2. GPCR/G Protein
  3. Protease Activated Receptor (PAR)
  4. tcY-NH2

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

Cat. No.: HY-P1263
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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.

For research use only. We do not sell to patients.

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tcY-NH2 Chemical Structure

tcY-NH2 Chemical Structure

CAS No. : 327177-34-4

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tcY-NH2 Related Antibodies

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Description

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].

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

tcY-NH2 Related Antibodies
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].

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

Animal Model: Brain death (BD) rat model[3]
Dosage: 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 mice[4]
Dosage: 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[6]
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.
Molecular Weight

739.86

Formula

C40H49N7O7
CAS No.
Sequence Shortening

{trans-Cinnamoyl}-YPGKF-NH2
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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tcY-NH2 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

tcY-NH2327177-34-4(trans-Cinnamoyl)-YPGKF-NH2Protease Activated Receptor (PAR)Thrombin receptorsPlateletthrombinthrombocytesinflammationimmunebrain death modelburn injury modelendostatinneutrophil migrationInhibitorinhibitorinhibit

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