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212329-37-8

中文名稱 MRS 1523
英文名稱 MRS 1523
CAS 212329-37-8
分子式 C23H29NO3S
分子量 399.55
MOL 文件 212329-37-8.mol
212329-37-8 結(jié)構(gòu)式 212329-37-8 結(jié)構(gòu)式

基本信息

中文別名
化合物 T16135
可分裝 5000/100MG
英文別名
MRS 1523 >98% (HPLC)
UUSHFEVEROROSP-UHFFFAOYSA-N
3-propyl-6-ethyl-5-[(ethylthio)carbonyl]-2 phenyl-4-propyl-3-pyridine carboxylate
3-Pyridinecarboxylic acid, 6-ethyl-5-[(ethylthio)carbonyl]-2-phenyl-4-propyl-, propyl ester

物理化學性質(zhì)

沸點551.3±50.0 °C(Predicted)
密度1.100±0.06 g/cm3(Predicted)
儲存條件2-8°C
溶解度DMSO: >10 mg/mL
酸度系數(shù)(pKa)1.44±0.28(Predicted)
形態(tài)oil
顏色無色至淺棕色

安全數(shù)據(jù)

WGK Germany3

常見問題列表

生物活性
MRS 1523 是一種有效的選擇性腺苷 A3 受體拮抗劑,對人和大鼠 A3 受體的 Ki 值分別為 18.9 nM 和 113 nM。在大鼠中,MRS 1523 對 A3 的選擇性分別是 A1 和 A2A 受體的 140 倍和 18 倍。MRS 1523 可以通過 N-type Ca channel 阻滯和抑制大鼠背根神經(jīng)節(jié)神經(jīng)元的動作電位而發(fā)揮抗痛覺過敏作用。
靶點

Ki: 18.9 nM (Human A 3 receptor), 113 nM (Rat A 3 receptor), 15.6 μM (A1 receptor) and 2.05 μM (A2A receptor)

體外研究

MRS 1523 (0.1-1 μM) treatment significantly antagonizes cell numbers to 40.7% and 57.4% of the control values, respectively, 30 min before the addition of cordycepin (60 μM). MRS1523 (1 μM) alone has any effect on tumor cell growth.
A partial blockade of the adenosine-5'-N-ethylcarboxamide (NECA)-induced migration is observed when human endothelial progenitor cells (hEPC) are co-incubated with MRS 1523 (1 nM). Furthermore, in 3-days hEPC, the treatment with MRS 1523 100 nM inhibits the NECA-induced migration by 70%. NECA-induced migration is blocked in dose-response fashion by MRS 1523 with calculated K i of 147 nM.

Cell Viability Assay

Cell Line: B16-BL6 cells
Concentration: 0.1 μM, 1 μM
Incubation Time: 24 hours, 48 hours, 72 hours
Result: Antagonized the growth suppression induced by cordycepin.
體內(nèi)研究

The expression and functional effects of A3 adenosine receptor (A3AR) on the excitability of small- to medium-sized, capsaicin-sensitive, dorsal root ganglion (DRG) neurons isolated from 3- to 4-week-old rats are investigated. The endogenous agonist adenosine reduces N-type Ca currents, and its effect is inhibited by 56% in the presence of A3AR antagonist MRS 1523. Current-clamp recordings demonstrated that neuronal firing of rat DRG neurons was also significantly reduced by A3AR activation in a MRS 1523-sensitive but PD173212-insensitive manner.

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