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Rabeprazole is a proton pump inhibitor that decreases the amount of acid produced in the stomach. Rabeprazole is used short-term to treat symptoms of gastroesophageal reflux disease (GERD) in adults and children who are at least 1 year old. 

  • Used for short term (4-8 weeks) for healing and symptomatic relief of erosive or ulcerative Gastroesophageal reflux disease (GERD).
  • Indicated for the maintenance of Healing of Erosive or Ulcerative Gastroesophageal Reflux Disease (GERD).
  • Indicated for the treatment of symptoms of Gastroesophageal Reflux Disease (GERD).
  • Used for short term (up to 4 weeks) for the treatment of Duodenal Ulcers.
  • For the treatment of Helicobacter pylori infection
  • For the treatment of peptic ulcers and bleeding peptic ulcers.
  • Zollinger-Ellison syndrome.
  • For the prophylaxis of Aspiration Pneumonia.

20 mg by intravenously

proton pump inhibitors are inactive at neutral pH. But, as soon as pH drops below 5, the drug rearranges into two positively charged ions and binds with H+K+ATPase enzyme by forming a covalent bond and inactivates the enzyme. It also inhibits the mucosal carbonic anhydrase enzyme.

Absorption& Distribution

Absolute bioavailability Rabeprazole I.V. is 100%. Rabeprazole is 96.3% bound to human plasma proteins.


Its involves getting absorbed into the parietal cells of the stomach, which are the cells that are responsible for secreting hydrochloric acid (HCl). At this point, rabeprazole is inactive. However, rabeprazole is then secreted into the secretory canaliculus of the parietal cells, which is the space from which acid secretion occurs. Here, acid secretion is mediated by the energy-dependent acid pumps,called hydrogen potassium adenosine triphosphatase (H+/K+ ATPase) pumps. These enzymatic pumps have cysteine amino acid residues. After being activated by gastric (stomach) acid to a reactive sulfenamide intermediate, rabeprazole permanently binds the cysteine residues, forming covalent, disulfide bonds. This action fundamentally alters the configuration of the acid pump, thereby inhibiting its activity. Thus, acid can no longer be secreted into the gastric lumen (the empty space of the stomach), and the pH of the stomach increases.


Following a single 20 mg oral dose of 14 C-labeled rabeprazole, approximately 90% of the drug was eliminated in the urine, primarily as thioether carboxylic acid; its glucuronide, and mercapturic acid metabolites. The remainder of the dose was recovered in the feces. Total recovery of radioactivity was 99.8%. No unchanged rabeprazole was recovered in the urine or feces.

  • liver problems
  • Interstitial Nephritis
  • Osteoporosis
  • Broken Bone
  • Inadequate Vitamin B12
  • low amount of magnesium in the blood
  • observational studies suggest that (PPI) therapy may be an increased risk for osteoporosis-related fractures of the hip, wrist, or spine.
  • The risk of fracture was increased in patients who received high dose, defined as multiple daily doses, and long-term PPI therapy (a year or longer).
  • Patients should use the lowest dose and shortest duration of PPI