Hirudin (C09-1138-225)

Hirudin is a thrombin inhibitor with blood anticoagulant property. Hirudin has potent anti-thrombotic, wound repair, anti-fibrosis, anti-tumor and anti-hyperuricemia effects. Hirudin also affects diabetic complications, cerebral hemorrhage, and others.In VitroHirudin inhibits the activity of thrombin, deprives the ability of thrombin to cleave fibrinogen, prevents the formation of fibrin and the cross-linking polymerization process of fibrin monomer in internal and external coagulation pathway. Hirudin reduces cell apoptosis of human microvascular endothelial cells (HMVECs) and suppresses the expression of p-JAK2 via antagonizing thrombin. Hirudin inhibits VEGF-Notch pathway and cell proliferation of HMVECs at high doses. Hirudin (3-10 mg/mL) reverses the abnormal proliferation and fibrosis in HK-2 cells caused by TGF-β1. Hirudin depresses the myocardial fibroblasts induced by angiotensin II by dose-dependently inhibits oxidative stress, regulates fibrosis-related factors, and represses the ERK1/2 pathway. MCE has not independently confirmed the accuracy of these methods. They are for reference only.In VivoHirudin increases the viability of rat random skin flap and reduces inflammatory responses . Hirudin promotes the wound healing in SD rats after laser surgery . Hirudin (10 and 15 mg/kg; i.g. once daily for 21 days) improves renal interstitial fibrosis to reduce renal tubule injury and inflammation in unilateral ureteral obstruction (UUO) mice. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Male balb/c mice with underwent unilateral ureteral ligation (UUO)Dosage: 10 and 15 mg/kg Administration: Oral gavage; 10 and 15 mg/kg, once daily for 21 days Result: Reduced renal damages and suppressed the upregulation of α-SMA, collagen deposition in UUO mice. Increased the level of fibrosis (collagen-I, FN, α-SMA), N-cad, slug and E-cad in UUO mice. Decreased the level of IL-1β, IL-6 and TNF-α, apoptosis of renal tubular cells in UUO mice. Decreased the expression of inflammatory factors, the occurrence of EMT, the incidence of fibrosis and the apoptosis of TGF-β-induced renal tubular epithelial cell.Form:Liquid. EC Number: 232-279-1 PubChem CID: 72941487 Isomeric SMILES: CC[C@H](C)[C@H]1C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](CSSC[C@H]2C(=O)NCC(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](CSSC[C@@H](C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N2)C(C)C)CC(=O)N)CO)CCC(=O)O)NC(=O)[C@H](CC(C)C)NC(=O)[C@@H]3CSSC[C@@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N3)CC(C)C)CC(=O)N)CCC(=O)N)CO)CCC(=O)O)[C@@H](C)O)NC(=O)[C@H](CC(=O)O)NC(=O)[C@H]([C@@H](C)O)NC(=O)[C@H](CC4=CC=C(C=C4)O)NC(=O)[C@H](C(C)C)NC(=O)[C@H](C(C)C)N)C(=O)N1)CCCCN)CC(=O)N)CCC(=O)N)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H]([C@@H](C)O)C(=O)NCC(=O)N[C@@H](CCC(=O)O)C(=O)NCC(=O)N[C@@H]([C@@H](C)O)C(=O)N5CCC[C@H]5C(=O)N[C@@H](CCCCN)C(=O)N6CCC[C@H]6C(=O)N[C@@H](CCC(=O)N)C(=O)N[C@@H](CO)C(=O)N[C@@H](CC7=CN=CN7)C(=O)N[C@@H](CC(=O)N)C(=O)N[C@@H](CC(=O)O)C(=O)NCC(=O)N[C@@H](CC(=O)O)C(=O)N[C@@H](CC8=CC=CC=C8)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H]([C@@H](C)CC)C(=O)N9CCC[C@H]9C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](CC1=CC=C(C=C1)OS(=O)(=O)O)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCC(=O)N)C(=O)O)CCC(=O)N)CC(=O)N)CCCCN)CCC(=O)O)CC(=O)O)CO)CC(C)C