MRS2690 disodium 

MRS2690 disodium is a selective P2Y14 receptor agonist. MRS2690 disodium inhibits adenylyl cyclase activity, thereby reducing intracellular cAMP levels and mediating concentration-dependent vasoconstriction of porcine coronary arteries. MRS2690 disodium 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. MRS2690 disodium can be used for ischemic heart disease^[1][2][3][4].

MRS2690 (0.001-10 μM) disodium elicits concentration-dependent contractions of porcine isolated coronary arteries at basal tone (log EC₅₀ = 6.30 M)^[1].
MRS2690 (0.001-10 μM) disodium shows enhanced concentration-dependent contractile responses in porcine coronary arteries pre-treated with Forskolin (HY-15371) plus U46619 (HY-108566) (R_max = 1.77 g),which can be blocked by the P2Y14 antagonist PPTN (HY-110322A), but not affected by the P2Y6 antagonist MRS2578 (HY-13104)^[1].
MRS2690 (10 μM) disodium significantly reduces forskolin-induced VASP phosphorylation (an indicator of cAMP levels) in porcine coronary arteries^[1].
MRS2690 (0.0001-1000 nM) disodium induces intracellular calcium mobilization in RBL-2H3 cells in a concentration-dependent manner with an EC₅₀ of 538 nM^[2].
MRS2690 (0.0001-100 nM) disodium stimulates [³⁵S]GTPγS binding to RBL-2H3 cell membranes in a concentration-dependent manner with an EC₅₀ of 8.1 nM^[2].
MRS2690 (1 μM) disodium activates P38 mitogen-activated protein kinase (MAPK) in RBL-2H3 cells^[2].
MRS2690 alone cannot induce β-hexosaminidase (HEX) release, but it concentration-dependently enhances antigen (DNP-BSA)-induced HEX release in RBL-2H3 cells primed with anti-DNP-BSA antibody, with an EC₅₀ of 103 nM^[2].
MRS2690 (1 μM, 50 min) disodium significantly enhances antigen (NP-BSA)-, C3a-induced β-hexosaminidase (β-Hex) release in LAD2 cells^[3].
MRS2690 (10-1000 nM) disodium significantly induces platelet-dependent neutrophil chemotaxis towards Macrophage derived chemokine (MDC, CCL22) in a concentration-dependent manner^[4].

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

626.33

C₁₅H₂₂N₂Na₂O₁₆P₂S

OC[C@H]1O[C@@H]([C@@H]([C@H]([C@@H]1O)O)O)OP(OP(OC[C@@H]2[C@@H](O)[C@@H](O)[C@H](N3C(NC(C=C3)=O)=S)O2)(O[Na])=O)(O[Na])=O

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]