INSERM U. 311, Etablissement de Transfusion Sanguine de Strasbourg, Strasbourg, France lntroduction as antithrombotic drugs (11). Similarly, the ATP analogues ARL66096 andARL67085 (previously known as FPL), which are potent antagonists of ADP induced platelet aggregation, have proved to be effective in arterial thrombosis models and are under clinical investigation (12). A rare congenital bleeding disorder with impairment of ADP induced platelet aggregation (13, 14) strikingly resembles the acquired thrombopa-thy resulting from ticlopidine or clopidogrel intake (15). Finally, patients with primary secretion defects have been shown to have lower numbers of ADP receptors than healthy donors, which emphasizes the role of ADP as a necessury cofactor in all platelet functions (16). Attempts to clone a speciftc P2T receptor have to date been unsuccessful and in addition more than one purinoceptor appears to be involved in the multiple effects of ADP on platelets (17-19). Thus one must now consider the<< YTf receptor>> as a pharmacological concept rather than as a molecular entity.