tcY-NH2 ((trans-Cinnamoyl)-YPGKF-NH2) TFA is a potent selective PAR4 antagonist peptide. tcY-NH2 TFA inhibits thrombin- and AY-NH 2 -induced platelet aggregation and endostatin release, and can be used in the research of inflammation, immunology. In Vitro tcY-NH2 TFA (0-500 μM) inhibits AYPGKF-NH 2 (10 μM)-induced platelet (obtained from male albino Sprague–Dawley rats) aggregation, with an IC 50 value of 95 μM. tcY-NH2 TFA potently activates aorta relaxation (RA) and gastric (LM) contraction, with IC 50 values of 64 μM (RA) and 1 μM (LM). tcY-NH2 TFA (Tc-YPGKF-NH 2 , 400 μM, 5 min) prevents endostatin release and platelet aggregation induced by thrombin or by AY-NH 2. tcY-NH2 TFA (5 μM, 15 min) decreases infarct size (IS) by 51%, and increases recovery of ventricular function by 26% in an isolated heart model . MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo tcY-NH2 TFA (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 TFA (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 TFA (intrapleural injection, 40 ng/kg for a single dose) inhibits neutrophil recruitment in experimental inflammation in mice . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Brain death (BD) rat modelDosage: 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 miceDosage: 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. Form:Solid IC50& Target:PAR4