protease activated receptor (par)

Atopaxar (E5555) 是一种高效、可口服的，选择性的，可逆的凝血酶受体蛋白酶激活受体-1 (PAR-1) 拮抗剂。它是一种抗血小板剂，能干扰血小板信号，可用于动脉粥样硬化血栓性疾病的研究。

AC-55541 (AOB2796) 是高选择性的蛋白酶激活受体 2(PAR2)激动剂，pEC50为6.7。它在 PI 水解测定和 Ca2+动态测定中的pEC50值为 5.9 和 6.6，在体内表现出伤害感受器活性。

SCH79797 dihydrochloride 是一种有效的特异性蛋白酶激活受体 1 (PAR1) 拮抗剂，IC50 为 70 nM，Ki 为 35 nM。SCH79797 dihydrochloride 具有抗增殖和促凋亡作用。

Parmodulin 2 (ML 161) 是一种蛋白酶激活受体 1(PAR1) 变构抑制剂，IC50为 0.26 μM。它是蛋白酶激活受体 1 (PAR1) 介导的血小板活化的抑制剂，可以抑制体外血小板聚集和体内血小板血栓形成。

Atopaxar hydrobromide 是可口服的，高效选择性的可逆凝血酶受体蛋白酶激活受体-1 拮抗剂。它是一种抗血小板剂，能干扰血小板信号，用于动脉粥样硬化血栓性疾病的研究。

Vorapaxar sulfate (Zontivity) 是一种选择性、口服活性和竞争性的凝血酶受体蛋白酶激活受体(PAR-1)拮抗剂，Ki 值为 8.1 nM。它剂量依赖性抑制凝血酶受体激活肽 (TRAP) 诱导的血小板聚集，是抗血小板药物。

AC-264613 是一种选择性蛋白酶激活受体 (PAR-2) 激动剂，pEC50为 7.5。

Vorapaxar (MK-5348) 是抗血小板药物，是一种选择性、口服活性和竞争性的凝血酶受体蛋白酶激活受体(PAR-1)拮抗剂，Ki 值为 8.1 nM。它靠剂量依赖性抑制凝血酶受体激活肽 (TRAP) 诱导的血小板聚集。

I-191 是选择性有效的蛋白酶激活受体 2 拮抗剂。

Protease-Activated Receptor-4 是蛋白酶激活受体 4 激动剂，具有抗血小板治疗。

Protease-Activated Receptor-2, amide (SLIGKV-NH2) 是 PAR2 的激动剂，IC50为 10.4 M。

PAR-2-IN-1 (IUN76750) 是一种 PAR-​2 信号通路抑制剂，具有抗炎和抗癌作用。

SLIGRL-NH2 (Protease-Activated Receptor-2 Activating Peptide) 为一种蛋白酶激活受体-2 (PAR-2) 激动剂，具有诱导非组胺能性瘙痒的功能。

PAR-4 Agonist Peptide, amide TFA (PAR-4-AP (TFA)) 是一种蛋白酶激活受体 4 (PAR-4) 激动剂，对 PAR-1 或 PAR-2 均无影响，其作用可被 PAR-4 拮抗剂阻断。

AZ3451 是蛋白酶激活受体 2 的变构拮抗剂，IC50值为 23 nM。

Protease-Activated Receptor-1, PAR-1 Agonist acetate 是一种选择性蛋白酶激活受体 1 (PAR-1) 激动剂肽。 它对应于 PAR1 栓系配体，可以选择性地模拟凝血酶通过该受体的作用。

Protease-Activated Receptor-1 (PAR-1) Agonist TFA is a selective peptide that acts as an agonist for the proteinase-activated receptor-1 (PAR-1). Corresponding to the tethered ligand of PAR-1, this compound mimics the actions of thrombin through the PAR-1 receptor[1][2].

Protease-Activated Receptor-3 (PAR-3) (1-6), human TFA is a peptide that acts as an agonist for the proteinase-activated receptor (PAR-3)[1].

Protease-Activated Receptor-1 (PAR-1) Agonist, a selective peptide, activates the PAR-1 receptor by mimicking the specific actions of thrombin. It corresponds to the PAR1 tethered ligand, facilitating selective activation of this receptor.

BMS-986141(UDM-003183) 是一种具有口服活性的选择性和高效性的凝血酶受体蛋白酶激活受体-4 (protease-activated receptor-4 (PAR-4)) 拮抗剂，其 IC50 值为 0.4 nM。BMS-98614 表现出显著的抗血栓作用。

PAR-2-IN-2 (compound P-596) 是一种蛋白酶激活受体 2 (PAR-2) 抑制剂，其对 SLIGKV 的 IC50 为 10.79 μM，而对 Trypsin 的 IC50 大于 200 μM。

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)

TFRGAP-amide, human PAR-3-derived tethered ligand sequence which does not activate PAR-3 but rather activates PAR-1 and PAR-2, either in Jurkat or in other PAR-expressing cells.

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 . RWJ-56110 dihydrochloride blocks angiogenesis and blocks the formation of new vessels in vivo. RWJ-56110 dihydrochloride induces cell apoptosis[1][2]. Proteinase-activated receptors (PARs) are a family of G protein-coupled receptors activated by the proteolytic cleavage of their N-terminal extracellular domain, exposing a new amino terminal sequence that functions as a tethered ligand to activate the receptors.RWJ56110 inhibits the aggregation of human platelets induced by both SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM) while being quite selective relative to collagen and the thromboxane mimetic U46619 [1].RWJ-56110 dihydrochloride is fully inhibits thrombin-induced RASMC proliferation with an IC50 value of 3.5 μM. RWJ-56110 dihydrochloride shows blockade of thrombin's action with RASMC calcium mobilization (IC50=0.12 μM), as well as with HMVEC (IC50=0.13 μM) and HASMC calcium mobilization (IC50=0.17 μM)[1].RWJ56110 (0.1-10 μM; 24-96 hours) inhibits endothelial cell growth dose-dependently, with half-maximal inhibitory concentration of RWJ56110 is approximately 10 μM[2].RWJ56110 (0.1-10 μM; 6 hours) inhibits DNA synthesis of endothelial cells in a thymidine incorporation assays. Endothelial cells are in fast-growing state (50-60% confluence), RWJ56110 inhibits cell DNA synthesis in a dose-dependent manner, but when cells that are in the quiescent state (100% confluent), the inhibitory effect of PAR-1 antagonists is much less pronounced[2].RWJ56110 (0.1-10 μM; pretreatment for 15 min) inhibits thrombin-induced Erk1/2 activation in a concentration-dependent manner. However, when endothelial cells are stimulated by FBS (final concentration 4%), it reduces partially the activated levels of Erk1/2[2].RWJ56110 (30 μM; 24 hours) has an inhibitory effect on endothelial cell cycle progression. It reduces the percentage of cells in the S phase, while alterations in the percentages of G1 and G2/M cells are less pronounced[2]. Western Blot Analysis[2] Cell Line: Endothelial cells [1]. Andrade-Gordon, et al.Design, synthesis, and biological characterization of a peptide-mimetic antagonist for a tethered-ligand receptor. oc Natl Acad Sci U S A. 1999 Oct 26;96(22):12257-62. [2]. Panagiota Zania, et al. Blockade of angiogenesis by small molecule antagonists to protease-activated receptor-1: association with endothelial cell growth suppression and induction of apoptosis. J Pharmacol Exp Ther. 2006 Jul;318(1):246-54.