MRS2179 (ammonium salt)
目录号 : GC44249A P2Y1 receptor antagonist
Cas No.:228264-19-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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).
| 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 |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 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 |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
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.