TcY-NH2 (TFA)

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].

Product Specifications

CAS Number

[1262750-73-1]

Product Name Alternative

(trans-Cinnamoyl) -YPGKF-NH2 (TFA)

UNSPSC

12352209

Target

Protease Activated Receptor (PAR)

Type

Peptides

Related Pathways

GPCR/G Protein

Applications

Metabolism-protein/nucleotide metabolism

Field of Research

Metabolic Disease; Inflammation/Immunology

Assay Protocol

https://www.medchemexpress.com/tcy-nh2-tfa.html

Purity

99.72

Solubility

DMSO : 100 mg/mL (ultrasonic)

Smiles

O=C(O)C(F)(F)F.NCCCC[C@@H](C(N[C@H](C(N)=O)CC1=CC=CC=C1)=O)NC(CNC([C@@H]2CCCN2C([C@@H](NC(/C=C/C3=CC=CC=C3)=O)CC4=CC=C(O)C=C4)=O)=O)=O

Molecular Formula

C42H50F3N7O9

Molecular Weight

853.88

References & Citations

[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.