tcY-NH2

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^[1][2][6]. In Vitro: 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^[1].
tcY-NH2 potently activates aorta relaxation (RA) and gastric (LM) contraction, with IC₅₀ values of 64 μM (RA) and 1 μM (LM)^[1].
tcY-NH2 (Tc-YPGKF-NH₂, 400 μM, 5 min) prevents endostatin release and platelet aggregation induced by thrombin or by AY-NH₂^[2].
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^[5]. In Vivo: 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^[3].
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 ^[4].
tcY-NH2 (intrapleural injection, 40 ng/kg for a single dose) inhibits neutrophil recruitment in experimental inflammation in mice^[6].