Adenosine receptor agonists deepen the inhibition of platelet aggregation by P2Y12 antagonists.
Adenosine receptor agonists deepen the inhibition of platelet aggregation by P2Y12 antagonists.
Vascul Pharmacol. 2018 Nov 21;:
Authors: Boncler M, Wzorek J, Wolska N, Polak D, Watala C, Rozalski M
Abstract
Several adenosine receptor (AR) agonists have been shown in the past to possess anti-platelet potential; however, the adjunctive role of AR agonists in anti-platelet therapy with the use of P2Y12 receptor inhibitors has not been elucidated so far. This in vitro aggregation-based study investigates whether the inhibition of platelet function mediated by cangrelor or prasugrel metabolite can be potentiated by AR agonists. It evaluates the effect of non-selective (2-chloroadenosine), A2A-selective (UK 432097, MRE 0094, PSB 0777) and A2B-selective AR agonists (BAY 60-6583) on platelet function in relation to their toxicity, specificity towards adenosine receptor subtypes, structure and solubility. UK 432097, 2-chloroadenosine, MRE 0094 and PSB 0777 were found to be more or less potent inhibitors of ADP-induced platelet aggregation when acting alone, and that they remained non-cytotoxic to the cells. These AR agonists were also effective in the potentiation of the effects exerted by P2Y12 antagonists. Considering the estimated IC50 value, UK 432097, showing a relatively high binding affinity to the A2A adenosine receptor, has been identified as the most potent anti-aggregatory agent. This compound diminished platelet aggregation at nan...
Source: Vascular Pharmacology - Category: Drugs & Pharmacology Authors: Boncler M, Wzorek J, Wolska N, Polak D, Watala C, Rozalski M Tags: Vascul Pharmacol Source Type: research