西他生坦鈉為一種小分子化合物，主要通過(guò)抑制內(nèi)皮素(Endothelin) 的作用而產(chǎn)生治療作用（內(nèi)皮素能調(diào)節(jié)血管收縮及血管平滑肌的生長(zhǎng)）。其對(duì)內(nèi)皮素A受體的作用是對(duì)B型內(nèi)皮素受體作用的6500倍，高選擇性的內(nèi)皮素A受體拮抗劑能增加血流與反轉(zhuǎn)血管收縮。Sitaxentan sodium是一種選擇性的endothelin A receptor (ETA)(內(nèi)皮素受體A）拮抗劑，IC50和K_i分別為1.4 nM和0.43 nM，比作用于ETB選擇性高7000倍。Phase 3。Sitaxentan sodium inhibits ET-1-induced stimulation of phosphoinositide turnover with a K_i of 0.69 nM and a pA2 of 8.0.Sitaxentan sodium has a serum half-life in the rat and the dog of 6 hours - 7 hours and 60?100% oral bioavailability. Orally administered Sitaxentan sodium is rapidly absorbed in both the rat and the dog with a t_1/2(abs) of 0.7 hours and 0.3 hours, respectively. Peak plasma concentrations occurred between 2 hours and 3 hours postdosing in the rat and between 45 minutes and 90 minutes in the dog. The pulmonary vasoconstrictor response to acute hypoxia (10% O₂ for 90 minutes) is prevented with Sitaxentan sodium (5 mg/kg infused i.v. 10 minutes prior to the onset of hypoxia). Sitaxentan sodium delivered i.v. 50 minutes after the onset of hypoxia reverses the established pulmonary vasoconstriction. Sitaxsentan blocks increased plasma endothelin levels. Sitaxsentan dose dependently (10 mg/kg and 50 mg/kg per day in the drinking water) attenuates right ventricular systolic pressure, right heart hypertrophy, and pulmonary vascular remodeling observed 3 weeks after a single subcutaneous injection of monocrotaline. Systemic administration of the ETA receptor antagonist Sitaxentan sodium significantly attenuates cerebral vasospasm after subarachnoid hemorrhage (SAH). Sitaxentan sodium reduces the development of hypoxic pulmonary vasoconstriction (HPV) in the pig. In addition, bolus injection of Sitaxentan sodium reverses already established HPV.

西他生坦鈉常見的不良反應(yīng)為頭痛、外周水腫。