ChemicalBook--->CAS DataBase List--->327177-34-4

327177-34-4

327177-34-4 Structure

327177-34-4 Structure
IdentificationBack Directory
[Name]

TCY-NH2
[CAS]

327177-34-4
[Synonyms]

TCY-NH2
M.W. 739.87 C40H49N7O7
trans-Cinnamoyl-YPGKF-NH2
TRANS-CINNAMOYL-YPGKF-AMIDE
trans-Cinnamoyl-YPGKF-NH2, tcY-NH2
TRANS-CINNAMOYL-TYR-PRO-GLY-LYS-PHE-NH2
trans-Cinnamoyl-Tyr-Pro-Gly-Lys-Phe-amide trifluoroacetate salt
L-Phenylalaninamide, N-[(2E)-1-oxo-3-phenyl-2-propen-1-yl]-L-tyrosyl-L-prolylglycyl-L-lysyl-
[Molecular Formula]

C40H49N7O7
[MDL Number]

MFCD06798369
[MOL File]

327177-34-4.mol
[Molecular Weight]

739.86
Chemical PropertiesBack Directory
[storage temp. ]

−20°C
[form ]

Powder
[Water Solubility ]

Soluble to 1 mg/ml in water
Safety DataBack Directory
[Safety Statements ]

22-24/25
Hazard InformationBack Directory
[Uses]

tcY-NH2 does not cause aggregation but blocks aggregation caused by receptor-activating peptide analogs (GY-NH2, AY-NH2), and thrombin without affecting ADP-mediated aggregation.
[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].

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.
[IC 50]

PAR4
[storage]

Store at -20°C
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