Proton pump inhibitors gastric acid production

Proton pump inhibitors (gastric acid secretion inhibitors, gastric add pump inhibitors) inhibit gastric acid secretion 90% greater than the H2 blockers because they block the final step of acid production. Both omeprazole (Prilosec) and lansoprazole (Prevacid) are proton pump inhibitors used for the treatment of peptic ulcers and GERD. Those with hepatic impairment should take these drags with caution and have liver enzymes monitored regularly. 

The proton pump inhibitors suppress gastric acid secretion by blocking the final step in the production of gastric acid by the gastric mucosa... 

Omeprazole is an antiulcer drug. It is a proton pump inhibitor. This substituted benzimidazole inhibits gastric acid secretion to help acid/peptic disorders and duodenal ulcers. It interferes with the proton pump in the mucous lining of the stomach, the last stage of acid production. It can turn off stomach acid in as little as one hour. Lansoprazole (no. 12) has a similar structure. 

Proton pump inhibitors Proton pump inhibitors block the final step of acid production and inhibit gastric acid secretion greater than the H2 blockers. Monitor liver enzymes if patient has liver function problems. Examples are ... 

V. cholerae is a gram-negative baciUus sharing similar characteristics with the family Enterobacteriaceae. Most pathology of cholera results from an enterotoxin (cholera toxin) produced by the bacteria. Conditions that reduce gastric acidity, such as the use of antacids, histamine-receptor blockers, or proton pump inhibitors or infections with Helicobacter pylori, increase the risk for clinical disease. Cholera toxin stimulates adenylate cyclase, which increases intracellular cAMP and results in inhibition of sodium and chloride absorption by microvillli and promotes the secretion of chloride and water by crypt cells. The toxin likely acts along the entire intestinal tract, but most fluid loss occurs in the duodenum. The net effect of the cholera toxin is isotonic fluid secretion (primarily in the small intestine) that exceeds the absorptive capacity of the intestinal tract (primarily the colon). This results in the production of watery diarrhea with electrolyte concentrations similar to that of plasma. 

Without reviewing the specific efficacy-related SAR, just like for 25, it becomes difficult to discern the phar-macophoric components in compound 26, which is a proton pump inhibitor (PIP) used to decrease gastric acid secretion. However, in this case the weak metabolic links are likely to be involved in efficacy, or they likely would have been excised during the lead optimization of this nonnatural product. Thus, the pyridine s para-methoxy group is likely to be requisite for activity, particularly since it appears that two methyl groups... 

The most potent suppressors of gastric acid secretion are inhibitors of the gastric H+K+-ATPase (proton pump). In typical doses, these drugs diminish the daily production of acid (basal and stimulated) by 80 to 95%. Five proton-pump inhibitors are available for clinical use omeprazole... 

Omeprazole (Prilosec, 21), the first H /K -ATPase inhibitor, also known as a proton pump inhibitor (PPI), was marketed as a treatment for gastric ulcers since 1988. It functions by preventing acid production in the mucosa. Omeprazole was the best-selling drug for several years until its patent expiration in 2001, at which time, esomeprazole (Nexium, 22), tihe (S)-enantiomer of racemic omeprazole (21), was launched. The mechanism of... 

An active substance, although initially released from its dosage form (and dissolved), may become unavailable for absorption due to reactimis with other medicines or food components [4]. An example is the formation of insoluble complexes of tetracycline with calcium or aluminium ions from antacids or milk products. Interaction (chelation or binding) with iron ions leads to a reduced absorption for a variety of active substances such as doxycycline, penicillamine, methyldopa and ciprofloxacin. The absorption of active substances showing pH-dependent dissolution behaviour may be influenced by medicines that influence the gastric pH, such as H2-antagonists, proton pump inhibitors and antacids. Antimycotic active substances such as ketoconazole or itraconazole dissolve better in acidic fluids. Therefore their bioavailability may be increased by the concomitant use of an acidic drink like cola, whereas the concomitant use of antacids or proton pump inhibitors is likely to reduce the bioavailability. Concomitant use of milk may increase the dissolution of acidic active substances, whereas fats from food may increase the bioavailability of lipophilic active substances like albendazole and griseofulvin. 

Proton pump inhibitors (PPIs) reduce gastric acid production in a pronounced and sustained manner. They are the most potent of the drugs that inhibit gastric acid secretion and are now widely used, essentially replacing the formerly heavily used histamine H2-receptor antagonists. 

Recombinant E. coli expressing the nitrobenzene dioxygenase from Cotncmonas sp. JS765 with amino acid substitutions at position 258 or 293 was used to increase the production of chiral sulfoxides from thioanisole, p-tolyl, Cl-thioanisole, and Br-thioanisole [44]. Chiral sulfoxides are mostly known as important precursors in the pharmaceuhcal industry [13]. For example, modafinil, marketed imder the name Provigil by Cephalon and prescribed for the treatment of imcontrollable sleepiness caused by narcolepsy or sleep apnea, has a chiral sulfoxide center [57, 58]. Esomeprazole, another chiral sulfoxide, is marketed by AstraZeneca imder the name Nexium as a proton pump inhibitor that reduces gastric acid secretion for treatment of gastroesophageal reflux disease [59]. 

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