Thromboxane synthase inhibitors and receptor antagonists.
Platelet activation plays a major role in myocardial infarction and in reocclusion following successful thrombolysis, as corroborated by several clinical studies using aspirin. However, the overall reduction of new vascular complications in patients with symptomatic arterial disease by aspirin was only around 25%. Therefore, there is great interest in finding new means to inhibit platelet activation more efficiently. One line of research has focused on ways to interfere with the action of thromboxane A2 in a more selective way than aspirin does. As such, the development of thromboxane synthase inhibitors, followed by thromboxane receptor antagonists, raised hopes for a better treatment. However, both classes of drugs have some drawbacks, which could be overcome by combining them. This aim has led to the development of compounds that intrinsically possess both activities. Ongoing research indicates that such a dual inhibitor may indeed be more powerful than either aspirin or drugs with the single actions.
Vermylen
J
J
Center for Thrombosis and Vascular Research, K.U. Leuven, Belgium.
Deckmyn
H
H
D001241:Aspirin / Q000494:pharmacology; D006801:Humans; D011982:Receptors, Prostaglandin / Q000187:drug effects*; D017482:Receptors, Thromboxane; D013930:Thromboxane-A Synthase / Q000037:antagonists & inhibitors*; D013931:Thromboxanes / Q000037:antagonists & inhibitors*
D011982:Receptors, Prostaglandin; D017482:Receptors, Thromboxane; D013931:Thromboxanes; D013930:Thromboxane-A Synthase; D001241:Aspirin