tcY-NH2
Purity: ≥95%
Biological Activity
tcY-NH2 is a selective PAR4 antagonist peptide. Inhibits endostatin release and platelet aggregation induced by thrombin.Technical Data
(Modifications: Tyr-1 = trans-Cinnamoyl-Tyr, Phe-5 = C-terminal amide)
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
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![[Nle4,D-phe7]-alpha-MSH | CAS No. 75921-69-6 | Melanocortin receptor agonist](https://resources.rndsystems.com/images/datasheets/structures/nle4-d-phe7-a-msh_3013.png "[Nle4,D-phe7]-alpha-MSH | CAS No. 75921-69-6 | Melanocortin receptor agonist")
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Background References
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Proteinase-activated receptor-4: evaluation of tethered ligand-derived peptides as probes for receptor function and as inflammatory agonists in vivo.
Hollenberg et al.
Br.J.Pharmacol., 2004;143:443 -
Proteinase-activated receptor 4 (PAR4): activation and inhibition of rat platelet aggregation by PAR4-derived peptides.
Hollenberg and Saifeddine
Can.J.Physiol.Pharmacol., 2001;79:439 -
Thrombin-induced platelet endostatin release is blocked by a proteinase activated receptor-4 (PAR4) antagonist.
Ma et al.
Br.J.Pharmacol., 2001;134:701
Product Datasheets
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Citations for tcY-NH2
The citations listed below are publications that use Tocris products. Selected citations for tcY-NH2 include:
4 Citations: Showing 1 - 4
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Thrombin induces morphological and inflammatory astrocytic responses via activation of PAR1 receptor.
Authors: Chen Et al.
Cell Death Discov. 2022;8:189
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Complement-activation fragment C4a mediates effector functions by binding as untethered agonist to protease-activated receptors 1 and 4.
Authors: Wang
Proc Natl Acad Sci U S A 2017;114(41):10948
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Thrombin-induced reactive oxygen species generation in platelets: A novel role for protease-activated receptor 4 and GPIbα.
Authors: Carrim Et al.
Br J Cancer 2015;6:640
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Non-hematopoietic PAR-2 is essential for matriptase-driven pre-malignant progression and potentiation of ras-mediated squamous cell carcinogenesis.
Authors: Sales Et al.
Redox Biol 2015;34:346
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