212329-37-8
212329-37-8 结构式
基本信息
可分装 5000/100MG
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
物理化学性质
常见问题列表
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)
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. |
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.