The continuing development of gastric acid pump inhibitors.

The synthesis and action of H2-receptor antagonists changed the understanding of gastric acid secretion as well as changing medical therapy for peptic ulcer disease. It is now known that peripheral regulation of gastric acid secretion depends largely, but not entirely, on histamine release from the enterochromaffin-like cell. There is, therefore, no final common pathway for stimulation of the parietal cell. In contrast, all stimuli converge to activate the acid pump, the H+,K(+)-ATPase. Inhibition of this pump by clinically useful drugs was achieved by developing derivatives of timoprazole, pyridyl-2-methylsulfinyl benzimidazole. Two of these derivatives, omeprazole and lansoprazole, have shown superiority in acid control and therefore in therapy for peptic ulcer disease compared to the available H2-receptor antagonists.