产品
编 号:F320761
分子式:C40H49N7O7
分子量:739.86
产品类型
结构图
CAS No: 327177-34-4
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产品详情
生物活性:
tcY-NH2 ((trans-Cinnamoyl)-YPGKF-NH2) is a potent selective PAR4 antagonist peptide. tcY-NH2 inhibits thrombin- and AY-NH2-induced platelet aggregation and endostatin release, and can be used in the research of inflammation, immunology.
体内研究:
tcY-NH2 (tail vein injection, 0.6 mg/kg for a single dose) alleviates liver injury in Brain death (BD) rat model, indicated by lower serum ALT/AST levels and better histomorphology.tcY-NH2 (intraperitoneal injection, 0.6 mg/kg for a single dose) increases posttraumatic activation of CD4+ Tregs within the draining lymph nodes in burn injury mice model .tcY-NH2 (intrapleural injection, 40 ng/kg for a single dose) inhibits neutrophil recruitment in experimental inflammation in mice.Animal Model:Brain death (BD) rat model
Dosage:0.6 mg/kg for a single dose
Administration:Tail vein injection for a single dose
Result:Reduced blood platelet activation and hepatic platelet accumulation.Attenuated the inflammatory response and apoptosis in the livers.Inhibited the activation of NF-κB and MAPK pathways induced by Brain death (BD).
Animal Model:Burn injury model of C57BL/6 N mice
Dosage:0.6 mg/kg for a single dose
Administration:Intraperitoneal injection
Result:Increased expression and phosphorylation of PKC-θ in the presence of platelets, without affecting early posttraumatic hemostasis.
Animal Model:BALB/c mice
Dosage:40 ng/kg for a single dose
Administration:Intrapleural injection
Result:Abolished the number of rolling and adhering neutrophils on the vessel wall.Inhibited CXCL8- and Cg-induced neutrophil migration into the pleural cavity of mice.
体外研究:
tcY-NH2 (0-500 μM) inhibits AYPGKF-NH2 (10 μM)-induced platelet (obtained from male albino Sprague–Dawley rats) aggregation, with an IC50 value of 95 μM.tcY-NH2 potently activates aorta relaxation (RA) and gastric (LM) contraction, with IC50 values of 64 μM (RA) and 1 μM (LM).tcY-NH2 (Tc-YPGKF-NH2, 400 μM, 5 min) prevents endostatin release and platelet aggregation induced by thrombin or by AY-NH2.tcY-NH2 (5 μM, 15 min) decreases infarct size (IS) by 51%, and increases recovery of ventricular function by 26% in an isolated heart model.