MRS2690 

MRS2690 is a selective P2Y14 receptor agonist. MRS2690 inhibits adenylyl cyclase activity, thereby reducing intracellular cAMP levels and mediating concentration-dependent vasoconstriction of porcine coronary arteries. MRS2690 induces intracellular calcium mobilization, activates P38 and stimulates [³⁵S]GTPγS binding to RBL-2H3 cell membranes. MRS2690 enhances antigen (NP-BSA)-, C3a-induced β-hexosaminidase (β-Hex) release. MRS2690can be used for ischemic heart disease^[1][2][3][4].

MRS2690 (0.001-10 μM) 在基础张力下引发猪孤立冠状动脉的浓度依赖性收缩 (log EC₅₀ = 6.30 M)^[1]。
MRS2690 (0.001-10 μM) 在预先用 Forskolin (HY-15371) 和 U46619 (HY-108566) 处理的猪冠状动脉中显示出增强的浓度依赖性收缩反应 (R_max = 1.77 g)，可被 P2Y14 拮抗剂 PPTN (HY-110322A) 阻断，但不受 P2Y6 拮抗剂 MRS2578 (HY-13104) 的影响^[1]。
MRS2690 (10 μM) 显著降低猪冠状动脉中 Forskolin 诱导的 VASP 磷酸化 (cAMP 水平的指标)^[1]。
MRS2690 (0.0001-1000 nM) 以浓度依赖性方式在 RBL-2H3 细胞中诱导细胞内钙动员，EC₅₀ 为 538 nM^[2]。
MRS2690 (0.0001-100 nM) 以浓度依赖性方式刺激 RBL-2H3 细胞膜的 [³⁵S]GTPγS 结合，EC₅₀ 为 8.1 nM^[2]。
MRS2690 (1 μM) 在 RBL-2H3 细胞中激活 P38 丝裂原活化蛋白激酶 (MAPK)^[2]。
MRS2690 单独不能诱导 β-己糖胺酶 (HEX) 释放，但在用抗 DNP-BSA 抗体预处理的 RBL-2H3 细胞中以浓度依赖性方式增强抗原 (DNP-BSA) 诱导的 HEX 释放，EC₅₀ 为 103 nM^[2]。
MRS2690 (1 μM, 50 min) 在 LAD2 细胞中显著增强抗原 (NP-BSA) 和 C3a 诱导的 β-己糖胺酶 (β-Hex) 释放^[3]。
MRS2690 (10-1000 nM) 显著诱导血小板依赖的中性粒细胞趋化性向巨噬细胞衍生趋化因子 (MDC, CCL22)^[4]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

582.37

C₁₅H₂₄N₂O₁₆P₂S

7077-89-6

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Abbas ZSB, et al. UDP-sugars activate P2Y14 receptors to mediate vasoconstriction of the porcine coronary artery. Vascul Pharmacol. 2018 Apr;103-105:36-46.  [Content Brief]

  [2]. Gao ZG, et al. UDP-glucose acting at P2Y14 receptors is a mediator of mast cell degranulation. Biochem Pharmacol. 2010 Mar 15;79(6):873-9.  [Content Brief]

  [3]. Gao ZG, et al. The role of P2Y(14) and other P2Y receptors in degranulation of human LAD2 mast cells. Purinergic Signal. 2013 Mar;9(1):31-40.  [Content Brief]

  [4]. Amison RT, et al. Lipopolysaccharide (LPS) induced pulmonary neutrophil recruitment and platelet activation is mediated via the P2Y1 and P2Y14 receptors in mice. Pulm Pharmacol Ther. 2017 Aug;45:62-68.  [Content Brief]