MRS2690 disodium is a selective agonist of the P2Y14 receptor. It inhibits adenylyl cyclase activity, thereby reducing intracellular cAMP levels and causing concentration-dependent vasoconstriction in porcine coronary arteries. MRS2690 disodium induces intracellular calcium mobilization, activates P38, and stimulates [35S]GTPγS binding on the membrane of RBL-2H3 cells. It also enhances the β-hexosaminidase (β-Hex) release induced by antigen (NP-BSA) and C3a. This compound is useful for research in ischemic heart disease.

MRS2690 (0.001-10 μM) disodium induces concentration-dependent contractions of isolated porcine coronary arteries under baseline tension, with a log EC 50 value of 6.30 M. In porcine coronary arteries pre-treated with Forskolin and U46619, it shows enhanced concentration-dependent contractions (R max = 1.77 g), which can be blocked by P2Y14 antagonist PPTN but remain unaffected by P2Y6 antagonist MRS2578. At 10 μM, MRS2690 disodium significantly reduces Forskolin-induced VASP phosphorylation in porcine coronary arteries, serving as an indicator of cAMP levels. Additionally, MRS2690 (0.0001-1000 nM) disodium induces intracellular calcium mobilization in RBL-2H3 cells in a concentration-dependent manner with an EC 50 of 538 nM. It enhances [35 S]GTPγS binding to RBL-2H3 cell membranes (EC 50 = 8.1 nM) and activates P38 MAPK in these cells at 1 μM. While unable to induce β-hexosaminidase (HEX) release on its own, MRS2690 enhances DNP-BSA induced HEX release in a concentration-dependent manner in RBL-2H3 cells pre-treated with anti DNP-BSA antibodies, with an EC 50 of 103 nM. Moreover, it significantly enhances NP-BSA and C3a induced β-hexosaminidase release in LAD2 cells at 1 μM for 50 minutes. Finally, MRS2690 (10-1000 nM) disodium significantly prompts platelet-dependent neutrophil chemotaxis towards macrophage-derived chemokine (MDC, CCL22) in a concentration-dependent fashion.