Mechanism of action<unk>  is a competitive antagonist of the μ-opiod receptors (MOR) in the gastrointestinal tract, with a Ki of 0.2 ng/mL. Activation of these receptors by endogenous or exogenous agonists reduces gastrointestinal motility, and<unk>  blocks this effect. Like most other peripherally-selective MOR antagonists, such as naloxegel and methylnaltrexone,<unk>  is selective for peripheral receptors because is effluxed by P-glycoprotein, which reduces its ability to cross the blood-brain barrier and affect the central nervous system. Pharmacokinetics Absorption Peak plasma concentration (Cmax) of<unk>  is reached approximately 2 hours after oral dosing, while the Cmax for metabolite occurs 36 hours after an oral dose.<unk> 's high affinity for the peripheral μ-receptor results in an absolute bioavailability less than 7%. Distribution 80% to 90% of systemically available<unk>  is bound to plasma protein. At steady state, the volume of distribution is approximately 30 liters. Metabolism<unk>  undergoes no significant hepatic metabolism, but is metabolized by intestinal flora. Gut metabolism produces an active metabolite with no clinically significant contribution to drug effect. Elimination<unk>  undergoes 35% renal excretion and greater than 50% biliary excretion. Drug metabolized by intestinal flora is excreted in the feces.<unk> 's half-life of elimination is 10 to 17 hours, while that of the gut metabolite is 10 to 18 hours.
Alvimopan
Fenoldopam
Tofisopam
Avacopan
Levosimendan
Hexoprenaline
Ergotamine
Bethanechol