Ecabet is an antiulcerative and gastroprotective agent.1,2,3,4 It reduces the viability of H. pylori grown under urea-supplemented acidic conditions in a concentration-dependent manner.1 Ecabet inhibits H. pylori urease activity in a pH-dependent manner (IC50s = 2.1-2.6 and >16 mg/ml at pH values of 5 and 8, respectively). It inhibits adhesion of H. pylori to MKN-28 cells when used at concentrations of 1 and 2 mg/ml.2 In vivo, ecabet (25 and 100 mg/kg, p.o.) increases levels of prostaglandin E2 in rat gastric mucosa.3 It inhibits formation of hemorrhagic lesions in esophageal mucosa and reduces gastric juice pepsin activity in a rat model of reflux induced by fore-stomach and pyloric ligation when administered at a dose of 30 mg/kg.4
1.Ito, Y., Shibata, K., Hongo, A., et al.Ecabet sodium, a locally acting antiulcer drug, inhibits urease activity of Helicobacter pyloriEur. J. Pharmacol.345(2)193-198(1998) 2.Hayashi, S., Sugiyama, T., Yachi, A., et al.Effect of ecabet sodium on Helicobacter pylori adhesion to gastric epithelial cellsJ. Gastroenterol.32(5)593-597(1997) 3.Kinoshita, M., Iwasaki, H., Yasoshima, A., et al.Effects of ecabet sodium (TA-2711), a new antiulcer agent, on gastrointestinal mucosal prostanoid production and morphology in ratsBiol. Pharm. Bull.16(12)1220-1225(1993) 4.Okuyama, K., Saito, N., Kume, E., et al.Ecabet sodium prevents esophageal lesions induced by the reflux of gastric juice in ratsInflammopharmacology15(2)90-94(2007)