Fig. 1. Mechanisms of action of endogenous apyrase.

eATP and eADP are scavenged by apyrase, leading to the generation of cardioprotective adenosine (eADO). Thus, administration of exogenous apyrase (APT102) boosts the endogenous control mechanism that converts a proinflammatory and prothrombotic environment, characterized by dominant P2 purinoceptor signaling, into an eADO P1 receptor signaling that is largely characterized by prevention of inflammatory responses and thrombosis, and cardioprotective mechanisms. Apyrase attenuates platelet activation mediated by P2Y₁, P2Y₁₂, and P2X₁ receptors, whereas clopidogrel blocks only P2Y₁₂ receptors. Thus, apyrase may be more effective for inhibiting platelet-rich thrombosis than P2Y₁₂ receptor antagonists.