In the last decade the incidence of thrombo-embolic diseases in which anti-platelet drugs may have been beneficial was estimated to be 2,500,000 patients affected by coronary artery diseases, 873,000 patients with cerebrovascular disease, i.e., stroke or transient ischemic attack, and 2,000,000 patients with peripheral arterial occlusive disease. However, even though G protein signaling pathways are known to be intimately involved in the genesis of thromboembolic events, it has not been possible to pharmacologically target G proteins as a means of decreasing blood platelet functi