protease activated receptor 4

Protease-Activated Receptor-4 diTFA,2454 is the proteinase-activated receptor-4 (PAR4)agonist

Protease-Activated Receptor-4 (PAR4) is a proteinase-activated receptor-4 agonist used in antiplatelet therapy.

BMS-986141(UDM-003183) is a selective and potent protease-activated receptor-4 (PAR-4) antagonist with oral activity and an IC50 value of 0.4 nM.BMS-98614 exhibits significant antithrombotic effects.

GB-110 hydrochloride selectively induces PAR2-mediated intracellular Ca2+ release in HT29 cells with an EC50 of 0.28 μM. GB-110 hydrochloride is a potent, orally active, and nonpeptidic protease activated receptor 2 (PAR2) agonist.

BMS-986120 is a first-in-class oral, reversible protease-activated receptor 4 (PAR4) antagonist with IC50s of 9.5 nM in human blood and 2.1 nM in monkey blood, exhibiting potent and selective antiplatelet effects[1][2].

UDM-001651 is an effective and orally bioavailable protease-activated receptor 4 antagonists (IC50=4 nM; Kd=1.4 nM). UDM-001651 displays antiplatelet potency (IC50=25 nM) in a γ-thrombin-induced platelet-rich plasma aggregation assay.

PAR4 antagonist3 (Compound 36) is a selective antagonist of protease-activated receptor 4 (PAR4). It exhibits antiplatelet activity with an IC50 of 26.1 nM and enhances metabolic stability in human liver microsomes, with a half-life (T1/2) of 97.6 minutes.

PAR4 antagonist4 (Compound 37) is a selective antagonist of protease-activated receptor 4 (PAR4). It exhibits antiplatelet activity with an IC50 of 14.2 nM. Moreover, PAR4 antagonist3 enhances metabolic stability in human liver microsomes, showing a half-life (T1/2) of 42.5 minutes.

PAR4 antagonist 2 (Compound 31) is a protease-activated receptor 4 (PAR4) antagonist with IC50 values of 95 nM for human PAR4 and 367 nM for mouse PAR4. It inhibits the activation of PAR4 through cleavage by the natural protease thrombin but has no effect on the synthetic PAR4 agonist peptide AYPGKF.

PAR2 (1-6) amide is a synthetic peptide agonist of proteinase-activated receptor 2 (PAR2) that corresponds to residues 1-6 of the amino terminal tethered ligand sequence of human PAR2 and residues 37-42 of the full-length sequence.1It binds to NCTC 2544 cells expressing human PAR2 (Ki= 9.64 μM in a radioligand binding assay) and induces calcium mobilization in the same cells (EC50= 0.075 μM).2PAR2 (1-6) amide (100 μM) reduces colony formation of A549 lung cancer cells.1It induces superoxide production and degranulation in isolated human eosinophils when used at a concentration of 500 μM.3PAR2 (1-6) amide (5 μmol/kg) induces tear secretion in rats when used in combination with amastatin .4 1.Bohm, S.K., Kong, W., Bromme, D., et al.Molecular cloning, expression and potential functions of the human proteinase-activated receptor-2Biochem. J.314(Pt 3)1009-1016(1996) 2.Kanke, T., Ishiwata, H., Kabeya, M., et al.Binding of a highly potent protease-activated receptor-2 (PAR2) activating peptide, [3H]2-furoyl-LIGRL-NH2, to human PAR2Br. J. Pharmacol.145(2)255-263(2005) 3.Miike, S., McWilliam, A.S., and Kita, H.Trypsin induces activation and inflammatory mediator release from human eosinophils through protease-activated receptor-2J. Immunol.167(11)6615-6622(2001) 4.Nishikawa, H., Kawai, K., Tanaka, M., et al.Protease-activated receptor-2 (PAR-2)-related peptides induce tear secretion in rats: Involvement of PAR-2 and non-PAR-2 mechanismsJ. Pharmacol. Exp. Ther.312(2)324-331(2005)

RWJ-56110 dihydrochloride is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 μM), showing no effect on PAR-2, PAR-3, or PAR-4. It inhibits the aggregation of human platelets induced by SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM), with high selectivity relative to U46619. RWJ-56110 dihydrochloride also blocks angiogenesis and the formation of new vessels in vivo, and induces cell apoptosis[1][2].

PAR 4 (1-6) TFA (GYPGQV TFA), a hexapeptide derived from protease-activated receptor 4 (PAR 4), serves as a specific agonist for PAR 4, exhibiting targeted activation properties.

PAR-4 Agonist Peptide, amide (AY-NH2), is an agonist of proteinase-activated receptor-4 (PAR-4).

SFNGGP-NH2 is a biologically active peptide that interacts with Protease-Activated Receptor 3 (PAR-3), a high-affinity thrombin receptor. Human cutaneous mast cells express PAR-3 mRNA, implicating a role in itch mechanotransduction, with both histamine-dependent and independent pathways reported. While PAR-3 alone does not induce itch, it may potentiate itch when co-expressed with PAR-4, enhancing thrombin's action. This suggests that PAR-3's primary function is not as a signal transmitter across the membrane, but rather as a cofactor necessary for PAR-4 activation.

Ala-parafluoroPhe-Arg-Cha-Cit-Tyr-NH2 is a biologically active peptide functioning as a selective agonist for Protease Activated Receptor 1 (PAR-1) [a subtype of G-protein coupled receptors involved in mediating thrombin's cellular effects]. Exhibiting high specificity for PAR-1 over PAR-2, its selectivity was assessed via cell-based calcium signaling assays in HEK293 cells. As an agonist, it is instrumental for in vivo investigations of PAR-1 activation. PAR-1 also collaborates with PAR-4, influencing thrombin-induced hepatocellular carcinoma within [coagulation type] tumor environments where thrombin generation occurs.

PAR-4 Agonist Peptide, amide TFA (PAR-4-AP (TFA)), is a selective activator of the proteinase-activated receptor-4 (PAR-4) that does not affect PAR-1 or PAR-2, and its activity can be inhibited by a PAR-4 antagonist.

PAR-4 (1-6) amide human, an N-terminal fragment of protease-activated receptor 4 (PAR4), induces platelet aggregation [1].

P4pal10 TFA, the TFA salt form of P4pal10, serves as an antagonist of the protease-activated receptor 4 (PAR4). This compound inhibits platelet aggregation and thrombin generation induced by tissue factor (TF), exhibiting anticoagulant and antithrombotic activities. Additionally, P4pal10 TFA alleviates carrageenan-induced edema and neutrophil infiltration, and ameliorates damage in rat myocardial ischemia/reperfusion (I/R) models.

RAG8 peptide is an antagonist of protease-activated receptor 4 (PAR 4), which inhibits late-stage platelet activation and reduces thrombosis without altering hemostasis or increasing bleeding risk. It is applicable in atherosclerosis research.