Disease relevance of Mosapride

• Mosapride, a 5HT-4 receptor agonist, improves insulin sensitivity and glycaemic control in patients with Type II diabetes mellitus [1].
• Coadministration of mosapride had no effect on respiratory depression induced by morphine (slope of 0.39 +/- 0.19 L/mm Hg CO2, P > .7) [2].
• The effect of mosapride, a novel prokinetic, on acid reflux variables in patients with gastro-oesophageal reflux disease [3].
• CONCLUSIONS: Treatment of functional dyspepsia with mosapride was not superior to placebo [4].
• The objective of this study is to perform an open study of mosapride citrate's effects on constipation, a prominent lower gastrointestinal tract disorder in parkinsonian patients [5].

Psychiatry related information on Mosapride

• During the day hours (0700-1900, light on), the local infusion of either 5-HT4 agonist, 5-MeOT (100 microM) or mosapride (10 microM), but not in their lower concentrations, into the bilateral hippocampus significantly increased motor activity as compared with the baseline values or the control rats [6].

High impact information on Mosapride

• METHODS: Thirty-four inpatients with Type II diabetes mellitus were randomly assigned to receive either mosapride (5 mg orally three times a day, n=17) or a placebo ( n=17) for 1 week (first study) [1].
• The 5-hydroxytryptamine 4 receptor agonist mosapride does not antagonize morphine-induced respiratory depression [2].
• Effects of famotidine, mosapride and tandospirone for treatment of functional dyspepsia [7].
• Mosapride stimulated contractile activity only in the gastric antrum and ileum [8].
• The aim of the present study was to evaluate whether a prokinetic benzamide, mosapride, enhances the R-R and R-IAS reflexes mediated via 5-HT4 receptors in the guinea pig [9].

Chemical compound and disease context of Mosapride

• The present study showed for the first time that mosapride citrate augmented lower gastrointestinal tract motility, as shown in CTT and videomanometry, and thereby ameliorated constipation in parkinsonian patients without serious adverse effects [5].
• In contrast to mosapride, cisapride causes embryonic lethality in teratology studies, and has been related to fatal cardiac arrhythmia in the adult [10].
• Intraarterial administration of mosapride, a prokinetic benzamide, accelerated intestinal motor activity and the concentration of dialysate ACh increased [11].
• Torsades de pointes ventricular tachycardia induced by mosapride and flecainide in the presence of hypokalemia [12].
• In nonerosive GERD, the addition of mosapride offers no benefit over pantoprazole alone [13].

Biological context of Mosapride

• Mosapride did not significantly influence the action potential duration (3 +/- 2.0% increase at 1.0 micromol/l, n = 6) [14].
• Mosapride was approximately 1000-fold less potent in blocking I(Kr) (IC50 = 4 micromol/l) [14].
• The selective 5-HT3 receptor antagonists ramosetron (YM060), YM114 (KAE-393), granisetron and ondansetron, and the substituted benzamides (5-HT4 receptor agonist/5-HT3 receptor antagonists) cisapride mosapride and SC-53116 dose-dependently enhanced gastric emptying in normal rats [15].
• During defecation, mosapride augmented the amplitude in rectal contraction (P < 0.05) and lessened the volume of postdefecation residuals [5].
• Influence of mosapride citrate on gastric motility and autonomic nervous function: evaluation by spectral analyses of heart rate and blood pressure variabilities, and by electrogastrography [16].

Anatomical context of Mosapride

• PROCEDURE: Electrical activity of the small intestine and cecum was recorded before and after mosapride administration by use of an electrogastrograph [17].
• Effects of mosapride, a 5-hydroxytryptamine 4 receptor agonist, on electrical activity of the small intestine and cecum in horses [17].
• We investigated the possible effects of mosapride, a digestive tract prokinetic agent, on glycemic control in diabetic patients complicated with gastropathy [18].
• CONCLUSIONS: Mosapride increases the rate of complete bolus transit in the esophagus, and enhances esophageal bolus transit in asymptomatic volunteers [19].
• The lower esophageal sphincter (LES) pressure and the number of transient LES relaxations did not change after mosapride vs. placebo [19].

Associations of Mosapride with other chemical compounds

• Ambulatory pH monitoring was performed after treatment with 40 mg mosapride citrate or placebo q.d.s. for 2 days in random order, using a double-blind crossover technique, with a washout period of at least 5 days [3].
• Electrophysiological characterization of the prokinetic agents cisapride and mosapride in vivo and in vitro: implications for proarrhythmic potential [14]?
• We compared the effects of four different 5-HT4 receptor agonists (cisapride, prucalopride, renzapride and mosapride) on cloned HERG channels with the objective to evaluate and compare their proarrhythmic potential [20].
• Other cytochrome P450 (CYP) 3A4 inhibitors, cimetidine, erythromycin, and clarithromycin, also inhibited the metabolism of cisapride and mosapride [21].
• A rapid high-performance liquid chromatography/positive ion electrospray tandem mass spectrometry method was developed and validated for the quantification of fexofenadine in human plasma using mosapride as internal standard [22].

Gene context of Mosapride

• Plasma gastrin levels (42.4+/-3.6 pg/ml) increased 60 min after administration of mosapride (p<0.01 vs. placebo) [23].
• Mosapride produced no significant effects on the recombinant HERG current [20].
• The affinity of TS-951 for the 5-HT4 receptor was higher than those of other agonists, 5-HT, cisapride, mosapride and renzapride [24].
• Mosapride improves food intake, while not worsening glycemic control and obesity, in ob/ob obese mice with decreased gastric emptying [25].
• Peak plasma motilin levels (18.6+/-1.7 pg/ml) were achieved 60 min after administration of mosapride (p<0.01 vs. placebo), and returned to baseline levels within a further 120 min [23].

Analytical, diagnostic and therapeutic context of Mosapride

• Improvement of glycemic control after treatment with mosapride for diabetic gastropathy [26].
• In ancillary experiments 10 rats received 100 mg/kg mosapride orally or placebo 50 minutes before intraperitoneal injection of 10 mg/kg morphine, followed 20 minutes later by injection of naloxone, and the respiratory frequency was monitored [2].
• In conscious dogs with force transducers implanted, mosapride (0.3-3 mg/kg i.v.) stimulated the antral motility without affecting the colonic motility [27].
• Mosapride citrate prolongs survival in stroke patients with gastrostomy [28].
• In order to analyze simultaneously the enantiomers of mosapride and M-1 in plasma, a simple and reproducible high-performance liquid chromatographic (HPLC) method has been developed [29].

References