par-4

PAR-4 Agonist Peptide, amide (AY-NH2) 是蛋白酶激活受体 4 (PAR-4) 的激动剂，对 PAR-1 或 PAR-2 均无影响，其作用可被 PAR-4 拮抗剂阻断。

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。

PAR-4 Agonist Peptide, amide acetate 是蛋白酶激活受体 4 (PAR-4) 的激动剂。

PAR 4 (1-6) 可用于生命科学领域的相关研究。其产品编号为 T36293，CAS号为 225779-44-2。

Prostate apoptosis response protein PAR-4 (2-7) [Homo sapiens] is a peptide with the sequence H2N-Ala-Thr-Gly-Gly-Tyr-Arg-OH, MW= 623.66.

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。

Trypsin 是一种可从鱼类分离出的丝氨酸蛋白酶，可水解赖氨酸或精氨酸羧基侧蛋白质。Trypsin 具有抗炎活性，可通过 PDCoV 的 S 糖蛋白与 pAPN 的相互作用诱导 PDCoV 感染的细胞膜融合，可激活 PAR2 和 PAR4，促进细胞增殖和分化。Trypsin 可用于促进伤口愈合和研究神经源性炎症。

ML-354 (VU0099704) 是一种具有选择性和高效性的 PAR4 拮抗剂，可用于研究心血管疾病。

Protease-Activated Receptor-4 diTFA 是蛋白酶激活受体 4 (PAR4) 激动剂。

tcY-NH2 TFA(327177-34-4 free base) 是一种选择性 PAR4 拮抗肽。抑制凝血酶诱导的内皮抑素释放和血小板聚集。

PAR-4 (1-6) amide human 是一个代表蛋白酶激活受体 4 (PAR4) N 末端片段的化学化合物。此化合物能够诱导血小板聚集。

PAR-4 (1-6), mouse 是多肽分子，其序列是 GYPGKF。

PAR4 antagonist6 (Compound 12) 作为一种效果显著的PAR4拮抗剂，其对hPAR4和mPAR4的IC50分别是134 nM和150 nM。

PAR4 antagonist7 (Compound 20f) 是一种具高选择性的PAR4拮抗剂，IC50值为1.72 nM。它能有效抑制由PAR4激动剂引发的血小板聚集。此外，PAR4 antagonist7 表现出优良的代谢稳定性，并在小鼠实验中未观察到出血倾向。

PAR4 antagonist8 (Compound 20f) 是口服活性并具选择性的PAR4拮抗剂，展现出出色的抗血栓作用。其IC50值是 15.32 nM，表明了其高效性。此外，PAR4 antagonist8 还能有效抑制由PAR4激动剂引发的人血小板聚集（IC50= 6.39 nM）和鼠血小板聚集，显示其广泛的生物活性。这种化合物具备良好的药代动力学特性，是抗血栓研究中极具价值的工具。

PAR4 antagonist1 (Compound 48) 是蛋白酶激活受体 4 (PAR4) 的拮抗剂，IC50为1.8 nM。在富血小板血浆 (PRP) 中，其对γ-凝血酶激活的PAR4的IC50为2 nM。PAR4 antagonist1 可用于抗血栓研究。

PAR4 antagonist5（compound 1）作为一种PAR4拮抗剂，展现出< 20 μM的IC50并有效抑制血小板聚集。该化合物主要应用于血栓栓塞性疾病的研究领域。

BMS-986120 is a first-in-class oral and reversible protease-activated receptor 4 (PAR4) antagonist. With IC50s of 9.5 nM and 2.1 nM in human and monkey blood, respectively. BMS-986120 has 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.

GYPGQV TFA (PAR 4 (1-6) TFA) 是一种六肽，作为蛋白酶激活受体 4 (PAR4) 片段，能特异性抑制PAR4。

Arylquin 1 是一种前列腺-凋亡-反应-4(Par-4)促分泌剂，靶向波形蛋白诱导 Par-4 分泌。Arylquin 1 通过诱导溶酶体膜通透性 (LMP) 诱导癌细胞非凋亡性细胞死亡。

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 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.

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