Abstract
Molsidomine or its active metabolite SIN-1A have antithrombotic properties in experimental models. This effect seems to be related, at least in part, to their antiplatelet activities. SIN-1A inhibited platelet adhesion to collagen, platelet aggregation, and the release reaction in in vitro experiments. SIN-1A acts as an early step of platelet activation by inhibiting calcium influx and phospholipase activity, which leads to inhibition of thromboxane formation and fibrinogen binding. Antiplatelet properties were observed after oral absorption in healthy volunteers and in patients with myocardial infarction after intravenous infusion.
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