MRS 1523

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.

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.