==== Reference: Usmani SS, Bedi G, Samuel JS, Singh S, Kalra S, Kumar P, et al. (2017) THPdb: Database of FDA-approved peptide and protein therapeutics. PLoS ONE 12(7) e0181748.====

Detailed description page of THPdb


Details of Th1060 which contains 3 entries.


Entry 1
(1) Primary information
ID1382
ThPP IDTh1060
Therapeutic Peptide/Protein NameInsulin, porcine
SequenceA chain: GIVEQCCTSICSLYQLENYCN; B chain: FVNQHLCGS view full sequnce in fasta
Functional ClassificationIa
Molecular Weight5795.6
Chemical FormulaC257H387N65O76S6
Isoelectric Point5.39
Hydrophobicity0.298
Melting Point (℃)N.A.
Half LifeN.A.
DescriptionInsulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure.
Indication/DiseaseFor the treatment of type I and II diabetes mellitus.
PharmacodynamicsInsulin 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.
Mechanism of ActionInsulin 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.
ToxicityN.A.
MetabolismInsulin is predominantly cleared by metabolic degradation via a receptor-mediated process.
AbsorptionN.A.
Volume of DistributionN.A.
ClearanceN.A.
CategoriesHypoglycemic Agents
Patents NumberN.A.
Date of IssueN.A.
Date of ExpiryN.A.
Drug InteractionN.A.
TargetInterferon alpha/beta receptor 2,Interferon alpha/beta receptor 1
Information of corresponding available drug in the market
Brand Namevetsulin
CompanyIntervet Inc (Merck Animal Health)
Brand Discriptionvetsulin is a sterile aqueous zinc suspension of purified porcine insulin.
Prescribed forvetsulin (porcine insulin zinc suspension) is indicated for the reduction of hyperglycemia and hyperglycemia-associated clinical signs in dogs and cats with diabetes mellitus
Chemical NameN.A.
Formulationpurified porcine insulin 40 IU (35% amorphous and 65% crystalline), Zinc (as chloride) 0.08 mg, Sodium acetate trihydrate 1.36 mg, Sodium chloride 7.0 mg, Methylparaben (preservative) 1.0 mg, pH is adjusted with hydrochloric acid and/or sodium hydroxide.
Physcial AppearanceVetsulin 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.
Route of AdministrationSubcutaneous Injection
Recommended DosageIn 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 hour intervals.
ContraindicationDogs 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.
Side EffectsIn 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.
Useful Linkhttp://dailymed.nlm.nih.gov/dailymed/archives/fdaDrugInfo.cfm?archiveid=101642
PubMed ID3053948, 3049614, 3330034, 3549531, 4280239
3-D StructureTh1060 (View) or (Download)


Entry 2
(2) Primary information
ID1383
ThPP IDTh1060
Therapeutic Peptide/Protein NameInsulin, porcine
SequenceA chain: GIVEQCCTSICSLYQLENYCN; B chain: FVNQHLCGS view full sequnce in fasta
Functional ClassificationIa
Molecular Weight5795.6
Chemical FormulaC257H387N65O76S6
Isoelectric Point5.39
Hydrophobicity0.298
Melting Point (℃)N.A.
Half LifeN.A.
DescriptionInsulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure.
Indication/DiseaseFor the treatment of type I and II diabetes mellitus.
PharmacodynamicsInsulin 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.
Mechanism of ActionInsulin 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.
ToxicityN.A.
MetabolismInsulin is predominantly cleared by metabolic degradation via a receptor-mediated process.
AbsorptionN.A.
Volume of DistributionN.A.
ClearanceN.A.
CategoriesHypoglycemic Agents
Patents NumberN.A.
Date of IssueN.A.
Date of ExpiryN.A.
Drug InteractionN.A.
TargetN.A.
Information of corresponding available drug in the market
Brand NameN.A.
CompanyN.A.
Brand DiscriptionN.A.
Prescribed forN.A.
Chemical NameN.A.
FormulationN.A.
Physcial AppearanceN.A.
Route of AdministrationN.A.
Recommended DosageN.A.
ContraindicationN.A.
Side EffectsN.A.
Useful LinkN.A.
PubMed ID3053948, 3049614, 3330034, 3549531, 4280240
3-D StructureTh1060 (View) or (Download)


Entry 3
(3) Primary information
ID1384
ThPP IDTh1060
Therapeutic Peptide/Protein NameInsulin, porcine
SequenceA chain: GIVEQCCTSICSLYQLENYCN; B chain: FVNQHLCGS view full sequnce in fasta
Functional ClassificationIa
Molecular Weight5795.6
Chemical FormulaC257H387N65O76S6
Isoelectric Point5.39
Hydrophobicity0.298
Melting Point (℃)N.A.
Half LifeN.A.
DescriptionInsulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure.
Indication/DiseaseFor the treatment of type I and II diabetes mellitus.
PharmacodynamicsInsulin 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.
Mechanism of ActionInsulin 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.
ToxicityN.A.
MetabolismInsulin is predominantly cleared by metabolic degradation via a receptor-mediated process.
AbsorptionN.A.
Volume of DistributionN.A.
ClearanceN.A.
CategoriesHypoglycemic Agents
Patents NumberN.A.
Date of IssueN.A.
Date of ExpiryN.A.
Drug InteractionN.A.
TargetHyaluronan,Transforming growth factor beta-1
Information of corresponding available drug in the market
Brand NameN.A.
CompanyN.A.
Brand DiscriptionN.A.
Prescribed forN.A.
Chemical NameN.A.
FormulationN.A.
Physcial AppearanceN.A.
Route of AdministrationN.A.
Recommended DosageN.A.
ContraindicationN.A.
Side EffectsN.A.
Useful LinkN.A.
PubMed ID3053948, 3049614, 3330034, 3549531, 4280241
3-D StructureTh1060 (View) or (Download)