Thromboxane A2 (TXA2) is generated in the lungs of people with asthma, and when it signals through the thromboxane receptor it causes bronchoconstriction, vasoconstriction, mucous secretion, and airway hyper-responsiveness.<unk>  inhibits the activity of the thromboxane receptor, blocking the effects of TXA2. Pharmacokinetics The pharmacokinetics of<unk>  have been studied in Japanese and Caucasian, including Indian, healthy volunteers. The plasma concentrations of<unk>  increase with increasing doses. The absorption of<unk>  is relatively rapid with maximum plasma concentrations of 4.6–6 μg/ml obtained in 3 to 4 hours. Steady state plasma concentrations of<unk>  are reached within 4–5 days.<unk>  is slowly cleared, mainly by hepatic biotransformation. The drug shows biexponential decay in plasma profiles with a mean elimination half-life of 22 hours. Approximately 20% of the administered dose is recovered in the urine, with 60% of the urinary recovery being in the form of conjugates
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