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Developments in the inhibition of gastric acid secretion

Journal

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
Volume 35, Issue 8, Pages 469-475

Publisher

WILEY
DOI: 10.1111/j.1365-2362.2005.01543.x

Keywords

gastrin (CCK2) receptor antagonist; gastrooesophageal reflux disease; H+,K+-ATPase; H-2-blocker; histamine (H-2) receptor antagonist; peptic ulcer; potassium-competitive acid blocker (P-CAB); proton pump inhibitor

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Understanding the physiology of gastric acid secretion and the pathophysiology of acid-related diseases (e.g. gastrooesophageal reflux and peptic ulcer) has led to the development of numerous ways to decrease acid exposure. Pharmacologically one can try to neutralize secreted acid by antacids, prevent stimulation of the parietal cell, improve mucosal defences and block the functioning of the proton pump. Proton pump inhibitors (PPIs) inhibit the final step of acid secretion, and are currently the most potent acid inhibitors. Major therapeutic improvement within the PPI class appears unlikely, as agents in this class share similar chemistry, mode of action, and pharmacokinetic profiles. New approaches that block acid secretion are now being developed. Gastrin (CCK2) receptor antagonists and potassium-competitive acid blockers (P-CABs) are in clinical development.

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