immune response from a Th1 type to a Th2 one, promotes suppressor T cells or acts as an altered peptide ligand. Studies in animals and in vitro systems suggest that upon its administration, glatiramer acetate-specific suppressor T-cells are induced and activated in the periphery. Some fraction of the injected material, either intact or partially hydrolyzed, is presumed to enter the lymphatic circulation, enabling it to reach regional lymph nodes, and some may enter the systemic circulation intact.	Glatiramer acetate (GA) exhibits strong and promiscuous binding to MHC molecules (HLA DRB1* variants) and consequent competition with various myelin antigens for their presentation to T cells. A further aspect of its action is potent induction of specific suppressor cells of the T helper 2 (Th2) type that migrate to the brain and lead to in situ bystander suppression. Furthermore, the GA-specific cells in the brain express the anti-inflammatory cytokines IL-10 and transforming growth factor beta, in addition to brain-derived neurotrophic factor, whereas they do not express the inflammatory cytokine IFN-gamma. Recent evidence also suggests that Glatiramer acetate directly inhibits dendritic cells and monocytes - both of which are circulating antigen presenting cells.	Adverse reactions include injection site reactions, vasodilatation, chest pain, asthenia, infection, pain, nausea, arthralgia, anxiety, and hypertonia.	Hydrolyzed by proteases								Glatiramer acetate, the active ingredient of COPAXONE, consists of the acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000 – 9,000 daltons. Glatiramer acetate is identified by specific antibodies. Chemically, glatiramer acetate is designated L-glutamic acid polymer with L-alanine, L-lysine and L-tyrosine, acetate (salt).		Each 1 ml of COPAXONE solution contains 20000 ug or 40000 ug of glatiramer acetate and the following inactive ingredient: 40000 ug of mannitol. The pH of the solutions is approximately 5.5 to 7.0. The biological activity of glatiramer acetate is determined by its ability to block the induction of experimental autoimmune encephalomyelitis (EAE) in mice.	Clear, colorless to slightly yellow, sterile, nonpyrogenic solution	Subcutaneous	COPAXONE is for subcutaneous use only. Do not administer intravenously. The dosing schedule depends on the product strength that is selected. The recommended doses are: COPAXONE 20000 ug per mL: administer once per day or COPAXONE 40000 ug per mL: administer three times per week and at least 48 h apart. COPAXONE 20000 ug per mL and COPAXONE 40000 ug per mL are not interchangeable.	COPAXONE is contraindicated in patients with known hypersensitivity to glatiramer acetate or mannitol.	most commonly associated with discontinuation were: injection site reactions, dyspnea, urticaria, vasodilatation, and hypersensitivity. The most common adverse reactions were: injection site reactions, vasodilatation, rash, dyspnea, and chest pain.	http://www.rxlist.com/copaxone-drug/side-effects-interactions.htm https://www.copaxone.com/  http://en.wikipedia.org/wiki/Glatiramer_acetate http://www.drugs.com/copaxone.html
FPDB21369	Th1120	Teriparatide	Parathyroid hormone precursor - Homo sapiens (1-34)SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNF	72	Bone Density Conservation Agents	Bone Density Conservation Agents	Ib	For the treatment of osteoporosis in men and postmenopausal women who are at high risk for having a fracture. Also used to increase bone mass in men with primary or hypogonadal osteoporosis who are at high risk for fracture.	Parathyroid hormone/parathyroid hormone-related peptide receptor	1556				4117.715	C181H291N55O51S2					Recombinant, human parathyroid hormone (PTH). It is a potent anabolic agent used to treat osteoporosis. It is manufactured and marketed by Eli Lilly and Company.	Clinical trials indicate that teriparatide increases predominantly trabecular bone in the lumbar spine and femoral neck; it has less significant effects at cortical sites. The combination of teriparatide with antiresorptive agents is not more effective than teriparatide monotherapy. The most common adverse effects associated with teriparatide include injection-site pain, nausea, headaches, leg cramps, and dizziness. After a maximum of two years of teriparatide therapy, the drug should be discontinued and antiresorptive therapy begun to maintain bone mineral density.	Teriparatide is the portion of human parathyroid hormone (PTH),amino acid sequence 1 through 34 of the complete molecule which contains amino acid sequence 1 to 84. Endogenous PTH is the primary regulator of calcium and phosphate metabolism in bone and kidney. Daily injections of teriparatide stimulate new bone formation leading to increased bone mineral density.	Effects of overexposure may include headaches, dizziness, dizziness, decreased blood pressured, decreased fetal survival, leg cramps, changes in clinical chemistry including increased in blood levels of calcium, decreased serum phosphorous, and increased urinary calcium and phosphorus.	Hepatic	Bioavailability is 95% following subcutaneous injection.	120 ml/kg	62000 ml/h [Women]  94000 ml/h [Men]	US6977077，US6770623，CA2314313，CA2325371	2003-08-20 00:00:00	2023-08-20 00:00:00		Treatment of Postmenopausal Women with Osteoporosis at High Risk for Fracture, Increase of Bone Mass in Men with Primary or Hypogonadal Osteoporosis at High Risk for Fracture, Treatment of Men and Women with Glucocorticoid-Induced Osteoporosis at High Risk for Fracture.		Each prefilled delivery device is filled with 2.7 ml to deliver 2.4 ml. Each mL contains 250 ug teriparatide (corrected for acetate, chloride, and water content), 410 ug glacial acetic acid, 100 ug sodium acetate (anhydrous), 45400 ug mannitol, 3000 ug Metacresol, and Water for Injection. In addition, hydrochloric acid solution 10% and/or sodium hydroxide solution 10% may have been added to adjust the product to pH 4. Each cartridge, pre-assembled into a delivery device, delivers 20 ug of teriparatide per dose each day for up to 672 h.	Sterile, colorless, clear, isotonic solution in a glass cartridge which is pre-assembled into a disposable delivery device (pen) for subcutaneous injection	Subcutaneous	Treatment of Postmenopausal Women with Osteoporosis at High Risk for Fracture. The recommended dose is 20 ug subcutaneously once a day. Increase of Bone Mass in Men with Primary or Hypogonadal Osteoporosis at High Risk for Fracture. he recommended dose is 20 ug subcutaneously once a day.	Hypersensitivity to teriparatide or to any of its excipients. Reactions have included angioedema and anaphylaxis		http://en.wikipedia.org/wiki/Teriparatide, http://www.forteo.com/,  http://www.rxlist.com/forteo-drug.htm,
FPDB21370	Th1124	Liraglutide	HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG	33	Unclassified		Ib	For use in/treatment of diabetes mellitus type 2.	Glucagon-like peptide 1 receptor	1576				3751.2	C172H265N43O51				approx. 13 h	Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.	Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11–15 h, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.	Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.	In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17400 ug subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS	During the initial 24 h following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.	Maximum concentrations of liraglutide are achieved at 8-12 h after dose. The mean peak and total exposures of liraglutide were 0.035 ug/ml and 0.96 ug·h/mL, respectively, for a subQ single dose of 600 ug. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 600 ug to 1800 ug. At 1800 ug Victoza, the average steady state concentration of liraglutide over 24 h was approximately 0.128 ug/ml AUC0-∞ was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-∞ from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.	SubQ 600 ug is approximately 13LIntravenous is approximately 70 ml/kg	The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1200 ml/h	US6268343，CA2264243	2001-08-23 00:00:00	2021-08-23 00:00:00		obese，type 2 diabetes mellitus		Each 1 ml of Saxenda solution contains 6000 ug of liraglutide and the following inactive ingredients: disodium phosphate dihydrate, 1420 ug; propylene glycol, 14000 ug; phenol, 5500 ug; and water for injection. Each pre-filled pen contains a 3 ml solution of Saxenda equivalent to 18000 ug liraglutide (free-base, anhydrous).Each 1 ml of Victoza solution contains 6000 ug of liraglutide. Each pre-filled pen contains a 3 ml solution of Victoza equivalent to 18000 ug liraglutide (free-base, anhydrous) and the following inactive ingredients: disodium phosphate dihydrate, 1420 ug; propylene glycol, 14000 ug; phenol, 5500 ug; and water for injection.	Saxenda is a clear, colorless solution，Victoza is a clear, colorless solution.	Subcutaneous	3000 ug daily，600 ug per day for one week. The 600 ug dose is a starting dose intended to reduce gastrointestinal symptoms during initial titration, and is not effective for glycemic control. After one week at 600 ug per day, the dose should be increased to 1200 ug. If the 1200 ug dose does not result in acceptable glycemic control, the dose can be increased to 1800 ug.	medullary thyroid carcinoma, Multiple Endocrine Neoplasia syndrome type 2 , hypersensitivity, Pregnancy，medullary thyroid carcinoma, Multiple Endocrine Neoplasia syndrome type 2, prior serious hypersensitivity reaction to Victoza.	Risk of Thyroid C-Cell Tumors, Acute Pancreatitis, Acute Gallbladder, Risk for Hypoglycemia with Concomitant Use of Anti-Diabetic Therapy , Heart Rate Increase, Renal Impairment, Hypersensitivity Reactions, Suicidal Behavior and Ideation.Nausea, Diarrhea, Vomiting, Constipation, Headache	http://www.rxlist.com/saxenda-drug.htm https://www.saxenda.com/ http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm427913.htm
FPDB21371	Th1127	Buserelin	pGlu-His-Trp-Ser-Tyr-D-Ser(tBu)-Leu-Arg-Pro-NHEt	36	Unclassified		IIIc	Buserelin may be used in the treatment of hormone-responsive cancers such as prostate cancer or breast cancer, estrogen-dependent conditions (such as endometriosis or uterine fibroids), and in assisted reproduction.	Lutropin-choriogonadotropic hormone receptor,Gonadotropin-releasing hormone receptor	1600				1298	C62H90N16O15				0.833333-1.333333 h by IV dose, 1.333333 h. By SC dose, 1-2 h by Intranasal dose	Buserelin is a luteinizing hormone-releasing hormone (LHRH) agonist. It is a synthetic hormone which stimulates the pituitary gland's gonadotrophin-releasing hormone receptor (GnRHR) and is used in prostate cancer treatment.		Buserelin stimulates the pituitary gland's gonadotrophin-releasing hormone receptor (GnRHR). Buserelin desensitizes the GnRH receptor, reducing the amount of LH and testosterone. However, there is a concomitant surge in LH and testosterone levels with the decrease in androgens, so antiandrogens must administered.										Treatment of endometriosis – an illness where some of the tissues that line the womb are found elsewhere in the body. As part of a treatment for infertility – it works by stopping the natural production of hormones that control ovulation. Synthetic hormones are then used to artificially stimulate ovulation. Your doctor should give you more information about how your treatment works， infertility		Each spray dose contains 150 ug of the active substance, buserelin as buserelin acetate. The other ingredients are citric acid, sodium citrate, sodium chloride and benzalkonium chloride in aqueous solution，Each 1 ml of solution contains 1 milligram of the active substance, buserelin as buserelin acetate. The other ingredients are, sodium chloride, sodium dihydrogen phosphate, sodium hydroxide, benzyl alcohol and water for injections	150 ug Nasal Spray Solution，1000 ug/ml Injection	Nasal spray，Subcutaneous	Treatment of endometriosis: The usual dose is one spray in each nostril three times each day. This is to make a total daily dose of 900 ug; Use the spray in the morning, at mid-day and in the evening; Treatment will be for a maximum of 4380 h;Treatment should be started on the first or second day of your menstrual period.This is to lower the chances you may be pregnant. Your doctor may perform a pregnancy test if there is any doubt; You may get a menstrual period after the first few weeks of using this medicine. You may also carry on getting breakthrough bleeding or spotting As part of treatment for infertility.Treatment starts on day 1 or day 21 of menstrual cycle. Daily dose is: 200 to 500 ug given as a single daily injection or 500 ug twice a day; Daily injections until blood tests show that levels of sex hormones are lowered. This usually takes one to three weeks; After this other hormones along with Suprecur Injection;Doctor determines the treatment time	Do not use this medicine and tell your doctor if: You are allergic (hypersensitive) to buserelin or goserelin, benzalkonium chloride or other ingredients of Suprecur Nasal Spray. Signs of an allergic reaction include: a rash, swallowing or breathing problems, swelling of your lips, face, throat or tongue;  You have abnormal menstrual bleeding where the cause is not endometriosis; You have a tumour that is not affected by hormones; You are pregnant or breast-feeding.This medicine is for use in women only. If you are not sure, talk to your doctor or pharmacist before using Suprecur Nasal Spray.Do not have this medicine and tell your doctor if: Allergy (hypersensitive) to buserelin or other similar medicines such as goserelin, or any of the other ingredients of Suprecur Injection. Abnormal menstrual bleeding Pregnancy or breast-feeding A tumour that is not affected by changes in hormone levels. This medicine is for use in women only. However there is another form of this medicine that can be used in men. Men should not use either form of this medicine if they have had their testicles removed.	Allergic reaction, diarrhoea, pain, swelling or a feeling of tension in stomach,  weight gain, difficulty in breathing, decreased urination. These could be signs of a serious side effect called ’Ovarian Hyperstimulation Syndrome’. This is more likely if you are taking other hormones as well as Suprecur Nasal Spray (buserelin) as part of a treatment for infertility.	http://www.drugs.com/uk/pdf/leaflet/468555.pdf
FPDB21372	Th1129	Tesamorelin	YADAIFTNSYRKVLGQLSARKLLQDIMSRQQGESNQERGARARL	44	Unclassified		Ib	Tesamorelin acetate is a synthetic analogue of human hypothalamic Growth Hormone Releasing Factor (hGRF) indicated to induce and maintain a reduction of excess abdominal fat in HIV-infected patients with lipodystrophy.	Growth hormone-releasing hormone receptor	1603				5135.9	C221H366N72O67S • xC2H4O2 where x averages 7.4 acetate counter ions per peptide molecule				26 and 0.633333 h	Stabilized synthetic peptide analogue of Growth Hormone Releasing Hormone (GHRH). It is used to treat excess abdominal fat in HIV-infected patients with lipodystrophy. It is a metabolic condition characterized by insulin resistance, fat redistribution and hyperlipidemia associated with antiretroviral therapy for HIV infection.	Tesamorelin stimulates growth hormone secretion, and subsequently increases IGF-1 and IGFBP-3 levels.	By acting on the pituitary cells in the brain, tesamorelin stimulates production and release of the endogenous hormone (hGRF). Tesamorelin therapy predisposes the patient to glucose intolerance and can also increase the risk of type 2 diabetes, so the drug is contraindicated in pregnancy.	Diarrhea, congestive heart failure, peripheral neuropathy, and loss of mobility were the four serious adverse events reported during the clinical studies	No formal metabolism studies have been performed in humans.	The absolute bioavailability was determined to be less than 4% in healthy adult subjects following a 2000 ug subcutaneous dose.	9400±3100 ml/kg in healthy subjects.10500±6100 ml/kg in HIV-infected patients.		US5861379	2015-11-30 00:00:00	2019-05-27 00:00:00		excess abdominal fat in HIV-infected patients with lipodystrophy		After reconstitution with the supplied diluent (Sterile Water for Injection, USP), a solution of EGRIFTA is clear and colorless. Each single-use vial of EGRIFTA contains 2000 ug of tesamorelin as the free base (2200 ug tesamorelin acetate, anhydrous) and the following inactive ingredient: 100000 ug mannitol, USP.	EGRIFTA is a sterile, white to off-white, preservative-free lyophilized powder for subcutaneous injection	Subcutaneous	The recommended dose of EGRIFTA is 2000 ug injected subcutaneously once a day.	Disruption of the Hypothalamic-pituitary Axis, Active Malignancy, Hypersensitivity and Pregnancy	rash, urticaria, arthralgia, extremity pain, peripheral edema, hyperglycemia, carpal tunnel syndrome, erythema, pruritis, pain, urticaria, irritation, swelling, hemorrhage	http://www.rxlist.com/egrifta-drug.htm http://www.egrifta.com/ http://www.drugs.com/egrifta.html
FPDB21373	Th1137	Teduglutide	HGDGSFSDEMNTILDNLAARDFINWLIQTKITD	33	Unclassified		Ia	Treatment of short bowel syndrome (SBS), malabsorption associated with the removal of the intestine, in adults patients who are dependent on parenteral support.	Glucagon-like peptide 2 receptor	1624				3752	C164H252N44O55S				Terminal half-life - 2 h.	Recombinant (E.coli derived) glucagon-like peptide-2 (GLP-2) analogue, made up of 33 amino acids. It differs from GLP-2 by one amino acid (A to G), which makes it more resistant to dipeptidyl peptidase-4 proteolysis, giving it a longer half-life as compared to endogenous GLP-2. FDA approved on December 21, 2012.	An enhancement of gastrointestinal fluid absorption (750-1000 ml/day) was observed following daily administrations of teduglutide. An increase in villus height and crypt depth of the intestinal mucosa was also noted. A decrease in fecal weight has also been observed. Teduglutide does not prolong the QTc interval.	Teduglutide is an analog of naturally occurring human glucagon-like peptide-2 (GLP-2), a peptide secreted by L-cells of the distal intestine in response to meals. GLP-2 increases intestinal and portal blood flow and inhibit gastric acid secretion. Teduglutide binds to the glucagon-like peptide-2 receptors located in enteroendocrine cells, subepithelial myofibroblasts and enteric neurons of the submucosal and myenteric plexus. This causes the release of insulin-like growth factor (IGF)-1, nitric oxide and keratinocyte growth factor (KGF). These growth factors may contribute to the increase in crypt cell growth and surface area of the gastric mucosa. Ultimately, absorption through the intestine is enhanced.	The most common adverse reactions (≥ 10%) across all studies with GATTEX are abdominal pain, injection site reactions, nausea, headaches, abdominal distension, upper respiratory tract infection. In addition, vomiting and fluid overload were reported in the SBS studies (1 and 3) at rates ≥ 10%.	Although a formal investigation has not been conducted, it is expected because teduglutide is a peptide-based drug, it will be degraded into smaller peptides and amino acids via catabolic pathways. The cytochrome P450 enzyme system is not involved in the metabolism of this drug.	The pharmacokinetic profile of teduglutide (when administered subcutaneously) is described by a one-compartment model with first order absorption in the abdomen, arm, and thigh. With escalating doses, teduglutide demonstrates linear pharmacokinetics. Absolute bioavailability, SubQ = 88%; Tmax, SubQ = 3-5 h;  Cmax, 50 ug/kg SubQ, SBS patients = 0.036 ug/ml; AUC, 50 ug/kg SubQ, SBS patients = 0.15 ug hr/mL; Teduglutide does not accumulate following multiple subcutaneous administrations.	Vd, healthy subjects = 103 ml/kg	Plasma clearance, healthy subjects = 123 ml/hr/kg;This value indicates that teduglutide is primarily cleared by the kidney.	US5789379，US7056886，US7847061	2016-12-22 00:00:00	2019-04-15 00:00:00		Short Bowel Syndrome (SBS)		Each single-use vial of GATTEX contains 5000 ug of teduglutide as a white lyophilized powder for solution for subcutaneous injection. In addition to the active pharmaceutical ingredient (teduglutide), each vial of GATTEX contains 3880 ug L-histidine, 15000 ug mannitol, 644 ug monobasic sodium phosphate monohydrate, 3434 ug dibasic sodium phosphate heptahydrate as excipients. No preservatives are present.	Teduglutide drug substance is a clear, colorless to light-straw–colored liquid.	Subcutaneous	50 ug/kg body weight administered by subcutaneous injection once daily		abdominal pain , injection site reactions, nausea, headaches , abdominal distension, upper respiratory tract infection.	http://www.rxlist.com/gattex-drug.htm https://www.gattex.com/  http://www.drugs.com/gattex.html
FPDB21374	Th1140	Insulin,isophane	A chain: GIVEQCCTSICSLYQLENYCN  B chain: FVNQHLCGSHLVEALYLVCGERGFFYTPKT	63	Antidiabetic Agents	Hypoglycemic Agents and Antidiabetic Agents	Ia	Used to improve glycemic control in patients with type 1 or type 2 diabetes mellitus.	Insulin receptor	1634				5808	C257H383N65O77S6	9				Recombinant (E.coli derived), Intermediate-acting insulin to improve glycemic control. It consists of a crystalline suspension of human insulin with protamine and zinc, which results in an intermediate-acting insulin with a slower onset of action and longer duration of activity compared to regular human insulin.	When 0.3 Units/kg of NPH insulin was subcutaneously administered, the onset of action was approximately 0.8 h. The duration of action was 13.2 h. The peak activity of NPH insulin occurs 4-6 h post-dose. Compared to insulin glargine, NPH insulin has a quicker onset of action and shorter duration of action.	The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism	Hypoglycemia is one of the most frequent adverse events experienced by insulin users.	Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process.	NPH insulin is generally well and rapidly absorbed from the site of injection. Absorption does not differ if it is subcutaneously administered in the thigh or abdomen. when 0.5 IU/kg of NPH insulin was given to adult type 1 diabetes patients before breakfast, the pharmacokinetic parameters are as follows: AUC (0-24 h) = 111,941 ± 77,941 pmol · l-1 · min-1; Cmax = 149 ± 121 pmol/l; Tmax = 480 ± 237 minute. It is important to note that NPH insulin has a high degree of patient variability in its absorption profile.	150 ml/kg						Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus,		Novolin N in an InnoLet disposable prefilled insulin syringe. Novolin N is commonly known as NPH, Human Insulin Isophane Suspension (recombinant DNA origin). The concentration of this product is 100 units of insulin per milliliter. It is a cloudy or milky suspension of human insulin with protamine and zinc. The insulin substance (the cloudy material) settles at the bottom of the insulin reservoir, therefore, the Novolin N InnoLet (nph, human insulin isophane suspension 3 ml disposable prefilled syringe) must be rotated up and down so that the contents are uniformly mixed before a dose is given	Novolin N InnoLet (nph, human insulin isophane suspension 3 ml disposable prefilled syringe)	Subcutaneous	0.5 U/kg/day SC (Type 1 Diabetes Mellitus), 0.5-1 units/kg/day in divided doses (Type 2 Diabetes Mellitus)	Tell your doctor or pharmacist if you have any medical conditions, pregnant, planning to become pregnant, or are breast-feeding; taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement; allergies to medicines, foods, or other substances; drink alcoholic beverages or smoke; heart problems (eg, heart failure); kidney or liver problems; nerve problems; adrenal, pituitary, or thyroid problems; or diabetic ketoacidosis; use 3 or more insulin injections per day; if you are fasting, have high blood sodium levels, or are on a low-salt (sodium) diet. Some MEDICINES MAY INTERACT with insulin isophane vials. Tell your health care provider if you are taking any other medicines, especially any of the following: Beta-blockers, Angiotensin-converting enzyme, (ACE) inhibitors, Thiazolidinediones Corticosteroids .	insulin allergy, Hypoglycemia, or low blood sugar, is the most common side effect of insulin. Symptoms of low blood sugar may include headache, hunger, sweating, pale skin, irritability, dizziness, feeling shaky, or trouble concentrating. Watch for signs of low blood sugar. Carry a piece of non-dietetic hard candy or glucose tablets with you in case you have low blood sugar. Tell your doctor if you have itching, swelling, redness, or thickening of the skin where you inject insulin isophane.	http://en.wikipedia.org/wiki/NPH_insulin http://www.drugs.com/mtm/insulin-isophane.html http://reference.medscape.com/drug/humulin-70-30-novolin-70-30-insulin-isophane-human-insulin-regular-human-999708
FPDB21375	Th1146	Lucinactant	KLLLLKLLLLKLLLLKLLLLK	21	Pulmonary Surfactants	Pulmonary surfactants	Ib	Intended for the prevention of respiratory distress syndrome (RDS) in premature infants at high risk for RDS.		1641				2470.2	C126H238N26O22					A new synthetic peptide containing surfactant for intratracheal use. It contains sinapultide, a novel, hydrophobic, 21-amino acid peptide (leucine and lysine repeating units, KL4 peptide) designed to mimic human surfactant protein-B (SB-P). It specifically mimics the C-terminal amphipathic helical domain of this protein. It also consists of phospholipids (dipalmitoylphosphatidylcholine, DPPC and palmitoyloleoyl phosphatidylglycerol,POPG) and a fatty acid (palmitic acid). It is completely devoid of animal-derived components. FDA approved it on March 6, 2012.	Lucinactant is a new synthetic surfactant containing a protein that mimics human surfactant protein-B, is effective at preventing respiratory distress syndrome (RDS) and related complications in preterm infants. Lucinactant has been shown to have antiinflammatory properties, is resistant to proteolytic degradation and oxidation, and has no potential for transmitting animal-derived diseases. Lucinactant has proven safe and effective in the prevention of RDS in preterm infants and as a treatment for MAS in full-term infants and for adult ARDS.	Pulmonary surfactant is a lipoprotein complex that is produced naturally in the lungs, where it lines the alveolar epithelium and serves to reduce surface tension, which facilitates alveoli expansion and allows gas exchange. Human surfactants contain phospholipids, predominantly dipalmitoylphosphatidylcholine (DPPC), in addition to surfactant proteins A, B, C and D. Surfactant is also a physical barrier to inhaled particle and noxious agents, enhances particle clearance, is involved in host defense against infection and possesses antiinflammatory properties. Several serious respiratory disorders have been associated with a loss or lack of endogenous surfactant. Lucinactant was designed to mimic the essential endogenous human surfactant protein B (SP-B).	Most common adverse reactions associated with the use of lucinactant are endotracheal tube reflux, pallor, endotracheal tube obstruction, and need for dose interruption.					US5407914	2012-06-03 00:00:00	2013-07-11 00:00:00		To prevent respiratory distress syndrome (RDS) in premature infants at high risk for RDS. It reduces the incidence of RDS at 24 h and mortality due to RDS.		Intratracheal Suspension: 8.5 ml suspension in a glass vial. Each mL contains 30000 ug phospholipids [22500 ug dipalmitoylphosphatidylcholine (DPPC) and 7500 ug palmitoyloleoyl-phosphatidylglycerol, sodium salt (POPG, Na)], 4050 ug palmitic acid (PA), and 862 ug sinapultide.	Suspension	Intratracheal administration	The recommended dose of surfaxin is 5.8 ml per kg birth weight. Up to 4 doses of surfaxin can be administered in the first 48 h of life. Doses should be given no more frequently than every 6 h.		Administration-related oxygen desaturation and bradycardia	http://www.drugbank.ca/drugs/DB04897
FPDB21376	Th1157	Sermorelin	YADAIFTNSYRKVLGQLSARKLLQDIMSRQ	30	Hormonal Agents	Hormone Replacement Agents	Ia	For the treatment of dwarfism, prevention of HIV-induced weight loss	Growth hormone-releasing hormone receptor	1666				3357.882	C149H246N44O42S	9.99	-0.33		0.183333-0.2 h	Sermorelin acetate is the acetate salt of an amidated synthetic 29-amino acid peptide (GRF 1-29 NH 2 ) that corresponds to the amino-terminal segment of the naturally occurring human growth hormone-releasing hormone (GHRH or GRF) consisting of 44 amino acid residues.	Sermorelin is used in the treatment of children with growth hormone deficiency or growth failure. Geref increases plasma growth hormone (GH) concentration by stimulating the pituitary gland to release GH. Geref is similar to the full-length native hormone (44 residues) in its ability to stimulate GH secretion in humans.	Sermorelin binds to the growth hormone releasing hormone receptor and mimics native GRF in its ability to stimulate growth hormone secretion.										Sermorelin is approved for diagnostic evaluation of pituitary function and also for increasing growth in children. Off label usage may include acute or age-related growth hormone insufficiency		Two vial presentations are available, Each vial contains 500 ug sermorelin (as the acetate) and 5000 ug mannitol. The pH is adjusted with dibasic sodium phosphate and monobasic sodium phosphate buffer. Each vial contains 3000 ug sermorelin (as the acetate) and 5000 ug mannitol. The pH is adjusted with dibasic sodium phosphate and monobasic sodium phosphate buffer.	Sermorelin is a sterile, non-pyrogenic, lyophilized powder	Subcutaneous Injection	A dosage of 0.2 - 0.3 ug once daily at bedtime by subcutaneous injection is recommended. It is also recommended that subcutaneous injection sites be periodically rotated.	Sermorelin should not be used by patients with a known sensitivity to sermorelin or any of the excipients	The most common treatment-related adverse event (occurring in about 1 patient in 6) is local injection reaction characterized by pain, swelling or redness. Other treatment-related adverse events had individual occurrence rates of less than 1% and include: headache, flushing, dysphagia, dizziness, hyperactivity, somnolence and urticaria.	http://www.rxlist.com/sermorelin-acetate-drug.htm http://en.wikipedia.org/wiki/Sermorelin
FPDB21377	Th1158	Aprotinin	RPDFCLEPPYTGPCKARIIRYFYNAKAGLCQTFVYGGCRAKRNNFKSAEDCMRTCGGA	58	Unclassified		IIa	For prophylactic use to reduce perioperative blood loss and the need for blood transfusion in patients undergoing cardiopulmonary bypass in the course of coronary artery bypass graft surgery who are at an increased risk for blood loss and blood transfusion.	Trypsin-1, Chymotrypsinogen B, Plasminogen, Kallikrein-!	1667				6511.439	C284H432N84O79S7			>100	Plasma half life: 2.5 h, Elimination half life: 10 h	Aprotinin, also known as bovine pancreatic trypsin inhibitor, BPTI (Trasylol, Bayer) is a protein, that is used as medication administered by injection to reduce bleeding during complex surgery, such as heart and liver surgery. Its main effect is the slowing down of fibrinolysis, the process that leads to the breakdown of blood clots. The aim in its use is to decrease the need for blood transfusions during surgery, as well as end-organ damage due to hypotension (low blood pressure) as a result of marked blood loss.	Aprotinin is a broad spectrum protease inhibitor which modulates the systemic inflammatory response (SIR) associated with cardiopulmonary bypass (CPB) surgery. SIR results in the interrelated activation of the hemostatic, fibrinolytic, cellular and humoral inflammatory systems. Aprotinin, through its inhibition of multiple mediators [e.g., kallikrein, plasmin] results in the attenuation of inflammatory responses, fibrinolysis, and thrombin generation. Aprotinin inhibits pro-inflammatory cytokine release and maintains glycoprotein homeostasis. In platelets, aprotinin reduces glycoprotein loss (e.g., GpIb, GpIIb/IIIa), while in granulocytes it prevents the expression of pro-inflammatory adhesive glycoproteins.	Aprotinin inhibits several serine proteases, specifically trypsin, chymotrypsin and plasmin at a concentration of about 125,000 IU/ml, and kallikrein at 300,000 IU/ml. Its action on kallikrein leads to the inhibition of the formation of factor XIIa. As a result, both the intrinsic pathway of coagulation and fibrinolysis are inhibited. Its action on plasmin independently slows fibrinolysis.		Aprotinin is slowly degraded by lysosomal enzymes.	100%(IV)			US5198534，CA2030783	1993-03-30 00:00:00		Captopril- aprotinin infused intravenously in a dose of 2 million KIU over two hours blocked the acute hypotensive effect of 100000 ug of captopril.Heparin- Aprotinin, in the presence of heparin, has been found to prolong the activated clotting time (ACT) as measured by a celite surface activation method，Tenecteplase- Aprotonin may antagonize the effect of Tenecteplase，Urokinase- Aprotonin may antagonize the effect of Urokinase	Trasylol (aprotinin) is indicated for prophylactic use to reduce perioperative blood loss and the need for blood transfusion in patients undergoing cardiopulmonary bypass in the course of coronary artery bypass graft surgery who are at an increased risk for blood loss and blood transfusion.		Each milliliter contains 10,000 KIU (Kallikrein Inhibitor Units) (1400 ug/ml) and 9000 ug sodium chloride in water for injection. Hydrochloric acid and/or sodium hydroxide is used to adjust the pH to 4.5-6.5.	It is supplied as a clear, colorless, sterile isotonic solution	Intravenous  administration	dosage is given as two regimens: Regimen A and Regimen B intial dose is same 1 ml (1400 ug or 10000 KIU) but loading dose and PumpPrime dose is 200 ml in case of regimen A and 100 ml in case of regimen B, and constant infusion rate is 50 ml/hr in A and 25 ml/hr in B.	Administration of Trasylol (aprotinin) to patients with a known or suspected previous aprotinin exposure during the last 8760 h is contraindicated. For patients with known or suspected history of exposure to aprotinin greater than 8760 h previously.	Ventricular fibrillation, heart arrest, bradycardia, congestive heart failure, hemorrhage, bundle branch block, myocardial ischemia, ventricular tachycardia, heart block, pericardial effusion, ventricular arrhythmia, shock, pulmonary hypertension. Hyperglycemia, hypokalemia, hypervolemia, acidosis. Arthralgia. Agitation, dizziness, anxiety, convulsion. Pneumonia, apnea, increased cough, lung edema.	http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=8a5982c6-825f-4d05-90f5-1519a7291d15
FPDB21378	Th1212	Insulin Pork	A chain GIVEQCCTSICSLYQLENYCN B chain FVNQHLCGSHLVEALYLVCGERGFFYTPKT	63	Antidiabetic Agents	Hypoglycemic Agents, Antidiabetic Agents	Ia	For the treatment of type I and II diabetes mellitus.	Insulin receptor, Insulin-like growth factor 1 receptor, Insulin-degrading enzyme, HLA class II histocompatibility antigen, DQ alpha 2 chain, HLA class II histocompatibility antigen, DQ beta 1 chain, Retinoblastoma-associated protein, Cathepsin D, Carboxypeptidase E, Neuroendocrine convertase 2, Neuroendocrine convertase 1, Protein NOV homolog, Low-density lipoprotein receptor-related protein 2, Insulin-like growth factor-binding protein 7, Synaptotagmin-like protein 4, Cytochrome P450 1A2	1821				5795.6	C257H387N65O76S6	5.39	0.218			Insulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure.	Insulin is used in the treatment of type I and type II diabetes. The primary activity of insulin is the regulation of glucose metabolism. In muscle and other tissues (except the brain), insulin causes rapid transport of glucose and amino acids intracellularly. It also promotes anabolism, and inhibits protein catabolism. In the liver, insulin promotes the uptake and storage of glucose in the form of glycogen, inhibits gluconeogenesis, and promotes the conversion of excess glucose into fat.	Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism.		Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process.										100 units/mL (U-100)	sterile suspension	Subcutaneous				https://www.drugs.com/drp/iletin-ii-nph-pork-100-units.html
FPDB21379	Th1213	Insulin Degludec	A chain GIVEQCCTSICSLYQLENYCN; B chain FVNQHLCGSHLVEALYLVCGERGFFYTPKT	63	Unclassified		Ia	Indicated to improve glycemic control in adults with diabetes mellitus.		1822				6103.97	C274H411N65O81S6				approximately 25 h	Insulin degludec differs from human insulin in that the amino acid threonine in position B30 has been omitted and a side-chain consisting of glutamic acid and a C16 fatty acid has been attached.	The glucose-lowering effect of TRESIBA after 192 h of once-daily dosing was measured in a euglycemic glucose clamp study enrolling 21 patients with type 1 diabetes. Figure 2 shows the pharmacodynamic effect of TRESIBA over time following 8 once-daily subcutaneous injections of 0.4 U/kg of TRESIBA in patients with type 1 diabetes.	The primary activity of insulin, including TRESIBA, is regulation of glucose metabolism. Insulin and its analogs lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production. Insulin also inhibits lipolysis and proteolysis, and enhances protein synthesis. TRESIBA forms multi-hexamers when injected into the subcutaneous tissue resulting in a subcutanous insulin degludec depot. The protracted time action profile of TRESIBA is predominantly due to delayed absorption of insulin degludec from the subcutaneous tissue to the systemic circulation and to a lesser extent due to binding of insulin-degludec to circulating albumin.		The affinity of insulin degludec to serum albumin corresponds to a plasma protein binding of > 99% in human plasma. The results of the in vitro protein binding studies demonstrate that there is no clinically relevant interaction between insulin degludec and other protein bound drugs.	After the first dose of TRESIBA, median onset of appearance was around one hour. Insulin degludec concentration reach steady state levels after 72-96 h of TRESIBA administration		The mean apparent clearance of insulin degludec is 30 ml/kg (2100 ml/h in 70 kg individual) after single subcutaneous dose of 0.4 U/kg.					TRESIBA is indicated to improve glycemic control in adults with diabetes mellitus.	LysB29(Ns-hexadecandioyl-y-Glu) des(B30) human insulin	100 units/mL (U-100) or 200 units/mL (U-200).	sterile, aqueous, clear, and colorless solution	Subcutaneous	Inject TRESIBA subcutaneously once-daily at any time of day. The recommended starting dose of TRESIBA in insulin naive patients with type 1 diabetes is approximately one-third to one-half of the total daily insulin dose. As a general rule, 0.2 to 0.4 units of insulin per kilogram of body weight can be used to calculate the initial total daily insulin dose in insulin naive patients with type 1 diabetes. The recommended starting dose of TRESIBA in insulin naive patients with type 2 diabetes mellitus is 10 units once daily.	During episodes of hypoglycemia; In patients with hypersensitivity to TRESIBA or one of its excipients.	Hypoglycemia; Hypersensitivity and allergic reactions; Hypokalemia.	http://www.rxlist.com/tresiba-drug/side-effects-interactions.htm
FPDB21380	Th1214	Insulin Beef	A chain: GIVEQCCASVCSLYQLENYCN; B chain: FVNQHLCGSHLVEALYLVCGERGFFYTPKT	63	Unclassified		Ia	For the treatment of type I and II diabetes mellitus.		1823				5733.5	C254H377N65O75S6					Insulin isolated from cattle pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure.	Insulin is used in the treatment of type I and type II diabetes. The primary activity of insulin is the regulation of glucose metabolism. In muscle and other tissues (except the brain), insulin causes rapid transport of glucose and amino acids intracellularly. It also promotes anabolism, and inhibits protein catabolism. In the liver, insulin promotes the uptake and storage of glucose in the form of glycogen, inhibits gluconeogenesis, and promotes the conversion of excess glucose into fat.	Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism.																		http://www.newdruginfo.com/pharmacopeia/usp28/v28230/usp28nf23s0_m40520.htm
FPDB21381		HEC-PT19	YBQGTFTSDYSIYLDEKAAKEFIEWLESA(SEQ ID NO: 11 )	36	Unclassified				GLP-1/GIP/GCGR		It is: B:Aib, 2-aminoisobutyric acid		The 17th lysine side chain amino group (OEG is 8-amino-3,6-dioxaoctanoic acid): -OEG-OEG-γGlu-CO-(CH2)16-CO2H	3529.42		4.08	-0.472				GLP-1R/GCGR/GIPR (EC50, nM)：0.149 16.300 NA	Combined GLP-1/GIP/GCGR						CN 115572326 A	44935			Treatment/Prevention of Metabolic Disorders and Related Conditions: Type II Diabetes; Obesity; Fatty Liver Disease (Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis); Dyslipidemia; Metabolic Syndrome							Nausea, vomiting	
FPDB21382		HEC-PT20	YBQGTFTSDYSIALDKKAQREFVEWLLSAGPSSGAPPPS (SEO ID NO: 12)	46	Unclassified				GLP-2/GIP/GCGR		It is: B:Aib, 2-aminoisobutyric acid		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid): : -OEG-OEG-γGlu-CO-(CH2)16-CO2H	4217.18		4.78	-0.544		2.8 h (mammalian reticulocytes, in vitro).		GLP-1R/GCGR/GIPR (EC50, nM)：9.657 50.270 7.634	Combined GLP-1/GIP/GCGR						CN 115572326 A	44936			Treatment/Prevention of Metabolic Disorders and Related Conditions: Type II Diabetes; Obesity; Fatty Liver Disease (Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis); Dyslipidemia; Metabolic Syndrome							Nausea, vomiting	
FPDB21383		HEC-PT24	YBQGTXTSDYSILLDRKAORDFIEWLLAGGPSSGAPPPS (SEQ ID NO: 13 )	46	Unclassified				GLP-3/GIP/GCGR		It is: B: Aib, 2-aminoisobutyric acid; X: (L)-α-Me-(2-F)-Phe		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)16-CO2H	4439.74		4.68	-0.382		2.8 h (mammalian reticulocytes, in vitro).			Combined GLP-1/GIP/GCGR						CN 115572326 A	44937			Treatment/Prevention of Metabolic Disorders and Related Conditions: Type II Diabetes; Obesity; Fatty Liver Disease (Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis); Dyslipidemia; Metabolic Syndrome							Nausea, vomiting	
FPDB21384		HEC-PT25	YBOGTXTSDYSILLDRKAQRDFIEWLLEGGPSSGAPPPS (SEQ ID NO: 14)	46	Unclassified				GLP-4/GIP/GCGR		It is: B: Aib, 2-aminoisobutyric acid; X: (L)-α-Me-(2-F)-Phe		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)16-CO2H	4388.61		4.44	-0.608		2.8 h (mammalian reticulocytes, in vitro).			Combined GLP-1/GIP/GCGR						CN 115572326 A	44938			Treatment/Prevention of Metabolic Disorders and Related Conditions: Type II Diabetes; Obesity; Fatty Liver Disease (Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis); Dyslipidemia; Metabolic Syndrome							Nausea, vomiting	
FPDB21385		HEC-PT26|||HEC-PT32	YBQGTXTSDYSILLDKKAQRDFIEWLLEGGPSSGAPPPS ( SEQ ID NO :15)	46	Unclassified				GLP-5/GIP/GCGR|||GLP-9/GIP/GCGR		It is: B: Aib, 2-aminoisobutyric acid; X: (L)-α-Me-(2-F)-Phe		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)16-CO2H|||The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid): -OEG-γGlu-CO-(CH2)16-CO2H	4251.42		4.44	-0.682		2.8 h (mammalian reticulocytes, in vitro).		GLP-1R/GCGR/GIPR (EC50, nM)：0.079 0.137 0.028|||GLP-1R/GCGR/GIPR (EC50, nM)：0.248 1.215 0.041	Combined GLP-1/GIP/GCGR						CN 115572326 A	44939|||44943			Treatment/Prevention of Metabolic Disorders and Related Conditions: Type II Diabetes; Obesity; Fatty Liver Disease (Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis); Dyslipidemia; Metabolic Syndrome							Nausea, vomiting	
FPDB21386		HEC-PT27	YBQGTXTSDYSILLDKKAAHEFIEWLLAGGPSSGAPPPS ( SEQID NO :16)	46	Unclassified				GLP-6/GIP/GCGR		It is: B: Aib, 2-aminoisobutyric acid; X: (L)-α-Me-(2-F)-Phe		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)16-CO2H	4131.32		4.75	-0.377		2.8 h (mammalian reticulocytes, in vitro).			Combined GLP-1/GIP/GCGR						CN 115572326 A	44940			Treatment/Prevention of Metabolic Disorders and Related Conditions: Type II Diabetes; Obesity; Fatty Liver Disease (Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis); Dyslipidemia; Metabolic Syndrome							Nausea, vomiting	
FPDB21387		HEC-PT28	YBQGTXTSDYSILLDEKAAQEFIEWLLAGGPSSGAPPPS ( SEQID NO :17)	46	Unclassified				GLP-7/GIP/GCGR		It is: B: Aib, 2-aminoisobutyric acid; X: (L)-α-Me-(2-F)-Phe		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)16-CO2H	4123.25		3.83	0.374					Combined GLP-1/GIP/GCGR						CN 115572326 A	44941			Treatment/Prevention of Metabolic Disorders and Related Conditions: Type II Diabetes; Obesity; Fatty Liver Disease (Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis); Dyslipidemia; Metabolic Syndrome							Nausea, vomiting	
FPDB21388		HEC-PT31	YBQGTXTSDYSIYLDKKAQQDFIEWLLEGGPSSGAPPPS ( SEQ ID NO :18)	46	Unclassified				GLP-8/GIP/GCGR		It is: B: Aib, 2-aminoisobutyric acid; X: (L)-α-Me-(2-F)-Phe		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)16-CO2H	4273.38		4.11	-0.787					Combined GLP-1/GIP/GCGR						CN 115572326 A	44942			Treatment/Prevention of Metabolic Disorders and Related Conditions: Type II Diabetes; Obesity; Fatty Liver Disease (Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis); Dyslipidemia; Metabolic Syndrome							Nausea, vomiting	
FPDB21389	P01275	Human GLP-1	HAEGIFTSDVSSYLEGOAAKEFIAWINKGRG	31	GLP-1 Receptor Agonists	GLP-1 receptor agonists (long-acting/short-acting).	Endogenous hormones (non-drug)	Type 2 diabetes (improving blood glucose control); obesity (suppressing appetite and reducing body weight).	GLP-1 receptor (widely distributed in the pancreas, gastrointestinal tract, central nervous system).					3355.71	C₁₄₉H₂₂₆N₄₀O₄₅S	5.5	-0.7		0.016667-0.033333 h	Administration route: subcutaneous injection.Recommended dosage: 600 ug/day initially, gradually increased to 1800 ug/day (for diabetes); 3000 ug/day (for obesity).	GLP-1R (EC50, nM)：0.046；GCGR (EC50, nM)：NA; GIPR (EC50, nM)：NA.	Activation of GLP-1 receptor → increased cAMP → promotion of insulin secretion by β cells.	Thyroid C-cell tumors (in animal experiments, human risk not confirmed). Acute pancreatitis (rare).	The peptide chain is metabolized by endonuclease/exonuclease without the involvement of hepatic CYP450.	The peptide chain is metabolized by endonuclease/exonuclease without the involvement of hepatic CYP450.	Subcutaneous injection bioavailability is approximately 55% (liraglutide).	Mainly degraded by proteolytic enzymes and excreted by the kidneys (liraglutide clearance is approximately 600 ml/h).	US8080515B2	40878	Circa 2030	Affected absorption: in combination with drugs that accelerate gastric emptying (e.g., metoclopramide) may reduce efficacy. Oral medications**: Spaced more than 1 h apart (e.g., oral contraceptives).	Refer to the package insert (e.g., semaglutide can also be used for cardiovascular risk reduction).	Different analogues have different names (e.g., liraglutide is a fatty acid-modified GLP-1 analog).	Pre-filled injection pen (solution)	It is mostly colorless to light yellow clear liquid (injection).	subcutaneous injection	600 ug/day initially, gradually increase to 1800 ug/day (diabetes); 3000 ug/day (obesity).	Personal or family history of medullary thyroid cancer. Multiple endocrine neoplasia type 2 (MEN2).	Nausea, vomiting, diarrhoea (usually transient). The risk of hypoglycaemia is low (may be increased with insulin/sulfonylureas).	https://www.sciencemag.org/
FPDB21390	P09681	Human GIP	YAEGTFISDYSIAMDKIHOQDFVNWLLAQKGKKNDWKHNITQ	42	Unclassified		Endogenous hormones	Endogenous insulin secretion and regulation of fat metabolism	GIP receptors (pancreatic B cells, fat cells)					4983.6	C225H354N60O65S	7.5	-0.6		0.083333-0.116667 h	Endogenous insulin secretion and regulation of fat metabolism	GLP-1R (EC50, nM)：NA；GCGR (EC50, nM)： 0.028; GIPR (EC50, nM)：NA.	Activates the GIP receptor → cAMP→ promotes insulin secretion and inhibits lipolysis		DPP-4 enzyme degradation (primary) renal clearance									Glucose-dependent insulinotropic polypeptide		Glucose-dependent insulinotropic polypeptide					：https://pubmed.ncbi.nlm.nih.gov/  。
FPDB21391		HPC-PT6	YSQGTFTSDYSILLDKKAQRDFIEWLLAGGPSSGAPPPS	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 Diabetes	GLP-9/GIP/GCGR					4800	C₂₃₀H₃₅₅N₅₉O₇₅S	4.8-5.5	-0.2		168-240 h		Glucose-dependent insulinotropic secretion, delayed gastric emptying, central appetite suppression	Combined GLP-1/GIP/GCGR	Reversible thyroid C-cell hyperplasia (rodent high dose), non-genotoxic	Proteolytic enzyme degradation (DPP-4 resistant design) + hepatic/renal clearance	Subcutaneous bioavailability ~70%	100-250 ml/kg	| 20-40 ml/h	CN 115572326 A	44940		Dose reduction in combination with sulfonylureas (risk of hypoglycemia); Avoid concomitant use with drugs that accelerate gastric emptying, such as metoclopramide	Glycemic control in adults with type 2 diabetes, weight management in obesity		.5000 ug/0.5 ml	Colorless to light yellow clear solution	subcutaneous injection	Start at 750 ug/week and gradually increase to 1.5 to 2250 ug/week	History of medullary thyroid cancer, multiple endocrine neoplasia type 2 (MEN2), pregnancy or lactation	| Common: nausea (30%-40%), vomiting (10%-15%), diarrhea (10%-20%)<br>Rare: acute pancreatitis (<0.1%), allergic reactions	https://web.expasy.org/protparam
FPDB21392		HEC-PT7	YSQGTFTSDYSILLDKKAORDFIEWLLAGGPSSGAPPPS	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, underlying nonalcoholic steatohepatitis	GLP-9/GIP/GCGR				The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)16-CO2H	4500	C₂₁₀H₃₂₅N₅₅O₆₅S	4.5-5.5	-0.3		168-240 h		Glucose-dependent insulin secretion, appetite suppression, and gastric emptying	Combined GLP-1/GIP/GCGR	Preclinical data show low systemic toxicity and potential risk: thyroid C-cell hyperplasia	Proteolytic enzyme degradation (DPP-4 resistant design) + renal clearance	| Subcutaneous injection bioavailability ~80%	100-300 ml/kg	20-50 ml/h	CN 115572326 A	44941		Combination of sulfonylureas may increase the risk of hypoglycemia; Avoid concomitant use with DPP-4 inhibitors	GLP-1 receptor (pancreatic β cells, hypothalamus		1500 ug/0.5 ml once weekly	Colorless to light yellow clear solution	subcutaneous injection	Start at 750 ug/week and increase to 1.5 to 2250 ug/week as tolerated	History of medullary thyroid cancer, multiple endocrine neoplasia type 2 (MEN2), severe gastrointestinal disease	Nausea (30%-40%), vomiting (10%-15%), diarrhea (10%-20%)<br>Rare: acute pancreatitis (<0.1%), allergic reactions	https://pubmed.ncbi.nlm.nih.gov/
FPDB21393		HEC-PT8	Y(dS)QGTFTSDYSILLDKKAQRDFIEWLLAGGPSSGAPPPS	40	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes mellitus (core indication), obesity	GLP-9/GIP/GCGR		Yes		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)16-CO2H	4700	C₂₂₅H₃₄₀N₅₈O₇₀S₂	4.0-4.8	-0.5		240-336 h		Glucose-dependent insulin secretion, inhibition of glucagon release, and delay gastric emptying	Combined GLP-1/GIP/GCGR	Preclinical data show reversible elevation of liver enzymes	Hepatic endothelial cell uptake + renal clearance	Subcutaneous injection bioavailability ~75%	80-150 ml/kg	15-30 ml/h	CN 115572326 A	44942		Combined warfarin should be used to monitor INR values; Avoid concomitant use with oral antibiotics	Adjuvant treatment of obesity with glycemic control and BMI 30kg/m² in adults with type 2diabetes mellitus		(2000 ug/0.5 ml every two weeks)	Colorless transparent solution (with sodium citrate buffer, mannitol stabilizer)	Subcutaneous injection (abdomen or thigh)	Start at 1000 ug/2 weeks and gradually increase to 2.0 to 3000 ug/2 weeks	History of medullary thyroid cancer, severe renal insufficiency	Nausea (25%-35%), headache (10%-15%)	https://pubmed.ncbi.nlm.nih.gov/
FPDB21394		HEC-PT9	YBQGTFTSDYSILLDKKAQRDFIEWLLAGGPSSGAPPPS	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, underlying nonalcoholic steatohepatitis	GLP-9/GIP/GCGR		It is: B:Aib, 2-aminoisobutyric acid		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)16-CO2H	5000	C₂₄₀H₃₇₀N₆₂O₈₀S	5.0-5.8	-0.1		240-336 h		Glucose-dependent insulinotropic secretion, delayed gastric emptying, central appetite suppression	Combined GLP-1/GIP/GCGR	Reversible hepatic steatosis (high dose in animal models), non-genotoxic	Hepatic metabolism (fatty acid oxidation) + renal clearance	Subcutaneous injection bioavailability ~75%	150-300 ml/kg	10-20 ml/h	CN 115572326 A	44943		Dose adjustment is required for combined insulin; Avoid concomitant use with strong inhibitors of CYP3A4	Glycemic control in adults with type 2 diabetes mellitus and obesity management with a BMI 30kg/m²		2000 ug/0.5 ml once every two weeks	Colorless clear solution (with citrate buffer, mannitol stabilizer)	subcutaneous injection	Start at 1000 ug/2 weeks and gradually increase to 2.0 to 3000 ug/2 weeks	History of medullary thyroid cancer, severe liver injury (Child-Pugh class C), allergy to β-alanine	Nausea (25%-35%), constipation (10%-15%)	https://web.expasy.org/protparam
FPDB21395		HEC-PT14	YBQGTXTSDYSILLDKKAORDFIEWLLAGG PSSGAPPPS	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, non-alcoholic steatohepatitis	GLP-1 receptor (pancreas, liver, hypothalamus)		Yes: B: Aib, 2-Amino-isobutyric acid		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid): : -OEG-OEG-γGlu-CO-(CH2)16-CO2H	5200	C₂₅₀H₃₈₅N₆₅O₈₅S	5.5-6.2	0.2		336-504 h		Glucose-dependent insulin secretion, regulation of hepatic lipid metabolism, central appetite suppression	Activates GLP-1 receptor →↑cAMP→ insulin secretion, inhibits hepatic lipogenesis, and regulates hypothalamic appetite center	Mildly elevated liver enzymes (reversible) without teratogenicity	Hepatic metabolism (fatty acid oxidation) + renal clearance	Subcutaneous injection bioavailability ~80%	100-200 ml/kg	8-15 ml/h	CN 115572326 A	44943		Avoid use in combination with strong CYP2C8 inhibitors (which may interfere with metabolism); Levels of fat-soluble vitamins should be monitored	Improvement of glycemic control in adult type 2 diabetes, weight management in obesity, and liver fibrosis in NASH		Nano liposome injection (5000 ug/ml, once a month)	Milky white translucent colloidal solution (phospholipid carrier)	Subcutaneous injection (abdomen or thigh)	Start at 2500 ug/month and adjust to 5000-7500 ug/month according to efficacy	Severe cholestasis, active autoimmune disease, hypersensitivity to phospholipid components	Nausea (20%-30%), fatigue (10%-15%)	https://web.expasy.org/protparam
FPDB21396		HEC-PT15	YBQGTXTSDYSILLDKKAQRDFIEWLLAGG PSSGAPPPS	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, atherosclerotic cardiovascular disease	GLP-1 receptor (metabolic regulation), vascular endothelial cell adhesion molecule		Yes: B: Aib, 2-Amino-isobutyric acid		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)16-CO2H	12000	C₂₅₀H₃₈₅N₆₅O₈₅S	6.0-6.8	-0.5		720-960 h		Glucose-dependent insulin secretion, inhibition of arterial plaque inflammation, regulation of lipid metabolism	<br>1. Activates GLP-1 receptors → insulin secretion/appetite <br>suppression2. PEG targets vascular endothelial → inhibits TNF-α/IL-6 inflammatory signaling	Mild complement activation (primate model), no genotoxicity	Hepatic metabolism (PEG chain hydrolysis) + renal clearance	Subcutaneous injection bioavailability ~90%	60-120 ml/kg	4-8 ml/h	CN 115572326 A	44943		Avoid concomitant antiangiogenic drugs (e.g., bevacizumab); Fat-soluble nutrients (e.g., vitamin D) should be taken 2 h apart	Adults with type 2 diabetes mellitus and ASCVD, obesity and carotid plaque		15000 ug/0.5 ml once monthly	Colorless transparent viscous solution	Subcutaneous injection (abdomen or thigh)	Start at 7500 ug/month and increase to 15 to 22500 ug/month as tolerated	Active autoimmune disease (e.g., lupus erythematosus), severe heart failure (NYHA class IV), allergy to PEG	Induration at the injection site (25%-35%), fatigue (10%-20%)	https://pubmed.ncbi.nlm.nih.gov/
FPDB21397		HEC-PT52	"YBQGTXTSDYSILLDEIAAKDFIEWLLEGGP
SSGAPPPS"	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, atherosclerotic cardiovascular disease	GLP-1R		B is 2-Aminoisobutyric acid (Aib), dS represents D-Ser: X is (L)-a-Me-(2-F)-Phe		The 20th lysine side chain amino group (OEG being 8-amino-3,6-dioxaoctanoic acid): :-OEG-OEG-γGlu-CO-(CH2)18-CO2H	4119.65	C₁₈₈H₂₈₈FN₄₀O₆₀S	3.71	-0.305		"The N-terminal of the sequence considered is Y (Tyr).
The estimated half-life is: 2.8 h (mammalian reticulocytes, in vitro).
                            0.166667 h (yeast, in vivo).
                            0.033333 h (Escherichia coli, in vivo)."		In vitro cell GLP-1R (EC50, nM): 1.721, GCGR (EC50, nM): 4.403, GIPR (EC50, nM): 0.610.	GLP-1 receptor agonists						CN 115572326 A	44943			Type 2 diabetes				subcutaneous injection				
FPDB21398		HEC-PT53	"YBQGTXTSDYSILLDEIAQKAFIEYLLEGGPS
SGAPPPS"	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, atherosclerotic cardiovascular disease	GLP-1R		2h65byvv3q2kz8zp9d45		The 20th lysine side chain amino group (OEG being 8-amino-3,6-dioxaoctanoic acid): :-OEG-OEG-γGlu-CO-(CH2)18-CO2H	4161.73	C₁₈₉H₂₈₈FN₄₁O₅₉S	3.83	-0.315		"The N-terminal of the sequence considered is Y (Tyr).
The estimated half-life is: 2.8 h (mammalian reticulocytes, in vitro).
                            0.166667 h (yeast, in vivo).
                            0.033333 h (Escherichia coli, in vivo)."		In vitro cell GLP-1R (EC50, nM): 0.973, GCGR (EC50, nM): 2.333, GIPR (EC50, nM): 0.152.	GLP-1 receptor agonists						CN 115572326 A	44943			Type 2 diabetes				subcutaneous injection				
FPDB21399		HEC-PT54	"HBQGTXTSDYSILLDEIAAKAFIEYLLEGGPS
SGAPPPS"	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, atherosclerotic cardiovascular disease	GLP-1R		2h65byvv3q2kz8zp9d45		The 20th lysine side chain amino group (OEG being 8-amino-3,6-dioxaoctanoic acid): :-OEG-OEG-γGlu-CO-(CH2)18-CO2H	4059.2	C₁₈₇H₂₈₅FN₄₁O₅₉	4.17	-0.228		"The N-terminal of the sequence considered is H (His).
The estimated half-life is: 3.5 h (mammalian reticulocytes, in vitro).
                            0.166667 h (yeast, in vivo).
                            >10 h (Escherichia coli, in vivo)."		In vitro cell GLP-1R (EC50, nM): 0.377, GCGR (EC50, nM): 1.103, GIPR (EC50, nM): 1.611.	GLP-1 receptor agonists						CN 115572326 A	44943			Type 2 diabetes				subcutaneous injection				
FPDB21400		HEC-PT61	"YBQGTXTSDYSILLDKKAQRDFIEWLLEGGP
SSGAPPPS"	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, atherosclerotic cardiovascular disease	GLP-1R		2h65byvv3q2kz8zp9d45		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)18-CO2H	4121.081	C₁₉₀H₂₈₈FN₄₂O₅₉	4.44	-0.682		"The N-terminal of the sequence considered is Y (Tyr).
The estimated half-life is: 2.8 h (mammalian reticulocytes, in vitro).
                            0.166667 h (yeast, in vivo).
                            0.033333 h (Escherichia coli, in vivo)."		In vitro cell GLP-1R (EC50, nM): 0.101, GCGR (EC50, nM): 0.217, GIPR (EC50, nM): 0.054.	GLP-1 receptor agonists						CN 115572326 A	44943			Type 2 diabetes				subcutaneous injection				
FPDB21401		HEC-PT72	"YBQGTXTSDYSILLDRKAQQDFIEWLLEGGP
SSGAPPPS"	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, atherosclerotic cardiovascular disease	GLP-1R		2h65byvv3q2kz8zp9d45		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)18-CO2H	4121.081	C₁₉₀H₂₈₈FN₄₂O₅₉	4.11	-0.672		"The N-terminal of the sequence considered is Y (Tyr).
The estimated half-life is: 2.8 h (mammalian reticulocytes, in vitro).
                            0.166667 h (yeast, in vivo).
                            0.033333 h (Escherichia coli, in vivo)."		In vitro cell GLP-1R (EC50, nM): 0.299, GCGR (EC50, nM): 0.522, GIPR (EC50, nM): 0.079.	GLP-1 receptor agonists						CN 115572326 A	44943			Type 2 diabetes				subcutaneous injection				
FPDB21402		HEC-PT73	"HBQGTXTSDYSILLDRIAAKDFIEWLLEGGP
SSGAPPPS"	39	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, atherosclerotic cardiovascular disease	GLP-1R		2h65byvv3q2kz8zp9d45		The 20th lysine side chain amino group (OEG being 8-amino-3,6-dioxaoctanoic acid): :-OEG-OEG-γGlu-CO-(CH2)18-CO2H	4686.2	C₂₀₁H₂₂₈N₄₂O₁₇F	4.43	-0.379		"The N-terminal of the sequence considered is H (His).
The estimated half-life is: 3.5 h (mammalian reticulocytes, in vitro).
                            0.166667 h (yeast, in vivo).
                            >10 h (Escherichia coli, in vivo)."		In vitro cell GLP-1R (EC50, nM): 0.477, GCGR (EC50, nM): 0.739, GIPR (EC50, nM): 0.463.	GLP-1 receptor agonists						CN 115572326 A	44943			Type 2 diabetes				subcutaneous injection				
FPDB21403		HEC-PT115	YBQGTXTSDYSILLDKKAQRAFIEYLLAGGP SSGAPPPS-NH2   B is 2-aminoisobutyric acid (Aib), dS indicates D-Ser: X is (L)-a-Me-(2-F)-Phe	92	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, atherosclerotic cardiovascular disease	GLP-1R		2h65byvv3q2kz8zp9d45		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)18-CO2H	4705.21	C₂₀₁H₂₃₀N₄₀O₁₄F	6.12	-0.421		"The N-terminal of the sequence considered is Y (Tyr).
The estimated half-life is: 2.8 h (mammalian reticulocytes, in vitro).
                            0.166667 h (yeast, in vivo).
                            0.033333 h (Escherichia coli, in vivo)."		In vitro cell GLP-1R (EC50, nM): 0.334, GCGR (EC50, nM): 0.141, GIPR (EC50, nM): 0.139.	GLP-1 receptor agonists						CN 115572326 A	44943			Type 2 diabetes				subcutaneous injection				
FPDB21404		HEC-PT116	"YBQGTXTSDYSILLDKKAQRAFIEWLLAGG
PSSGAPPPS-NH2"	41	GLP-1 Receptor Agonists	GLP-1 receptor agonists		Type 2 diabetes, obesity, atherosclerotic cardiovascular disease	GLP-1R		2h65byvv3q2kz8zp9d45		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)18-CO2H	4722.23	C₂₀₂H₂₃₃N₄₁O₁₆F	6.12	-0.41		"The N-terminal of the sequence considered is Y (Tyr).
The estimated half-life is: 2.8 h (mammalian reticulocytes, in vitro).
                            0.166667 h (yeast, in vivo).
                            0.033333 h (Escherichia coli, in vivo)."		In vitro cell GLP-1R (EC50, nM): 0.224, GCGR (EC50, nM): 0.095, GIPR (EC50, nM): 0.110.	GLP-1 receptor agonists						CN 115572326 A	44943			Type 2 diabetes				subcutaneous injection				
FPDB21405		HEC-PT117	"YBHGTXTSDYSILLDKKAQRAFIEWLLAGG
PSSGAPPPS-NH2"	41	Unclassified			Type 2 diabetes, obesity, atherosclerotic cardiovascular disease	GLP-1R		2h65byvv3q2kz8zp9d45		The amino group on the side chain of the 17th lysine (OEG is 8-amino-3,6-dioxaoctanoic acid):: -OEG-γGlu-CO-(CH2)18-CO2H	4722.23	C₂₀₁H₂₃₂N₄₁O₁₅F	6.75	-0.403		"The N-terminal of the sequence considered is Y (Tyr).
The estimated half-life is: 2.8 h (mammalian reticulocytes, in vitro).
                            0.166667 h (yeast, in vivo).
                            0.033333 h (Escherichia coli, in vivo)."		In vitro cell-based GLP-1R (EC50, nM): 0.277; GCGR (EC50, nM): 0.090; GIPR (EC50, nM): 0.073.	GLP-1 receptor agonists						CN 115572326 A	44943			Type 2 diabetes				subcutaneous injection				
FPDB21406		1	k8-GLP-1(7-37)	4	GLP-1 Receptor Agonists	Antidiabetic agent / GLP-1 receptor agonist.								3837					1.2h		potency (EC5o, pM)55±19		Common toxicities include gastrointestinal effects (nausea, vomiting).	Likely degraded by neprilysin (NEP)anddipeptidyl peptidase-4 (DPP-4)enzymes	Administered subcutaneously with slow absorption into systemic circulation.	Low volume of distribution (typical for peptide drugs), confined primarily to plasma and extracellular fluid.	Renal clearance predominates; metabolism via proteolytic enzymes.					Type 2 diabetes mellitus		Subcutaneous injection (solution or lyophilized powder).	quid (prefilled pen) or powder for reconstitution.	Subcutaneous injection.	500–1000 ug weekly	Personal/family history of medullary thyroid carcinoma (MTC).	* Nausea, diarrhea, constipation, headache.	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5846677/
FPDB21407		2	K8(C16-γ-Glu)R26,34-GLP 1(7-37)	9	Unclassified								The ε-amino group of the 8th lysine residue is modified by γ-Glu	3820		4.5–5.5				A long-acting, acylated GLP-1 analog engineered for once-weekly subcutaneous administration Modifications improve resistance to enzymatic degradation and prolong systemic exposure.	potency (EC50, pM) 1260 ± 210																			https://www.fda.gov/drugs
FPDB21408		3	K18(C16-γ-Glu)R26,34-GLP-1(7-37)	9	Unclassified								The ε-amino group of the 18th lysine side chain is modified by γ-Glu.	3779							potency (EC5o, pM)35.2±6.2																			
FPDB21409		4	K23(C16-γ-Glu)R26，34-GLP-1(7-37)	9	Unclassified								The ε-amino group of the lysine at position 23 is modified by γ-Glu	3751					20±2h		potency (EC5o, pM)30.1±3.3																			
FPDB21410		5	K26(C16-γ-Glu)R34-GLP 1(7-37)	9	Unclassified								The ε-amino group of the 26th lysine residue is modified by γ-Glu	3778					14±2h		potency (EC5o, pM)61.0±7.1																			
FPDB21411		6	K27(C16-γ-Glu)R26,34-GLP 1(7-37)	9	Unclassified								The ε-amino group of the 27th lysine residue is modified by γ-Glu	3751							potency (EC5o, pM)36.3±0.3																			
FPDB21412		7	K34(C16-γ-Glu)-R26-GLP-1（7-37)	9	Unclassified								The ε-amino group of lysine at position 34 is modified by γ-glutamyl.	3694					13h		potency (EC5o, pM)121±26																			
FPDB21413		8	K36(C16-γ-Glu)R26,34-GLP-1(7-36)	9	Unclassified								γ-Glu modification of the side chain amino group of lysine at position 36	3880					12±2h		potency (EC5o, pM)36.4±2.1																			
FPDB21414		9	K38(C16-γ-Glu)-R26,34-GLP-1(7-38)	9	Unclassified								The ε-amino group of the 38th lysine residue is modified by γ-Glu	3893							potency (EC5o, pM)53.0±2.8																			
FPDB21415		10	K26,34 (bis-C16-diacid)-GLP-1 (7-37)	14	Unclassified								The side chain amino groups of lysines at positions 26 and 34 are modified by (di--C16-diacid)	4091							potency (EC5o, pM)70007																			
FPDB21416		11	K26,34(bis-γ-Glu-C16)-GLP-1(7-37)	11	Unclassified								The side-chain amino groups of lysines at positions 26 and 34 are modified with (di-γ-Glu-C16)	4035							potency (EC5o, pM)16700±3700																			
FPDB21417		12	K26,34 (di-γ-Glu-C14)-GLP-1(7-37)	10	Unclassified								The side chain amino groups of lysines at positions 26 and 34 are modified with (di-γ-Glu-C14)	3780							potency (EC5o, pM)3050±350																			
FPDB21418		13	K26(bis-C12-diacid),K34(bis-C12-diacid)-GLP-1(7-37)	25	Unclassified			for type 2 diabetes	GLP-1R				A bis-C12-diacid modification is attached to the side chains of lysines (Lys, K) at positions 26 and 34.	3780						"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：177±52	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21419		14	K26（C16-diacid）-R34-GLP-1(7-37)	12	Unclassified			for type 2 diabetes	GLP-1R				"A C16-diacid modification is attached to the side chain of lysine (Lys, K) at position 26. 

The natural amino acid at position 34 (usually glutamic acid E or lysine K) is replaced with arginine (Arg, R)."	3653						"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：154±66	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21420		15	K26（C14-diacid）-R34-GLP-1(7-37)	12	Unclassified			for type 2 diabetes	GLP-1R				"At lysine (Lys, K) at position 26, a C14-diacid modification is attached to the side chain.

R34: The natural amino acid at position 34 (usually glutamic acid E or lysine K) is replaced with arginine (Arg, R)."	3624						"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：72±0.7	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21421		16	K26（γ-Glu-C18）-R34-GLP-1(7-37)	9	Unclassified			for type 2 diabetes	GLP-1R				"A (γ-Glu-C18) modification is attached to the side chain of lysine (Lys, K) at position 26.

R34: The 34th naturally occurring amino acid (typically glutamic acid, E, or lysine, K) is replaced with arginine (Arg, R)."	3779						"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：194±24	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21422		17	K26（γ-Glu-C14）-R34-GLP-1(7-37)	9	Unclassified			for type 2 diabetes	GLP-1R				"A (γ-Glu-C14) modification is attached to the side chain of lysine (Lys, K) at position 26.

R34: The natural amino acid at position 34 (usually glutamic acid E or lysine K) is replaced with arginine (Arg, R)."	3723						"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：22.0±7.1	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21423		18	K26（γ-Glu-C12）-R34-GLP-1(7-37)	9	Unclassified			for type 2 diabetes	GLP-1R				"A (γ-Glu-C12) modification is attached to the side chain of lysine (Lys, K) at position 26.

R34: The natural amino acid at position 34 (usually glutamic acid E or lysine K) is replaced with arginine (Arg, R)."	3695					15±3 h	"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：27.3±8.4	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21424		19	K26（γ-Glu-C16）-desamino-H7R34-GLP-1(7-37)	18	Unclassified			for type 2 diabetes	GLP-1R				"On the side chain of lysine (Lys, K) at position 26: a hexadecyl (C16) group is attached via a γ-glutamyl linkage, resulting in fatty acylation modification. The 7th amino acid, histidine (His, H):
Remove the α-amino group (-NH₂), retaining the imidazole ring side chain. The 34th arginine (Arg, R) is substituted for the native glycine (Gly, G)."	3737						"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：687±129	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21425		20	K26（GABA-C16）-R34-GLP-1(7-37)	10	Unclassified			for type 2 diabetes	GLP-1R				"A (GABA-C16) modification is attached to the side chain of lysine (Lys, K) at position 26.

R34: The natural amino acid at position 34 (usually glutamic acid E or lysine K) is replaced with arginine (Arg, R)."	3707					31±4 h	"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：84.4±22.1	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21426		21	                                   K26（â -Ala-C16）-R34-GLP-1(7-37)	9	Unclassified			for type 2 diabetes	GLP-1R				"A (â-Ala-C16) modification is attached to the side chain of lysine (Lys, K) at position 26.

R34: The natural amino acid at position 34 (usually glutamic acid E or lysine K) is replaced with arginine (Arg, R)."	3694					8.8±1 h	"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：113±3	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21427		22	K26（Iso-Nip-C16）-R34-GLP-1(7-37)	12	Unclassified			for type 2 diabetes	GLP-1R				"An (Iso-Nip-C16) modification is attached to the side chain of lysine (Lys, K) at position 26.

R34: The natural amino acid at position 34 (usually glutamic acid E or lysine K) is replaced with arginine (Arg, R)."	3733						"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：410±120	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21428		23	K34（γ-Glu-C16）-desamino-H7R34-GLP-1(7-37)	18	Unclassified			for type 2 diabetes	GLP-1R				At lysine (Lys, K) at position 34 side chain: a palmitoyl (C16) is attached through γ-glutamyl (γ-Glu) forming a fatty acyl modification. At histidine (His, H) at position 7: the α-amino group (-NH₂) is removed, retaining the imidazole side chain. Arginine (Arg, R) at position 34 replaces the natural glycine (Gly, G).	3737						"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：2360±370	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21429		24	K34（C8）-desamino-H7R34-GLP-1(7-37)	15	Unclassified			for type 2 diabetes	GLP-1R				At the 34th lysine (Lys, K) side chain: a (C8) is attached to form a fatty acylation modification. At the 7th histidine (His, H): the α-amino group (-NH₂) is removed, retaining the imidazole side chain. At the 34th arginine (Arg, R), the natural glycine (Gly, G) is replaced.	3496						"A series of very potent derivatives of the 30-amino acid peptide hormone glucagon-like peptide-1
(GLP-1) is described. The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin."	potency (EC50, pM)：236±66	"The principle of fatty acid derivatization has been
used to protract the action of insulin by facilitating
binding to serum albumin."						US6268343B1	37103			Type 2 diabetes				"injection or through
an alternative way feasible for peptides (pulmonal,
buccal)."				
FPDB21430		25	desamino-H7R26-GLP-1(7-37)	13	Unclassified				GLP-1 receptor		"Abbreviations used for acyl groups in lysine N_x005f_x005f_x000f_
-acylated peptides: γ-Glu-C8 ) γ-L-glutamoyl(NR-octanoyl); γ-Glu-C14 ) γ-Lglutamoyl(NR-tetradecanoyl);
γ-Glu-C16 ) γ-L-glutamoyl(NR-hexadecanoyl); γ-Glu-C18 ) γ-L-glutamoyl(NR-octadecanoyl); C8 ) octanoyl;
C12-diacid ) ω-carboxyundecanoyl; C16-diacid ) ω-carboxypentadecanoyl; C20-diacid ) ω-carboxynonadecanoyl; GABA-C16 ) γ-aminobutyroyl(Nγ-hexadecanoyl);
 Iso-Nip-C16 ) 1-(hexadecanoyl)piperidyl-4-carboxy. Data are given as mean ( SD of two individual
experiments with triplicate samples."		K34 γ-Glu-C8	3625						"The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin. GLP-1 had a potency (EC50) of 0.000055 uM for
the cloned human GLP-1 receptor. Many of the compounds had similar or even higher potencies,
despite quite large substituents. All compounds derivatized with fatty acids equal to or longer
than 12 carbon atoms were very protracted compared to GLP-1 and thus seem suitable for
once daily administration to type 2 diabetic patients. A structure-activity relationship was
obtained. GLP-1 could be derivatized with linear fatty acids up to the length of 16 carbon atoms,
sometimes longer, almost anywhere in the C-terminal part without considerable loss of potency.
Derivatization with two fatty acid substituents led to a considerable loss of potency. A structureactivity
 relationship on derivatization of specific amino acids generally was obtained. It was
found that the longer the fatty acid, the more potency was lost. Simultaneous modification of
the N-terminus (in order to obtain better metabolic stability) interfered with fatty acid
derivatization and led to loss of potency."	EC50, pM 169 ±1	"Derivatization with both short and long
fatty acids and amino acid-derived spacers led to
compounds that were highly potent. Several compounds
were both very potent and had plasma half-lives above
10 h, making them suitable as drugs for treatment of
type 2 diabetes using once daily administration"										Type 2 diabetes				"need to be administered by injection or through
an alternative way feasible for peptides (pulmonal,
buccal"	27% 4100 ug			
FPDB21431		26|||27|||28	K36R26,34-GLP-1(7-36)	5	Unclassified				GLP-1 receptor		"Abbreviations used for acyl groups in lysine N_x005f_x005f_x000f_
-acylated peptides: γ-Glu-C8 ) γ-L-glutamoyl(NR-octanoyl); γ-Glu-C14 ) γ-Lglutamoyl(NR-tetradecanoyl);
γ-Glu-C16 ) γ-L-glutamoyl(NR-hexadecanoyl); γ-Glu-C18 ) γ-L-glutamoyl(NR-octadecanoyl); C8 ) octanoyl;
C12-diacid ) ω-carboxyundecanoyl; C16-diacid ) ω-carboxypentadecanoyl; C20-diacid ) ω-carboxynonadecanoyl; GABA-C16 ) γ-aminobutyroyl(Nγ-hexadecanoyl);
 Iso-Nip-C16 ) 1-(hexadecanoyl)piperidyl-4-carboxy. Data are given as mean ( SD of two individual
experiments with triplicate samples."		K36 C20-diacid|||K36 C16-diacid|||K36 γ-Glu-C18	3651|||3595|||3722					13 ± 4h	"The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin. GLP-1 had a potency (EC50) of 0.000055 uM for
the cloned human GLP-1 receptor. Many of the compounds had similar or even higher potencies,
despite quite large substituents. All compounds derivatized with fatty acids equal to or longer
than 12 carbon atoms were very protracted compared to GLP-1 and thus seem suitable for
once daily administration to type 2 diabetic patients. A structure-activity relationship was
obtained. GLP-1 could be derivatized with linear fatty acids up to the length of 16 carbon atoms,
sometimes longer, almost anywhere in the C-terminal part without considerable loss of potency.
Derivatization with two fatty acid substituents led to a considerable loss of potency. A structureactivity
 relationship on derivatization of specific amino acids generally was obtained. It was
found that the longer the fatty acid, the more potency was lost. Simultaneous modification of
the N-terminus (in order to obtain better metabolic stability) interfered with fatty acid
derivatization and led to loss of potency."	EC50, pM 210±14|||EC50, pM 7.89 ± 1.21|||EC50, pM 116 ±3	"Derivatization with both short and long
fatty acids and amino acid-derived spacers led to
compounds that were highly potent. Several compounds
were both very potent and had plasma half-lives above
10 h, making them suitable as drugs for treatment of
type 2 diabetes using once daily administration"										Type 2 diabetes				"need to be administered by injection or through
an alternative way feasible for peptides (pulmonal,
buccal"	8% 500 ug|||11% 600 ug|||27% 3700 ug			
FPDB21432		29|||30|||31|||32	R26,34-GLP-1(7-38)	4	Unclassified				GLP-1 receptor		"Abbreviations used for acyl groups in lysine N_x005f_x005f_x000f_
-acylated peptides: γ-Glu-C8 ) γ-L-glutamoyl(NR-octanoyl); γ-Glu-C14 ) γ-Lglutamoyl(NR-tetradecanoyl);
γ-Glu-C16 ) γ-L-glutamoyl(NR-hexadecanoyl); γ-Glu-C18 ) γ-L-glutamoyl(NR-octadecanoyl); C8 ) octanoyl;
C12-diacid ) ω-carboxyundecanoyl; C16-diacid ) ω-carboxypentadecanoyl; C20-diacid ) ω-carboxynonadecanoyl; GABA-C16 ) γ-aminobutyroyl(Nγ-hexadecanoyl);
 Iso-Nip-C16 ) 1-(hexadecanoyl)piperidyl-4-carboxy. Data are given as mean ( SD of two individual
experiments with triplicate samples."		K38 C16-diacid|||K38 C12-diacid|||K38 γ-Glu-C18|||K38 γ-Glu-C14	3808|||3752|||3935|||3880						"The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin. GLP-1 had a potency (EC50) of 0.000055 uM for
the cloned human GLP-1 receptor. Many of the compounds had similar or even higher potencies,
despite quite large substituents. All compounds derivatized with fatty acids equal to or longer
than 12 carbon atoms were very protracted compared to GLP-1 and thus seem suitable for
once daily administration to type 2 diabetic patients. A structure-activity relationship was
obtained. GLP-1 could be derivatized with linear fatty acids up to the length of 16 carbon atoms,
sometimes longer, almost anywhere in the C-terminal part without considerable loss of potency.
Derivatization with two fatty acid substituents led to a considerable loss of potency. A structureactivity
 relationship on derivatization of specific amino acids generally was obtained. It was
found that the longer the fatty acid, the more potency was lost. Simultaneous modification of
the N-terminus (in order to obtain better metabolic stability) interfered with fatty acid
derivatization and led to loss of potency."	EC50, pM 5.60 ±3.5|||EC50, pM 4.19 ±0.98|||EC50, pM 115±21|||EC50, pM 54± 1	"Derivatization with both short and long
fatty acids and amino acid-derived spacers led to
compounds that were highly potent. Several compounds
were both very potent and had plasma half-lives above
10 h, making them suitable as drugs for treatment of
type 2 diabetes using once daily administration"										Type 2 diabetes				"need to be administered by injection or through
an alternative way feasible for peptides (pulmonal,
buccal"	26% 3900 ug|||16% 900 ug|||11% 3600 ug			
FPDB21433		33	G8R26,34-GLP-1(7-38)	5	Unclassified				GLP-1 receptor		"Abbreviations used for acyl groups in lysine N_x005f_x005f_x000f_
-acylated peptides: γ-Glu-C8 ) γ-L-glutamoyl(NR-octanoyl); γ-Glu-C14 ) γ-Lglutamoyl(NR-tetradecanoyl);
γ-Glu-C16 ) γ-L-glutamoyl(NR-hexadecanoyl); γ-Glu-C18 ) γ-L-glutamoyl(NR-octadecanoyl); C8 ) octanoyl;
C12-diacid ) ω-carboxyundecanoyl; C16-diacid ) ω-carboxypentadecanoyl; C20-diacid ) ω-carboxynonadecanoyl; GABA-C16 ) γ-aminobutyroyl(Nγ-hexadecanoyl);
 Iso-Nip-C16 ) 1-(hexadecanoyl)piperidyl-4-carboxy. Data are given as mean ( SD of two individual
experiments with triplicate samples."		K38 γ-Glu-C16	3894						"The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin. GLP-1 had a potency (EC50) of 0.000055 uM for
the cloned human GLP-1 receptor. Many of the compounds had similar or even higher potencies,
despite quite large substituents. All compounds derivatized with fatty acids equal to or longer
than 12 carbon atoms were very protracted compared to GLP-1 and thus seem suitable for
once daily administration to type 2 diabetic patients. A structure-activity relationship was
obtained. GLP-1 could be derivatized with linear fatty acids up to the length of 16 carbon atoms,
sometimes longer, almost anywhere in the C-terminal part without considerable loss of potency.
Derivatization with two fatty acid substituents led to a considerable loss of potency. A structureactivity
 relationship on derivatization of specific amino acids generally was obtained. It was
found that the longer the fatty acid, the more potency was lost. Simultaneous modification of
the N-terminus (in order to obtain better metabolic stability) interfered with fatty acid
derivatization and led to loss of potency."	EC50, pM 328 ±14	"Derivatization with both short and long
fatty acids and amino acid-derived spacers led to
compounds that were highly potent. Several compounds
were both very potent and had plasma half-lives above
10 h, making them suitable as drugs for treatment of
type 2 diabetes using once daily administration"										Type 2 diabetes				"need to be administered by injection or through
an alternative way feasible for peptides (pulmonal,
buccal"	38% 5000 ug			
FPDB21434		34	E37R26,34-GLP-1(7-38)	5	Unclassified				GLP-1 receptor		"Abbreviations used for acyl groups in lysine N_x005f_x005f_x000f_
-acylated peptides: γ-Glu-C8 ) γ-L-glutamoyl(NR-octanoyl); γ-Glu-C14 ) γ-Lglutamoyl(NR-tetradecanoyl);
γ-Glu-C16 ) γ-L-glutamoyl(NR-hexadecanoyl); γ-Glu-C18 ) γ-L-glutamoyl(NR-octadecanoyl); C8 ) octanoyl;
C12-diacid ) ω-carboxyundecanoyl; C16-diacid ) ω-carboxypentadecanoyl; C20-diacid ) ω-carboxynonadecanoyl; GABA-C16 ) γ-aminobutyroyl(Nγ-hexadecanoyl);
 Iso-Nip-C16 ) 1-(hexadecanoyl)piperidyl-4-carboxy. Data are given as mean ( SD of two individual
experiments with triplicate samples."		K38 γ-Glu-C16	3981						"The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin. GLP-1 had a potency (EC50) of 0.000055 uM for
the cloned human GLP-1 receptor. Many of the compounds had similar or even higher potencies,
despite quite large substituents. All compounds derivatized with fatty acids equal to or longer
than 12 carbon atoms were very protracted compared to GLP-1 and thus seem suitable for
once daily administration to type 2 diabetic patients. A structure-activity relationship was
obtained. GLP-1 could be derivatized with linear fatty acids up to the length of 16 carbon atoms,
sometimes longer, almost anywhere in the C-terminal part without considerable loss of potency.
Derivatization with two fatty acid substituents led to a considerable loss of potency. A structureactivity
 relationship on derivatization of specific amino acids generally was obtained. It was
found that the longer the fatty acid, the more potency was lost. Simultaneous modification of
the N-terminus (in order to obtain better metabolic stability) interfered with fatty acid
derivatization and led to loss of potency."	EC50, pM 27.2±0.1	"Derivatization with both short and long
fatty acids and amino acid-derived spacers led to
compounds that were highly potent. Several compounds
were both very potent and had plasma half-lives above
10 h, making them suitable as drugs for treatment of
type 2 diabetes using once daily administration"										Type 2 diabetes				"need to be administered by injection or through
an alternative way feasible for peptides (pulmonal,
buccal"	26% 5100 ug			
FPDB21435		35|||36	E37G8R26,34-GLP-1(7-38)	6	Unclassified				GLP-1 receptor		"Abbreviations used for acyl groups in lysine N_x005f_x005f_x000f_
-acylated peptides: γ-Glu-C8 ) γ-L-glutamoyl(NR-octanoyl); γ-Glu-C14 ) γ-Lglutamoyl(NR-tetradecanoyl);
γ-Glu-C16 ) γ-L-glutamoyl(NR-hexadecanoyl); γ-Glu-C18 ) γ-L-glutamoyl(NR-octadecanoyl); C8 ) octanoyl;
C12-diacid ) ω-carboxyundecanoyl; C16-diacid ) ω-carboxypentadecanoyl; C20-diacid ) ω-carboxynonadecanoyl; GABA-C16 ) γ-aminobutyroyl(Nγ-hexadecanoyl);
 Iso-Nip-C16 ) 1-(hexadecanoyl)piperidyl-4-carboxy. Data are given as mean ( SD of two individual
experiments with triplicate samples."		K38 γ-Glu-C16|||K38 γ-Glu-C18	3967|||3995					11±1h	"The compounds were all derivatized with fatty acids in order to protract
their action by facilitating binding to serum albumin. GLP-1 had a potency (EC50) of 0.000055 uM for
the cloned human GLP-1 receptor. Many of the compounds had similar or even higher potencies,
despite quite large substituents. All compounds derivatized with fatty acids equal to or longer
than 12 carbon atoms were very protracted compared to GLP-1 and thus seem suitable for
once daily administration to type 2 diabetic patients. A structure-activity relationship was
obtained. GLP-1 could be derivatized with linear fatty acids up to the length of 16 carbon atoms,
sometimes longer, almost anywhere in the C-terminal part without considerable loss of potency.
Derivatization with two fatty acid substituents led to a considerable loss of potency. A structureactivity
 relationship on derivatization of specific amino acids generally was obtained. It was
found that the longer the fatty acid, the more potency was lost. Simultaneous modification of
the N-terminus (in order to obtain better metabolic stability) interfered with fatty acid
derivatization and led to loss of potency."	EC50, pM 135 ±7|||EC50, pM 213±30	"Derivatization with both short and long
fatty acids and amino acid-derived spacers led to
compounds that were highly potent. Several compounds
were both very potent and had plasma half-lives above
10 h, making them suitable as drugs for treatment of
type 2 diabetes using once daily administration"										Type 2 diabetes				"need to be administered by injection or through
an alternative way feasible for peptides (pulmonal,
buccal"	29% 2900 ug|||32% 3200 ug			
FPDB21436		1	GLP-1(7-38)-CO-(CH2)8CH3(C10)K(yGlu-C10)	16	GLP-1 Receptor Agonists	Short-acting GLP-1 analogues			Glucagon-Like Peptide-1 Receptor				y-Glu	3481.9		5.8		31-32	1.2h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Short-acting and highly active: The chain is long and shortIt leads to weak albuminbindingandsemi-attenuationInsufficient period	"Lysine at the 26th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Rapid subcutaneous absorption and early peak	Low (with less tissue distribution.）	high									inject subcutaneously	55±19pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21437		2	GLP-1(7-38)-CO-(CHz),CH3(C11)KlyGlu-C11)	18	GLP-1 Receptor Agonists	Medium-efficiency GLP-1 analogues			Glucagon-Like Peptide-2 Receptor				y-Glu	3495.9		5.8		28-30	0.8h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Medium efficiency and high activity: The chain length is significantly extended by halfDecline period (6 times that of C10)	"Lysine at the 27th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Medium absorption rate	Medium	Medium									inject subcutaneously	39±17pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21438		3	GLP-1(7-38)-CO-(CH2)oCH3(C12)KlyGlu-C12)	18	GLP-1 Receptor Agonists	Long-acting GLP-1 analogues			Glucagon-Like Peptide-3 Receptor				y-Glu	3509.9		5.8		43-45	5.1h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Medium-efficiency high activity: The activity is superior to that of natural GLP-1.The half-life is close to the lower limit of clinical demand	"Lysine at the 28th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Slow and continuous absorption	Higher (albumin nodules.	low									inject subcutaneously	66±23pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21439		4	GLP-1(7-38)-CO-(CH2)12CH3(C14)KlyGlu-C14)	17	GLP-1 Receptor Agonists	Long-acting GLP-1 analogues			Glucagon-Like Peptide-4 Receptor				y-Glu	3538		5.8		53-55	7.6h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Medium to long-lasting high activity: Optimal activity retention, half The decline period is still less than once a day	"Lysine at the 29th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Slow and continuous absorption	high	low									inject subcutaneously	29±7pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21440		5	GLP-1(7-38)-CO-(CH2)4CH3(C16, Liraglutide) KlyGIu-C16	28	GLP-1 Receptor Agonists	Long-acting GLP-1 analogues			Glucagon-Like Peptide-5 Receptor				y-Glu	3566.1		5.8		62-64	9h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Long-lasting high activity: Optimal balance (Liraglutide)The prototype meets the requirement of one-time daily administration	"Lysine at the 30th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Release slowly. It is suitable for once a day	high	Extremely low									inject subcutaneously	27±2pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	· Injection site reaction (swelling, induration) · Dyslipidemia (theoretical risk )	
FPDB21441		6	GLP-1(7-38)-CO-(CH2)16CH3(C18)KlyGlu-C18)	17	GLP-1 Receptor Agonists	Long-acting GLP-1 analogues			Glucagon-Like Peptide-6 Receptor				y-Glu	3594.1		5.8		68-70	16h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Long-lasting medium activity: A chain that is too long slightly reduces activity.The half-life is prolonged but the clinical gain is limited	"Lysine at the 31th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Slow release	high	Extremely low									inject subcutaneously	61±7pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	· Injection site reaction (swelling, induration) · Dyslipidemia (theoretical risk )	
FPDB21442		7	GLP-1(7-38)-CO-(CH2)eCH3(C10)K(Gaba-C10)	17	GLP-1 Receptor Agonists	Short-acting GLP-1 analogues			Glucagon-Like Peptide-7 Receptor				Gaba	3481.9		6		31-32	21h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Short-acting and high-activity: Spacer Gaba has a long-lasting effect Weaker than y-Glu	"Lysine at the 32th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Absorb quickly	low	high									inject subcutaneously	170±40pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21443		8	GLP-1(7-38)-CO-(CH2)9CH3(C11)K(Gaba-C11)	16	GLP-1 Receptor Agonists	Short-acting GLP-1 analogues			Glucagon-Like Peptide-8 Receptor				Gaba	3495.9		6		28-30	1.6h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Short-acting ultra-high activity: The most active.Strong but with insufficient half-life	"Lysine at the 33th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Medium absorption rate	Low - medium	high									inject subcutaneously	28±5pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21444		9	GLP-1(7-38)-CO-(CHz)1oCH3(C12)K(Gaba-C12)	18	GLP-1 Receptor Agonists	Medium-efficiency GLP-1 analogues			Glucagon-Like Peptide-9 Receptor				Gaba	3509.9		6		43-45	1.7h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Short effect and high activity: The chain length effect is weak in Gaba series	"Lysine at the 34th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Moderate absorption	Medium	Medium									inject subcutaneously	8.6±3.6pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21445		10	GLP-1(7-38)-CO-(CH2)12CH3(C14)K(Gaba-C14)	16	GLP-1 Receptor Agonists	Medium - and long-acting GLP-1 analogues			Glucagon-Like Peptide-10 Receptor				Gaba	3538		6		53-55	2.4h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Medium efficiency and high activity: Half-life remains.Deficiency (Compared with y-Glu of the same chain length.Compound 4:9.0h	"Lysine at the 35th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Slow absorption	Higher	Low - medium									inject subcutaneously	19±1pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21446		11	GLP-1(7-38)-CO-(CH2),CH3(C11K(BAla-C11)	16	GLP-1 Receptor Agonists	Short-acting GLP-1 analogues			Glucagon-Like Peptide-11 Receptor				β-Ala	3495.9		6.2			4.6h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Short-acting high activitY: β - Ala spacer has the weakest long-acting effect (compared with Y-Glu homocin 2: 5.1h )	"Lysine at the 36th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Fast absorption	low	high									inject subcutaneously	35±11pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21447		12	GLP-1(7-38)-CO-(CH2)oCHz(C12)K(BAla-C12)	18	GLP-1 Receptor Agonists	Medium-efficiency GLP-1 analogues			Glucagon-Like Peptide-12 Receptor				B-Ala	3509.9		6.2			1.2h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Short-acting and highly active: Increased chain length Improvement is limited	"Lysine at the 37th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Moderate absorption	Medium	Medium									inject subcutaneously	37±6pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21448		13	GLP-1(7-38)-CO-(CH2)12CH3(C14)K(BAla-C14)	16	GLP-1 Receptor Agonists	Long-acting GLP-1 analogues			Glucagon-Like Peptide-13 Receptor				β-Ala	3538		6.2			2.8h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Medium efficiency and high activity: Long chain required ≥C14 is close to medium efficacy and remains weak On the y-Glu series	"Lysine at the 38th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Slow absorption	Higher	low									inject subcutaneously	27±3pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	The gastrointestinal tolerance is slightly better.However, the duration of the therapeutic effect is short	
FPDB21449		14	GLP-1(7-38)-CO-(CHz)u4CH3(C16)KID-yGIu-C16)	20	GLP-1 Receptor Agonists	Long-acting GLP-1 analogues			Glucagon-Like Peptide-14 Receptor				D-y-Glu	3566.1		5.8			6.5h	Fatty acid chain length drives long-acting , while  spacer optimizes and maintains receptor activity	Long-lasting and highly active: Chiral change(Type D) does not affect the activity.Long-lasting performance, with a half-life slightly higher than Liraglutide	"Lysine at the 39th position of the compound is linked to fatty acid chains with different lengths through a spacer. After subcutaneous injection, fatty acid chains reversibly combine with albumin in blood to form a ""storage pool"", which slowly releases active peptides and significantly prolongs the half-life."		The mechanism of protractionof acylated peptides is based onbinding to the fatty acid binding sites on albumin.	Slow release	high	low									inject subcutaneously	55±15pmol/L	· Renal insufficiency: C16-C18 compounds(5,6,14) Decreased clearance through the kidneys → Regulators are needed Quantity.· Obese patients: The lipophilicity of fatty acid chains may increaseTissue distribution volume → Exposure level needs to be monitored.	· Injection site reaction (swelling, induration) · Dyslipidemia (theoretical risk )	
FPDB21450		15	K26(α-Glu-CO-(CH2)14CH3)-GLP-1(7-37)	13	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(α-Glu-CO-(CH2)14CH3)	3652					12h		Potency(pmol/L):76±1	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21451		16	K26(CO-(CH2)14CH3)-GLP-1(7-37)	10	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(CO-(CH2)14CH3)	3537					16h		Potency(pmol/L):4440±440	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21452		17	K26(Triethylenglycol-CO-(CH2)14CH3)-GLP-1(7-37)	26	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(Triethylenglycol-CO-(CH2)14CH3)	3672					13h		Potency(pmol/L):1570±60	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21453		18	K26(SO2-(CH2)11CH3)-GLP-1(7-37)	10	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(SO2-(CH2)11CH3)	3531					15h		Potency(pmol/L):2110±210	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21454		19	K26(β-Ala-SO2-(CH2)11CH3)-GLP-1(7-37)	13	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(β-Ala-SO2-(CH2)11CH3)	3601					9.4h		Potency(pmol/L):350±20	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21455		20	K26(γ-Glu-CO-(CH2)7CH=CH2)-GLP-1(7-37)	15	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(γ-Glu-CO-(CH2)7CH=CH2)	3298					1.9		Potency(pmol/L):36±0.4	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21456		21	K26(γ-Glu-CO-(CH2)10NHCO-CH3)-GLP-1(7-37)	17	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(γ-Glu-CO-(CH2)10NHCO-CH3)	3578					2		Potency(pmol/L):160±30	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21457		22	K26(γ-Glu-CO-(CH2)10NH2)-GLP-1(7-37)	13	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(γ-Glu-CO-(CH2)10NH2)	3624					1.1		Potency(pmol/L):140±30	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21458		23	K26(β-Ala-CO-(CH2)11NH2)-GLP-1(7-37)	13	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(β-Ala-CO-(CH2)11NH2)	3580					2		Potency(pmol/L):110±20	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21459		24	K26(γ-Glu-CO-(CH2)110H)-GLP-1(7-37)	12	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(γ-Glu-CO-(CH2)110H)	5010					2.6		Potency(pmol/L):45±8	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21460		25	K26(β-Ala-CO-(CH2)150H)-GLP-1(7-37)	12	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(β-Ala-CO-(CH2)150H)	5513					4.6		Potency(pmol/L):65±7	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21461		26	K26(β-Ala-CO-(CH2)10SO3H)-GLP(7-37)	14	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(β-Ala-CO-(CH2)10SO3H)	3630					2.5		Potency(pmol/L):110±50	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21462		27	K26(γ-Glu-CO-CH20(CH2)8CH3)-GLP-1(7-37)	15	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(γ-Glu-CO-CH20(CH2)8CH3)	3625					1.7		Potency(pmol/L):81±19	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21463		28	K26(γ-Glu-CO-(CH2)2O(CH2)9CH3)-GLP-1(7-37)	16	GLP-1 Receptor Agonists	GLP-1 Receptor Agonist, GLP-1 RA			GLP-1R				K26(γ-Glu-CO-(CH2)2O(CH2)9CH3)	3298					3.1		Potency(pmol/L):70±20	"The mechanism of action of GLP-1 is to stimulate insulin secretion,
stimulate beta-cell function, increase beta-cell mass, and to
decrease glucagon secretion, gastric emptying, and appetite.3,4
Physiologically, GLP-1 is secreted from the L-cells in the
intestine as a response of meal ingestion."										Type 2 diabetes,Obesity				Subcutaneous				
FPDB21464		29	HAEGTFTSDVSSYLEGQAAKEFIAWLVK[Arg34(γ-Glu-CO-CH₂O(CH₂)₂O(CH₂)₂O(CH₂)₂CH₃)]GRG	52	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R				Arg34 side chain -NH-γ-Glu-CO-CH₂-(O-CH₂-CH₂)₃-CH₃	3486.7027	C₁₇₈H₂₇₅N₄₅O₅₄S₁	6.32	-0.45		0.2h		Potency(pmol/L):320±150											Type 2 diabetes				Subcutaneous				DOI: 10.1021/jm070861j
FPDB21465		30	HAEGTFTSDVSSYLEGQAAKEFIAWLVK[Arg34(γ-Glu-CO-(CH₂)₈CH(OH)CH₂(OH)(CH₂)₆OH)]GRG	53	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R				Arg34 side chain -NH-γ-Glu-CO-(CH₂)₈-CH(OH)-CH₂(OH)-(CH₂)₆-OH	3612.8435	C₁₉₄H₃₀₃N₄₅O₅₇S₁	5.89	-0.62		2.3h		Potency(pmol/L):210±20											Type 2 diabetes				Subcutaneous				DOI: 10.1021/jm070861j
FPDB21466		31	HAEGTFTSDVSSYLEGQAAKEFIAWLVK[Arg34(8-Aminooctanoyl-CO-(CH₂)₆CH₃)]GRG	53	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R				Arg34 side chain -NH-8-Aminooctanoyl-CO-(CH₂)₆-CH₃	3437.7828	C₁₇₅H₂₇₇N₄₅O₅₂S₁	10.12	0.38		2.5h		Potency(pmol/L):48±4											Type 2 diabetes				Subcutaneous				DOI: 10.1021/jm070861j
FPDB21467		32	HAEGTFTSDVSSYLEGQAAKEFIAWLVK[Arg34(9-Aminononanoyl-CO-(CH₂)₆CH₃)]GRG	53	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R				Arg34 side chain -NH-9-Aminononanoyl-CO-(CH₂)₆-CH₃	3451.7985	C₁₇₆H₂₇₉N₄₅O₅₂S₁	10.15	0.41		4.5h		Potency(pmol/L):64±12											Type 2 diabetes				Subcutaneous				DOI: 10.1021/jm070861j
FPDB21468		33	HAEGTFTSDVSSYLEGQAAKEFIAWLVK[Arg34(10-Aminodecanoyl-CO-(CH₂)₆CH₃)]GRG	53	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R				Arg34 side chain -NH-10-Aminodecanoyl-CO-(CH₂)₆-CH₃	3465.8142	C₁₇₇H₂₈₁N₄₅O₅₂S₁	10.18	0.44		4.3h		Potency(pmol/L):39±12											Type 2 diabetes				Subcutaneous				DOI: 10.1021/jm070861j
FPDB21469		34	HAEGTFTSDVSSYLEGQAAKEFIAWLVK[Arg34(5-Aminopentanoyl-CO-(CH₂)₄NHCO-(CH₂)₄CH₃)]GRG	60	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R				Arg34 side chain -NH-5-Aminopentanoyl-CO-(CH₂)₄-NH-CO-(CH₂)₄-CH₃	3482.7677	C₁₇₉H₂₈₄N₄₆O₅₄S₁	9.85	0.28		2h		Potency(pmol/L):74±35											Type 2 diabetes				Subcutaneous				
FPDB21470		35	HAEGTFTSDVSSYLEGQAAKEFIAWLVK[Arg34(β-Ala-CO-(CH₂)₁₀NHCO-(CH₂)₂CH₃)]GRG	49	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R				Arg34 side chain -NH-β-Ala-CO-(CH₂)₁₀-NH-CO-(CH₂)₂-CH₃	3494.7679	C₁₈₂H₂₉₅N₄₇O₅₅S₁	9.78	0.42		3.4h		Potency(pmol/L):48±2											Type 2 diabetes				Subcutaneous				
FPDB21471		36	HAEGTFTSDVSSYLEGQAAKEFIAWLVK[Arg34(γ-Glu-CO-(CH₂)₁₄CH₃)]GRG-OH	45	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R				Arg34 side chain -NH-γ-Glu-CO-(CH₂)₁₄-CH₃	3651.9348	C₁₇₀H₂₇₀N₅₀O₅₃S₁	6.8	0.55		18h		Potency(pmol/L):400±100											Type 2 diabetes				Subcutaneous				
FPDB21472		37	HAEGTFTSDVSSYLEGQAAKEFIAWLVK[Arg34(γ-Glu-CO-(CH₂)₉Phenyl)]GRG	47	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R				Arg34 side chain -NH-γ-Glu-CO-(CH₂)₉-Phenyl	3528.7649	C₁₈₅H₂₈₈N₄₆O₅₆S₁	6.15	0.18		2.4h		Potency(pmol/L):31±14											Type 2 diabetes				Subcutaneous				
FPDB21473		38	HAEGTFTSDVSSYLEGQAAKEFIAWLVK[Arg34(γ-Glu-CO-(CH₂)₄Cyclohexyl)]GRG	51	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R				Arg34 side chain -NH-γ-Glu-CO-(CH₂)₄-Cyclohexyl	3464.7341	C₁₇₅H₂₇₅N₄₅O₅₅S₁	6.35	0.25		2.0h		Potency(pmol/L):73±1											Type 2 diabetes				Subcutaneous				
FPDB21474		39|||41|||42	GLP-1(7-37)-γ-Glu	6	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R										3.0h|||6.0h|||6.8h		Potency(pmol/L):26±2|||Potency(pmol/L):260±80|||Potency(pmol/L):18±10											Type 2 diabetes				Subcutaneous				
FPDB21475		40	GLP-1(7-37)-	3	GLP-1 Receptor Agonists	Synthesis of Acylated GLP-1 Analogue			GLP-1R										1.4h		Potency(pmol/L):380											Type 2 diabetes				Subcutaneous				
FPDB21476		43	GLP-1(7-37)-β-Ala	6	Unclassified				GLP-1R										8.8h		Potency(pmol/L):360±150											Type 2 diabetes				Subcutaneous				
FPDB21477		31	"[GLP-1(7-37) sequence: Aib8, Arg34]  
       |  
       Lys26-ε-NH-CO-(Benzyl-BAla-2xOEG)-CO-(C18 diacid)-COOH"	51	Unclassified				GLP-1R					4699.3	C₂₀₅H₃₂₀N₄₆O₆₂						"GLP-1R potency (EC50, pM)
(SEM) 0% HAS:5990 (1040)"											"approved for once-daily
treatment of diabetes as well as obesity."								
FPDB21478		32	H-Aib-E-G-T-F-T-Aib-D-V-S-S-Y-L-E-G-Q-A-A-K(γGlu-2xOEG-C20diacid)-E-F-I-A-W-L-V-K-G-R-R-OH	51	Unclassified				GLP-1R					4735.2	C₂₀₄H₃₂₁N₄₄O₆₂						"GLP-1R potency (EC50, pM)
(SEM) 0% HAS:11.5 (1.3)"											"approved for once-daily
treatment of diabetes as well as obesity."								
FPDB21479		33	H-Aib-E-G-T-F-T-Aib-D-V-S-S-Y-L-E-G-Q-A-A-K(γGlu-2xOEG-C22diacid)-E-F-I-A-W-L-V-K-G-R-R-OH	51	Unclassified				GLP-1R					4763.2	C₂₀₆H₃₂₅N₄₄O₆₂						"GLP-1R potency (EC50, pM)
(SEM) 0% HAS:24.4 (2.9)"											"approved for once-daily
treatment of diabetes as well as obesity."								
FPDB21480		34	"[GLP-1(7-37) backbone: 26Lys, 34Arg, 36Lys (acylated)]  
       |  
       Lys36-ε-NH-(2xOEG)-CO-C18diacid-COOH"	50	Unclassified				GLP-1R					4569.1	C₁₉₄H₃₀₇N₄₆O₆₀						"GLP-1R potency (EC50, pM)
(SEM) 0% HAS:7.0 (0.3)"											"approved for once-daily
treatment of diabetes as well as obesity."								
FPDB21481		35	"[GLP-1(7-37): Aib8, Lys27]  
       |  
       Lys27-ε-NH-γGlu-2xOEG-CO-C18diacid-COOH"	34	Unclassified				GLP-1R					4922.3	C₂₁₂H₃₃₆N₄₇O₆₅						"GLP-1R potency (EC50, pM)
(SEM) 0% HAS:4.6 (0.4)"											"approved for once-daily
treatment of diabetes as well as obesity."								
FPDB21482		36	"[GLP-1(7-37): Aib8, Lys16]  
       |  
       Lys16-ε-NH-γGlu-2xOEG-CO-C18diacid-COOH"	34	Unclassified				GLP-1R					4908.3	C₂₁₁H₃₃₄N₄₇O₆₆						"GLP-1R potency (EC50, pM)
(SEM) 0% HAS:9.9 (1.4)"											"approved for once-daily
treatment of diabetes as well as obesity."								
FPDB21483		37	"[GLP-1(7-37): Aib8, Aib22, Aib25, 37Lys]  
       |  
       Lys37-ε-NH-OEG-CO-C18diacid-COOH"	36	Unclassified				GLP-1R					4665.3	C₂₀₀H₃₁₆N₄₉O₆₁						"GLP-1R potency (EC50, pM)
(SEM) 0% HAS:40.9 (0.4)"											"approved for once-daily
treatment of diabetes as well as obesity."								
FPDB21484		38	GLP-1(7-37)-[Aib8, Lys22(C18 diacid-yGlu-2xOEG)]	24	Unclassified				GLP-1R					4815.3	C₂₀₉H₃₃₁N₄₆O₆₅						"GLP-1R potency (EC50, pM)
(SEM) 0% HAS:2.7 (0.1)"											"approved for once-daily
treatment of diabetes as well as obesity."								
FPDB21485		39	GLP-1(7-37)-[Aib8, Lys25(C18 diacid-γGlu-2xOEG)]	23	Unclassified				GLP-1R					4923.4	C₂₁₂H₃₃₇N₄₈O₆₆						"GLP-1R potency (EC50, pM)
(SEM) 0% HAS:41.8 (4.1)"											"approved for once-daily
treatment of diabetes as well as obesity."								
FPDB21486		23	E3 chimera 2(GCGR GLP-1R)	16	Unclassified				GLP-1R					3383							EC50 (nM):GCGR:2.4±1   GLP-1R:0.028±0.011											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."								
FPDB21487		24	E16 GLP-1-NH2 Des-R30(GCGR GLP-1R)	18	Unclassified				GLP-1R					3213.85							EC50 (nM):GCGR>1000   GLP-1R:0.011±0.003											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."								
FPDB21488		25	K20 T29-NH2(GCGR GLP-1R)	12	Unclassified				GLP-1R					3480.66							EC50 (nM):GCGR:0.12±0.04   GLP-1R:0.13±0.05											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."								
FPDB21489		26	K12 E16 lactam(GCGR GLP-1R)	16	Unclassified				GLP-1R					3506							EC50 (nM):GCGR:0.046±0.016   GLP-1R:0.051±0.002											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."								
FPDB21490		27	E16 K20 lactam(GCGR GLP-1R)	16	Unclassified				GLP-1R					3506							EC50 (nM):GCGR:0.058±0.032   GLP-1R:0.049±0.008											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."								
FPDB21491		28	K20 E24 lactam (GCGR GLP-1R)	16	Unclassified				GLP-1R					3464.06							EC50 (nM):GCGR:0.078±0.039   GLP-1R:0.24±0.10											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."								
FPDB21492		29	E24 K28 lactam(GCGR GLP-1R)	16	Unclassified				GLP-1R					3478							EC50 (nM):GCGR:0.076±0.069   GLP-1R:0.18±0.01											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."								
FPDB21493		30	Aib2 C24 chimera 2(GCGR GLP-1R)	19	Unclassified				GLP-1R					3413.142							EC50 (nM):GCGR:0.59±0.12   GLP-1R:0.014±0.002											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."								
FPDB21494		31	Aib2 C24 40k(GCGR GLP-1R)	13	Unclassified				GLP-1R					43428.443							EC50 (nM):GCGR:2.9±1.0   GLP-1R:0.036±0.014											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."								
FPDB21495		32	Aib2 C24 chimera 2 lactam(GCGR GLP-1R)	25	Unclassified				GLP-1R					3394.498							EC50 (nM):GCGR:0.055±0.011   GLP-1R:0.013±0.005											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."								
FPDB21496		33	Aib2 C24 lactam 40k(GCGR GLP-1R)	19	Unclassified				GLP-1R					43369.19							EC50 (nM):GCGR:0.67±0.26   GLP-1R:0.059±0.029											"the efficacy of a new peptide with agonism at the glucagon and GLP-1 receptors that has potent, sustained satiationinducing
 and lipolytic effects. Selective chemical modification to glucagon resulted in a loss of specificity, with minimal change to 
inherent activity. The structural basis for the co-agonism appears to be a combination of local positional interactions and a change 
in secondary structure. Two co-agonist peptides differing from each other only in their level of glucagon receptor agonism were 
studied in rodent obesity models. Administration of PEGylated peptides once per week normalized adiposity and glucose tolerance 
in diet-induced obese mice. Reduction of body weight was achieved by a loss of body fat resulting from decreased food intake and 
increased energy expenditure. These preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate 
degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects."