| Indication |
For the treatment of acid-reflux disorders (GERD), peptic ulcer
disease, H. pylori eradication, and prevention of gastroinetestinal
bleeds with NSAID use. |
| Pharmacodynamics |
Esomeprazole is a compound that inhibits gastric acid secretion
and is indicated in the treatment of gastroesophageal reflux disease
(GERD), the healing of erosive esophagitis, and H. pylori
eradication to reduce the risk of duodenal ulcer recurrence.
Esomeprazole belongs to a new class of antisecretory compounds, the
substituted benzimidazoles, that do not exhibit anticholinergic or H2
histamine antagonistic properties, but that suppress gastric acid
secretion by specific inhibition of the H+/K+
ATPase at the secretory surface of the gastric parietal cell. By doing
so, it inhibits acid secretion into the gsatric lumen. This effect is
dose-related and leads to inhibition of both basal and stimulated acid
secretion irrespective of the stimulus. |
| Mechanism of action |
Esomeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H+/K+-ATPase
in the gastric parietal cell. By acting specifically on the proton
pump, Esomeprazole blocks the final step in acid production, thus
reducing gastric acidity. |
| Absorption |
90% |
| Volume of distribution |
- 16 L [healthy volunteers]
|
| Protein binding |
97% |
| Metabolism |
Mainly hepatic. Esomeprazole is completely metabolized by the
cytochrome P450 system via CYP2C19 and CYP3A4. Metabolism produces
inactive hydroxy and desmethyl metabolites, which have no effect on
gastric acid secretion. Less than 1% of the parent drug is excreted in
urine. |
| Route of elimination |
Approximately 80% of the administered dose of esomeprazole is
excreted as metabolites in urine and the remaining 20% is excreted in
feces. |
| Half life |
1-1.5 hours |
| Clearance |
Not Available |
| Toxicity |
Blurred vision, confusion, drowsiness, dry mouth, flushing headache, nausea, rapid heartbeat, sweating |
