Mosapride facilitates acetylcholine release from the enteric cholinergic neurons. It does not block K+ channels or D2 dopaminergic receptors. Mosapride is a selective 5-HT4 receptor agonist with no affinity for 5-HT1, 5-HT2, adrenalineα1, adrenalineα2 or dopamine D2 receptors.
In vivo
Mosapride augmented lower gastrointestinal motility in animal models and in patients with lower gastrointestinal disorders. It enhanced defecation responses in animal models. In human, after oral administration of single doses of mosapride 5-40 mg, peak mosapride concentrations (Cmax) were reached after about 1 hour. Both the Cmax and area under the concentration-time curve from time zero to infinity (AUC∞) increased in a dose-proportional manner. There were no significant differences in the pharmacokinetic profiles of mosapride administered as single or multiple doses. Mosapride is excreted in the urine and faeces. It is primarily metabolized in the liver by cytochrome P450 3A4 to the active metabolite, a des-4-fluorobenzyl compound.