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tcY-NH2 TFA - 99%, high purity , CAS No.1262750-73-1

COA

Grade & Purity:

≥99%

Cas Number: 1262750-73-1
Molecular Weight: 853.88
PubChem CID: 71311594

In stock

Item Number

T646845

Grouped product items
SKU	Size	Availability	Price	Qty
T646845-1mg	1mg	Available within 8-12 weeks(?) Production requires sourcing of materials. We appreciate your patience and understanding.	$200.90
T646845-5mg	5mg	Available within 8-12 weeks(?) Production requires sourcing of materials. We appreciate your patience and understanding.	$580.90

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Class A GPCR (4138) GPCR/G Protein (3172) Protease Activated Receptor (PAR) (55)

Basic Description

Specifications & Purity	≥99%
Biochemical and Physiological Mechanisms	tcY-NH2 ((trans-Cinnamoyl)-YPGKF-NH2) TFA is a potent selective PAR4 antagonist peptide. tcY-NH2 TFA inhibits thrombin- and AY-NH 2 -induced platelet aggregation and endostatin release, and can be used in the research of inflammation, immunology[
Storage Temp	Desiccated,Store at -80°C
Shipped In	Ice chest + Ice pads This product requires cold chain shipping. Ground and other economy services are not available.
Product Description	tcY-NH2 ((trans-Cinnamoyl)-YPGKF-NH2) TFA is a potent selective PAR4 antagonist peptide. tcY-NH2 TFA inhibits thrombin- and AY-NH 2 -induced platelet aggregation and endostatin release, and can be used in the research of inflammation, immunology. In Vitro tcY-NH2 TFA (0-500 μM) inhibits AYPGKF-NH 2 (10 μM)-induced platelet (obtained from male albino Sprague–Dawley rats) aggregation, with an IC 50 value of 95 μM. tcY-NH2 TFA potently activates aorta relaxation (RA) and gastric (LM) contraction, with IC 50 values of 64 μM (RA) and 1 μM (LM). tcY-NH2 TFA (Tc-YPGKF-NH 2 , 400 μM, 5 min) prevents endostatin release and platelet aggregation induced by thrombin or by AY-NH 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 . MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo 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. 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. tcY-NH2 TFA (intrapleural injection, 40 ng/kg for a single dose) inhibits neutrophil recruitment in experimental inflammation in mice . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Brain death (BD) rat modelDosage: 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 miceDosage: 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 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. Form:Solid IC50& Target:PAR4

Names and Identifiers

Smiles	C1C[C@H](N(C1)C(=O)[C@H](CC2=CC=C(C=C2)O)NC(=O)/C=C/C3=CC=CC=C3)C(=O)NCC(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CC4=CC=CC=C4)C(=O)N.C(=O)(C(F)(F)F)O
Isomeric SMILES	C1C[C@H](N(C1)C(=O)[C@H](CC2=CC=C(C=C2)O)NC(=O)/C=C/C3=CC=CC=C3)C(=O)NCC(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CC4=CC=CC=C4)C(=O)N.C(=O)(C(F)(F)F)O
PubChem CID	71311594
Molecular Weight	853.88

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