Sucralfate binds to duodenal and gastric ulcers and to gastric erosions produced by ethanol and anti-inflammatory drugs. The affinity of sucralfate for defective mucosa is explained by the drug's viscous adhesiveness and the formation of polyvalent bridges between the negatively charged sucralfate polyanions and positively charged proteins present in high concentrations in mucosal lesions. Sucralfate also buffers acid, inhibits the action of pepsin, and adsorbs bile salts. These properties of sucralfate enable the drug to act as an effective barrier to the penetration of acid, pepsin, and bile salts. Evidence to support such a comprehensive protective barrier effect is presented. Sucralfate also binds to uninjured mucosa and is believed to exert a similar "barrier" effect on regenerated and normal mucosa. Other possible mechanism for sucralfate's antiulcer effect include depletion of acid, pepsin, and bile salts from the the gastric secretion. Animal data show that the action of sucralfate is sustained because of its viscous adhesiveness, slow reaction with acid, and high affinity for defective mucosa.