Thromboxane A 2 (TXA 2 ) and prostacyclin (PGI 2 ) are two labile products formed from arachidonic acid by the way of cyclooxygenase. An overproduction of thromboxane A 2 has been detected in a series of diseases whereby this prostanoid is assumed to contribute to the underlying pathomechanisms by its potent stimulation of platelet aggregation and smooth muscle contraction. This increased TXA 2 biosynthesis is frequently accompanied by a stimulation of prostacyclin formation which is one of the most potent inhibitors of platelet aggregation and smooth muscle contraction. Therefore, TXA 2 prostaglandin endoperoxide H 2 receptor antagonists, thromboxane synthase inhibitors and drugs which combine both activities have been developed with the aim to suppress the formation and/or the action of thromboxane A 2 . Since prostacyclin has been demonstrated to counterbalance the pathological effects of TXA 2 , several PGI 2 agonists have also been developed. This review will highlight the evolution and some of the latest findings in the field of prostacyclin and thromboxane A 2 modulators mainly those which are under clinical evaluation or marketed.
Keywords: thromboxane A2 TXA2, prostacylin modulators, TXA2 biosynthesis, prostaglandin endoperoxide H2 receptor antagonists, thormboxane synthase inhibitors, TXSIs, TXA2 PGH2 receptor antagonists TXRAs, Prostanoid thromboxane A2 receptor antagonists, Non Prostanoid thromboxane A2 receptor antagonists, sulotroban, Combined thromboxane A2 receptor antagonists, prostaglandin D2, prostaglandin E2, prostaglandin H2, prostaglandin G2, prostaglandin F2