(R)-Omeprazole is the inactive isomer of omeprazole , a gastric proton-pump inhibitor. A stereoselective hydroxylation of (R)-omeprazole is mediated primarily by cytochrome P450 (CYP) 2C19, whereas CYP3A4 favors sulfoxidation of the active (S)-enantiomer . (R)-Omeprazole has been shown to act as a reversible direct-acting and metabolism-dependent inhibitor of CYP2C19 in pooled human liver microsomes (IC50 = 8.1 μM).
5-hydroxy Omeprazole is a major metabolite of omeprazole , an inhibitor of the gastric H+ K+-ATPase pump.[1] 5-hydroxy Omeprazole is produced from omeprazole by the action of cytochrome P450 (CYP) isoform 2C19, a monooxygenase. [2][3] CYP2C19 polymorphisms significantly influence the metabolism of omeprazole, and individuals may be classified as homozygous extensive metabolizers, heterozygous extensive metabolizers, and poor metabolizers.[1]
Omeprazole acid is a medication used in the treatment of gastroesophageal reflux disease, peptic ulcer disease, and Zollinger–Ellison syndrome. It is also used to prevent upper gastrointestinal bleeding in people who are at high risk. Omeprazole is a proton pump inhibitor and as such blocks the release of stomach acid.
Omeprazole N-oxide, a metabolite of the gastric proton pump inhibitor omeprazole, serves as a potential impurity in commercial omeprazole preparations.
Esomeprazole hemistrontium, also known as (S)-Omeprazole, is a potent and orally active proton pump inhibitor that effectively reduces acid secretion by inhibiting the H+, K+-ATPase in gastric parietal cells. This compound exhibits promising potential for research in symptomatic gastroesophageal reflux disease [1] [2] [3].
Esomeprazole potassium salt ((S)-Omeprazole potassium salt) is an effective and orally active proton pump inhibitor that works by inhibiting the H+, K+-ATPase enzyme in the gastric parietal cells, leading to a reduction in acid secretion. It is a promising compound for investigating symptomatic gastroesophageal reflux disease [1] [2] [3].