For research use only. Not for therapeutic Use.
tcY-NH2 ((trans-Cinnamoyl)-YPGKF-NH2) TFA is a potent selective PAR4 antagonist peptide. tcY-NH2 TFA 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 TFA (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 TFA potently activates aorta relaxation (RA) and gastric (LM) contraction, with IC50 values of 64 μM (RA) and 1 μM (LM)[1].
tcY-NH2 TFA (Tc-YPGKF-NH2, 400 μM, 5 min) prevents endostatin release and platelet aggregation induced by thrombin or by AY-NH2[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[5].
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[3].
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 [4].
tcY-NH2 TFA (intrapleural injection, 40 ng/kg for a single dose) inhibits neutrophil recruitment in experimental inflammation in mice[6].
| Catalog Number | I045728 |
| CAS Number | 1262750-73-1 |
| Synonyms | (2S)-N-[2-[[(2S)-6-amino-1-[[(2S)-1-amino-1-oxo-3-phenylpropan-2-yl]amino]-1-oxohexan-2-yl]amino]-2-oxoethyl]-1-[(2S)-3-(4-hydroxyphenyl)-2-[[(E)-3-phenylprop-2-enoyl]amino]propanoyl]pyrrolidine-2-carboxamide;2,2,2-trifluoroacetic acid |
| Molecular Formula | C42H50F3N7O9 |
| Purity | ≥95% |
| InChI | InChI=1S/C40H49N7O7.C2HF3O2/c41-22-8-7-14-31(38(52)46-32(37(42)51)24-28-12-5-2-6-13-28)44-36(50)26-43-39(53)34-15-9-23-47(34)40(54)33(25-29-16-19-30(48)20-17-29)45-35(49)21-18-27-10-3-1-4-11-27;3-2(4,5)1(6)7/h1-6,10-13,16-21,31-34,48H,7-9,14-15,22-26,41H2,(H2,42,51)(H,43,53)(H,44,50)(H,45,49)(H,46,52);(H,6,7)/b21-18+;/t31-,32-,33-,34-;/m0./s1 |
| InChIKey | WQJKBSZTPQERHW-USBDLMLUSA-N |
| SMILES | C1CC(N(C1)C(=O)C(CC2=CC=C(C=C2)O)NC(=O)C=CC3=CC=CC=C3)C(=O)NCC(=O)NC(CCCCN)C(=O)NC(CC4=CC=CC=C4)C(=O)N.C(=O)(C(F)(F)F)O |
| Reference | [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. [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. [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. [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. [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. [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. |
