Epoxy compounds usually have stronger nucleophilic ability, because the alkyl group on the oxygen atom makes the bond angle smaller, which makes the lone pair of electrons react more dissimilarly with the electron-deficient system. Compound: 5-Methoxy-2-[[(4-methoxy-3,5-dimethyl-2-pyridyl)methyl]thio]benzimidazole, is researched, Molecular C17H19N3O2S, CAS is 73590-85-9, about Effect of hypoxia on oxidative and reductive pathways of omeprazole metabolism by the isolated perfused rat liver.Recommanded Product: 73590-85-9.
The effect of hypoxia on the elimination of H168-68 (omeprazole)(I) [73590-58-6] a potent inhibitor of gastric acid secretion, was studied in the isolated perfused rat liver. During normal oxygenation, a 10 mg bolus dose was eliminated rapidly (half-life (T1/2)-β = 8.0 min), while under hypoxic conditions T1/2β was increased to 81.6 min. Upon reoxygenation, T1/2β returned to 9.6 min. During hypoxia, perfusate concentrations of an oxidative metabolite (I-sulfone [88546-55-8]) were reduced by 68%, while those of the reductively-generated I-sulfide [73590-85-9] increased 4-fold. With reoxygenation, both formation and elimination of the sulfone were increased, whereas, which had accumulated during the hypoxic period, was eliminated rapidly. These findings were duplicated in steady-state experiments, in which omeprazole clearance during hypoxia fell by at least 70%, and sulfide concentrations in perfusate rose from undetectable levels to 200 ng/mL (at least a 10-fold increase). Sulfone concentrations did not change with hypoxia, consistent with a reduction in both its formation and elimination rates. Thus, the hepatic elimination of omeprazole is severely retarded by hypoxia, but this effect is promptly reversed by reoxygenation. The increased formation of the reductive metabolite during hypoxia is not of sufficient magnitude to sustain the normal hepatic elimination of omeprazole.
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Reference:
Ether – Wikipedia,
Ether | (C2H5)2O – PubChem