tcY-NH2  (Synonyms: (trans-Cinnamoyl)-YPGKF-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].

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

739.86

C₄₀H₄₉N₇O₇

327177-34-4

{trans-Cinnamoyl}-YPGKF-NH2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Morley D Hollenberg, et al. Proteinase-activated receptor-4: evaluation of tethered ligand-derived peptides as probes for receptor function and as inflammatory agonists in vivo. Br J Pharmacol. 2004 Oct;143(4):443-54.  [Content Brief]

  [2]. L Ma, et al. Thrombin-induced platelet endostatin release is blocked by a proteinase activated receptor-4 (PAR4) antagonist. Br J Pharmacol. 2001 Oct;134(4):701-4.  [Content Brief]

  [3]. Hongbo Fang, et al. Blocking protease-activated receptor 4 alleviates liver injury induced by brain death. Biochem Biophys Res Commun. 2022 Mar 5;595:47-53.  [Content Brief]

  [4]. Matthias Bock, et al. Platelets differentially modulate CD4 + Treg activation via GPIIa/IIIb-, fibrinogen-, and PAR4-dependent pathways. Immunol Res. 2022 Apr;70(2):185-196.  [Content Brief]

  [5]. Jennifer L Strande, et al. Inhibiting protease-activated receptor 4 limits myocardial ischemia/reperfusion injury in rat hearts by unmasking adenosine signaling. J Pharmacol Exp Ther. 2008 Mar;324(3):1045-54.  [Content Brief]

  [6]. Lindisley F Gomides, et al. Blockade of proteinase-activated receptor 4 inhibits neutrophil recruitment in experimental inflammation in mice. Inflamm Res. 2014 Nov;63(11):935-41.  [Content Brief]