2-Cl-IB-MECA is a highly selective A3 adenosine receptor agonist with Ki value of 0.33nM, displaying 2500- and 1400-fold selectivity over A1 and A2A receptors, respectively.
2-Cl-IB-MECA is a selective A3 adenosine receptor (A3AR) agonist (Ki=0.33 nM). Intravenous administration of 200 micrograms/kg 2-Cl-IB-MECA resulted in a short-lasting hypotension, which was accompanied by a 50-100-fold increase in plasma histamine concentrations. Administration of a second dose of 2-Cl-IB-MECA did not elicit any hemodynamic effects. Also no histamine release was observed after the second dose[3]. Pretreating wild-type (WT) mice with Cl-IB-MECA reduced myocardial infarct size induced by 30 min of coronary occlusion and 24 h of reperfusion at doses (30 and 100 mug/kg) that concomitantly reduced blood pressure and stimulated systemic histamine release. Cl-IB-MECA protects against myocardial ischemia/reperfusion injury in mice principally by activating the A(3)AR (A(3) adenosine receptor) [4]. Cl-IB-MECA is able to enhance TNF-α production in LPS-treated macrophages in an NF-κB- dependent manner[5]. Cl-IB-MECA suppressed erythroblast growth and maturation at doses >/=50 mumol/l through a mechanism of cell cycle inhibition and accumulation of cells in the G1/G0 phase[6].
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