A better knowledge of platelet activation mechanisms has made it possible to develop antiplatelet agents that are capable of inhibiting primary haemostasis at very precise levels. Many of these agents block the synthesis or receptor of an hemostasis I agonist. Thus, the thromboxane A2 receptor can be blocked, or its synthesis can be interrupted, by thromboxane synthetase inhibitors, by cyclooxygenase inhibitors, or by omega 3 fatty acids which are competitive inhibitors. Inhibitors of thrombin (hirudin), PAF acether and serotonin (ketanserin) also are available. Other antiplatelet agents secreted by endothelial cells act as haemostasis I antagonists by elevating platelet cAMP or cGMP levels (prostacyclins and analogues, nitrate derivatives). Monoclonal antibodies and RGD peptides directly inhibit the glycoproteins that are responsible for platelet adhesion or aggregation, but their users are faced with problems of cost and route of administration. Of all these new antiplatelet agents, only ticlopidine, which has an imperfectly known mode of action, has proved effective in multiple situations, but its use is limited by its side-effects.