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1 were elevated at baseline and decreased with sitaxsentan.
3 were randomized to receive placebo (n = 60), sitaxsentan 100 mg (n = 55), or sitaxsentan 300 mg (n =
6 ctive therapy (101 [15%] iloprost, 118 [18%] sitaxsentan, 204 [31%] sildenafil, and 233 [36%] subcuta
8 bo (n = 60), sitaxsentan 100 mg (n = 55), or sitaxsentan 300 mg (n = 63) orally once daily for 12 wee
9 245 patients were treated: placebo (n = 62), sitaxsentan 50 mg (n = 62) or 100 mg (n = 61), or OL (6M
10 The placebo-subtracted treatment effect for sitaxsentan 50 mg was 24.2 m (p = 0.07) and for OL bosen
11 limit of normal) was 6% for placebo, 5% for sitaxsentan 50 mg, 3% for sitaxsentan 100 mg, and 11% fo
12 determined the acute hemodynamic effects of sitaxsentan, a selective ET(A) receptor antagonist, in p
14 selective endothelin receptor-A antagonists sitaxsentan and ambrisentan are currently undergoing inv
15 used the selective ET(A) receptor antagonist sitaxsentan at increasing rates (0.3125 to 10 mg/min) in
19 ive endothelin A (ET(A)) receptor antagonist sitaxsentan for the treatment of pulmonary arterial hype
20 udy, the selective ET(A) receptor antagonist sitaxsentan improved six-min walk (6MW) distance, World
25 to 1 of 3 doses (1.5, 3.0, or 6.0 mg/kg) of sitaxsentan or placebo as an intravenous infusion over 1
26 with the selective ET(A) receptor antagonist sitaxsentan, orally once daily at a dose of 100 mg, impr
27 istration of the selective ET(A)R antagonist sitaxsentan prevented podocyte loss, formation of the hy
28 ion trial, once a day treatment of 100 mg of sitaxsentan statistically significantly improved 6-min w
29 agonism and the subsequent identification of sitaxsentan (TBC11251, 1) as a clinical development comp
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