Esomeprazole strontium is a proton pump inhibitor. It suppresses gastric acid secretion by specific inhibition H+/K+ ATPase in the gastric parietal cell. The S- and R-isomers of omeprazole are protonated and converted in the acidic compartment of the parietal cell forming the active inhibitor, the achiral sulphenamide. By acting specifically on the proton pump, esomeprazole blocks the final step in acid production, thus reducing gastric acidity. The drug is indicated for the treatment of gastroesophageal reflux disease, reduction the risk of NSAID-associated gastric ulcer, eradication of H.pylori, and pathological hypersecretory conditions.

Ufiprazole (Omeprazole sulfide) is a metabolite of Omeprazole, which is a proton pump inhibitor. Omeprazole sulfide has been shown to be a direct-acting inhibitor of CYP2C19 in pooled human liver microsomes. Ufiprazole is also a weak BRS-3 agonist.

Pumaprazole is imidazopyridine derivative patented by Byk Gulden Lomberg Chemische Fabrik GmbH for the treatment of gastrointestinal diseases. Pumaprazole acts as a reversibly binding acid pump antagonist. Pumaprazole differs from covalently binding proton pump inhibitors (PPIs), such as omeprazole, both with respect to chemical structure and mode of interaction with the gastric H(+)/K(+)-ATPase. In preclinical models, the single dose of Pumaprazole is able to elevate intragastric pH in the dog with gastric fistula under pentagastrin or carbachol stimulation from pH 1 to about pH 7 while still displaying a dose-dependent, well-controllable duration of action of a few hours.

Omeprazole sulfone is the major metabolite of the omeprazole, gastric proton pump inhibitor. Metabolite is formed by the sulfoxidation of the omeprazole under the action of cytochrome P450 (CYP)3A4. Omeprazole sulfone is found in plasma and shows elimination rate–limited kinetics in vivo. Omeprazole sulfone has been shown to act as a reversible direct-acting and metabolism-dependent inhibitor of CYP2C19.