Abstract

Rabeprazole, a proton pump inhibitor, is used for individuals with ulcers. The prodrug is transformed into an active sulphenamide form by the acidic conditions present in the parietal cells. Rabeprazole inhibits the H+K+ ATPase of the gastric cells, leading to a decrease in the generation of stomach acid in both normal and stimulated situations. The present review was based on the pharmacokinetics and toxicological profile of Rabeprazole. Once absorbed into the body, approximately 96.3–97% of rabeprazole is bound to plasma proteins. In humans, the half-life of rabeprazole is approximately one hour. The peak concentration of rabeprazole in human plasma following a single oral dose does not appear until around 3.5 hours later. Rabeprazole is metabolised mostly by the liver. Once the liver has metabolised the medicine, 90% of it will be excreted via the kidneys. The elimination fraction is 10%. Rabeprazole is mostly metabolised by the cytochrome P450 enzymes CYP2C19 and CYP3A4. . It concluded that in the human pylorus, it decreased muscular tone, maximal contraction values, and contraction frequencies. When diclofenac sodium SR, glucosamine, diacerein, calcium, and vitamin D preparations were administered in addition to rabeprazole, the patients experienced GI bleeding, fatty liver grade 1, mild epigastric discomfort, black stools, and decreased haemoglobin content.

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