Home>>MRS2179 (ammonium salt)

MRS2179 (ammonium salt)

目录号 : GC44249

A P2Y1 receptor antagonist

MRS2179 (ammonium salt) Chemical Structure

Cas No.:228264-19-5

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1mg
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10mg
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产品描述

MRS2179 is a competitive purinergic P2Y1 receptor antagonist (Kb = 102 nM).[1] It is selective for P2Y1 over P2Y2, P2Y4, P2Y6, P2Y12, and P2Y13, as well as P2X1-4, receptors at 10 µM.2,3 MRS2179 reduces phospholipase C (PLC) activity induced by the P2Y receptor agonist 2-methylthioadenosine diphosphate with an IC50 value of 331 nM in turkey erythrocyte membranes that endogenously express high levels of the P2Y1 receptor.[1] It inhibits platelet shape change and aggregation induced by ADP in washed isolated human platelets when used at a concentration of 10 µM.[4] MRS2179 (50 mg/kg, i.v.) prolongs the length of tail bleeding time in mice, as well as decreases platelet thrombus formation in a mouse model of iron chloride-induced arterial thrombosis.[4],[5]

Reference:
[1]. Nandanan, E., Camaioni, E., Jang, S.-Y., et al. Structure-activity relationships of bisphosphate nucleotide derivatives as P2Y1 receptor antagonists and partial agonists. J. Med. Chem. 42(9), 1625-1638 (1999).
[2]. von Kügelgen, I. Pharmacological profiles of cloned mammalian P2Y-receptor subtypes. Pharmacol. Ther. 110(3), 415-432 (2006).
[3]. Brown, S.G., King, B.F., Kim, Y.-C., et al. Activity of novel adenine nucleotide derivatives as agonists and antagonists at recombinant rat P2X receptors. Drug Dev. Res. 49(4), 253-259 (2000).
[4]. Tovar, C., Higgins, B., Deo, D.D., et al. Small-molecule inducer of cancer cell polyploidy promotes apoptosis or senescence: Implications for therapy. Cell Cycle 9(16), 3364-3375 (2010).
[5]. Lenain, N., Freund, M., Léon, C., et al. Inhibition of localized thrombosis in P2Y1-deficient mice and rodents treated with MRS2179, a P2Y1 receptor antagonist. J. Thromb. Haemost. 1(6), 1144-1149 (2003).

Chemical Properties

Cas No. 228264-19-5 SDF
化学名 2′-deoxy-N-methyl-3′-adenylic acid, 5′-(dihydrogen phosphate), ammonium salt, hydrate
Canonical SMILES OP(OC[C@@H]1[C@@H](OP(O)(O)=O)C[C@H](N2C=NC3=C2N=CN=C3NC)O1)(O)=O.N
分子式 C11H17N5O9P2•XNH3[XH2O] 分子量 425.2
溶解度 42.5mg/ml in water 储存条件 Store at -20°C
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1 mM 2.3518 mL 11.7592 mL 23.5183 mL
5 mM 0.4704 mL 2.3518 mL 4.7037 mL
10 mM 0.2352 mL 1.1759 mL 2.3518 mL
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Research Update

Massive efflux of adenosine triphosphate into the extracellular space immediately after experimental traumatic brain injury

Exp Ther Med 2021 Jun;21(6):575.PMID:33850547DOI:10.3892/etm.2021.10007.

The aim of the current study was to determine effects of mild traumatic brain injury (TBI), with or without blockade of purinergic ATP Y1 (P2Y1) receptors or store-operated calcium channels, on extracellular levels of ATP, glutamate, glucose and lactate. Concentrations of ATP, glutamate, glucose and lactate were measured in cerebral microdialysis samples obtained from the ipsilateral cortex and underlying hippocampus of rats with mild unilateral controlled cortical impact (CCI) or sham injury. Immediately after CCI, a large release of ATP was observed in the cortex (3.53-fold increase of pre-injury value) and hippocampus (2.97-fold increase of pre-injury value), with ATP returning to the baseline levels within 20 min post-injury and remaining stable for during the 3-h sampling period. In agreement with the results of previous studies, there was a significant increase in glutamate 20 min after CCI, which was concomitant with a decrease in extracellular glucose (20 min) and an increase in lactate (40-60 min) in both brain regions after CCI. Addition of a selective P2Y1 receptor blocker (MRS2179 ammonium salt hydrate) to the microdialysis perfusate significantly lowered pre-injury ATP and glutamate levels, and eliminated the post-CCI peaks. Addition of a blocker of store-operated calcium channels [2-aminoethoxy diphenylborinate (2-APB)] to the microdialysis perfusate significantly lowered pre-injury ATP in the hippocampus, and attenuated the post-CCI peak in both the cortex and hippocampus. 2-APB treatment significantly increased baseline glutamate levels, but the values post-injury did not differ from those in the sham group. Pre-injury glucose levels, but not lactate levels, were increased by MRS2179 and decreased by 2-APB. However, none of these treatments substantially altered the CCI-induced reduction in glucose and increase in lactate in the cortex. In conclusion, the results of the present study demonstrated that a short although extensive release of ATP immediately after experimental TBI can be significantly attenuated by blockade of P2Y1 receptors or store-operated calcium channels.