Taprostene (CG-4203), a synthetic and chemically stable analogue of Prostacyclin (PGI2), effectively protects the endothelium and myocardium following acute myocardial ischemia and reperfusion in cats. It enhances cytoprotective actions and minimizes undesired hemodynamic effects [1].

Taprostene, administered intravenously at 100 ng/kg/min starting 30 minutes after occlusion of the left anterior descending coronary artery and continuing through 1 hour of reperfusion in a 6-hour myocardial ischemia (MI) model with reperfusion in anesthetized cats, significantly reduces plasma creatine phosphokinase activity in the MI + Taprostene group compared to the MI + vehicle group. This compound exhibits a multifaceted activity profile, including inhibition of platelet aggregation at much lower concentrations than those needed for significant vasodilation in rabbit aortic rings, suggesting antiaggregatory and cytoprotective roles in circulatory shock, acute inflammatory conditions, and rat models of myocardial hypoxia and permanent ischemia. Initial tests with varying infusion rates from 50 to 200 ng/kg/min determined an optimal rate that minimized vasodilatory (hemodynamic) effects while maintaining cardioprotective benefits. Taprostene also effectively prevents neutrophil adherence to myocardial endothelium in areas of ischemia and reperfusion injury [1]. This study employed adult male cats weighing between 2.5 to 3.5 kg, using a dosage of 100 ng/kg infused intravenously at 100 ng/kg/min for the duration of the 5.5-hour experiment [1]. Notably, in six cat aortic rings, concentrations of 1-100 ng/mL of Taprostene did not induce vasorelaxation, achieving a 34% relaxation at 300 ng/mL, with an EC50 of 520 ng/mL, which is 26 times higher than the concentration needed for its antiplatelet effect in cat platelet-rich plasma.