BMS-98614 is an orally active, selective thrombin receptor protease-activated receptor-4 (PAR-4) antagonist with an IC50 value of 0.4 nM. BMS-98614 has excellent antithrombotic effect[1][2].
Atopaxar (E5555) is a potent, orally active, selective and reversible thrombin receptor protease-activated receptor-1 (PAR-1) antagonist. Atopaxar interferes with platelet signaling. Atopaxar can be used for the research of atherothrombotic disease[1][2].
I-191 is a protease-activated receptor 2 (PAR-2) signaling pathway inhibitor extracted from patent WO2015048245A1. I-191 inhibits PAR-2 activators such as SLIGKV, Trypsin, and Thrombin with IC50s of 0.0014 μM, 0.0023 μM, 0.32 μM, respectively[1].
AY77 is a calcium-biased PAR2 agonist. AY77 shows an EC50 of 0.17 and 2 nM in PAR2-mediated the activation in the Gq pathway and recruitment of β-arrestin-2, respectively. AY77 potently induces intracellular Ca2+ release[1][2].
PAR-4 Agonist Peptide, amide TFA (PAR-4-AP TFA; AY-NH2 TFA) is a proteinase-activated receptor-4 (PAR-4) agonist, which has no effect on either PAR-1 or PAR-2 and whose effects are blocked by a PAR-4 antagonist[1].
Protease-Activated Receptor-3 (PAR-3) (1-6), human is a proteinase-activated receptor (PAR-3) agonist peptide[1].
I-287 is a potent, selective, orally active inhibitor of PAR2, negative PAR2 allosteric modulator, inhibits PAR2-mediated activation of Gq and G12/13 but not Gi/o proteins (IC50=45-390 nM);I-287 is a negative allosteric modulator (NAM) and not an orthosteric competitive antagonist of hPAR2.I-287 inhibits PAR2-mediated activation of DAG/Ca2+/PKC and RhoA/SRF-RE, as well as FAK and ERK1/2 signaling pathways, shows no effect on PAR2-mediated recruitment of βarrestin2 and receptor internalization.I-287 inhibits PAR2-induced secretion of IL-8 cytokine in vitro and reduces Freund's adjuvant (CFA)-induced paw edema model in mice.
Vorapaxar is a protease-activated receptor (PAR-1) antagonist that inhibits thrombin-induced platelet activation.
Q94 hydrochloride, a selective PAR1 antagonist (IC50=916 nM), can selectively block PAR1/Gαq interaction and signalling. Q94 hydrochloride blocks PAR1-mediated increases in both CCL2 mRNA and protein levels in a dose-dependent manner. Q94 hydrochloride also completely blocks thrombin-induced ERK1/2 and MLC phosphorylation[1].
ENMD-1068 is a selective protease-activated receptor 2 (PAR2) antagonist. ENMD-1068 reduces hepatic stellate cell activation and collagen expression by inhibiting TGF-β1/Smad signaling. ENMD-1068 also inhibits the proliferation of endometrial cells and induces apoptosis of epithelial cells in the lesion. ENMD-1068 can be used in the study of endometriosis and liver fibrosis[1][2].
AZ-8838 (AZ8838) is a potent, and selective PAR2 antagonist with Kd of 125 nM; shows excellent selectivity over PAR1 and PAR4 (>50 uM).
ENMD-1068 hydrobromide is a potent PAR2 antagonist. ENMD-1068 hydrobromide attenuates joint inflammation in a dose-dependent manner. ENMD-1068 hydrobromide can be used in research of joint inflammation[1].
GB-88 is a selective, orally PAR2 antagonist, inhibits PAR2 activates Ca(2+) release with an IC 50 of 2 µM[1].
TFLLRN-NH2 is a biological active peptide. (PAR-1 Agonist)
SCH79797 dihydrochloride is a highly potent, selective nonpeptide protease activated receptor 1 (PAR1) antagonist. SCH79797 dihydrochloride inhibits binding of a high-affinity thrombin receptor-activating peptide to PAR1 with an IC50 of 70 nM and a Ki of 35 nM. SCH79797 dihydrochloride inhibits thrombin-induced platelet aggregation with an IC50 of 3 μM. SCH79797 dihydrochloride has antiproliferative and pro-apoptotic effects, and limits myocardial ischemia/reperfusion injury in rat hearts. SCH79797 dihydrochloride also potently prevents PAR1 activation in vascular smooth muscle cells, endothelial cells, and astrocytes[1][2][3][4].
AZ3451 is a protease-activated receptor-2 (PAR2) antagonist.
Trypsin is an enzyme that hydrolyzes proteins at the carboxyl side of the Lysine or Arginine. Trypsin activates PAR2 and PAR4. Trypsin induces cell-to-cell membrane fusion in PDCoV infection by the interaction of S glycoprotein of PDCoV and pAPN. Trypsin also promotes cell proliferation and differentiation. Trypsin can be used in the research of wound healing and neurogenic inflammation[1][2][3][4][6].
Parstatin(human), a cell-penetrating PAR-1 thrombin receptor agonist peptide, is a potent inhibitor of angiogenesis[1][2].
TRAP-6 amide TFA is a PAR-1 thrombin receptor agonist peptide[1].
Protease-Activated Receptor-1, PAR-1 Agonist is a thrombin-specific, protease-activated receptor 1 (PAR-1)-specific agonist peptide[1].
P4pal10 is a PAR4 antagonist. P4pal10 prevents the thrombin-mediated aggregation of mouse platelets in vivo. P4pal10 significantly reduced both the oedema and the granulocyte infiltration induced by Carrageenan (HY-125474)[1].
TRAP-6 is a protease-activated receptor 1 (PAR1) agonist. Sequence: Ser-Phe-Leu-Leu-Arg-Asn.
FLLRN is a biological active peptide. (PAR1-specific antagonist peptide)
TFLLR-NH2 (TFA) is a selective PAR1 agonist with an EC50 of 1.9 μM.
PAR-4 Agonist Peptide, amide is a proteinase-activated receptor-4 (PAR-4) agonist, which has no effect on either PAR-1 or PAR-2 and whose effects are blocked by a PAR-4 antagonist.
Protease-Activated Receptor-2 Activating Peptide is an agonist of Protease-Activated Receptor-2 (PAR-2).
UDM-001651 is a potent, selective, and orally bioavailable protease-activated receptor 4 (PAR4) antagonist (IC50=4 nM; Kd=1.4 nM). UDM-001651 shows antiplatelet potency (IC50=25 nM) in a γ-thrombin-induced platelet-rich plasma aggregation assay (γ-Thr PRP)[1].
RWJ-56110 dihydrochloride is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 uM) and shows no effect on PAR-2, PAR-3, or PAR-4. RWJ-56110 dihydrochloride inhibits the aggregation of human platelets induced by both SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM), quite selective relative to U46619 (HY-108566). RWJ-56110 dihydrochloride blocks angiogenesis and blocks the formation of new vessels in vivo. RWJ-56110 dihydrochloride induces cell apoptosis[1][2].