Treatment for Acid-Related Disorders

Omeprazole, lansoprazole, pantoprazole, and rabeprazole are substituted benzimidazoles that act to inhibit gastric acid biological process by covalently attractiveness to the proton pump (H+/K+ ATPase), the test common tract for acid body fluid. The PPIs are secreted in the canalicular luminous flux unit of the parietal cell, where they are concentrated and activated by redemption to sulfonamides in the acid state of affairs.
Although rabeprazole is activated at a higher pH, it may be less acid stable than the other PPIs. In their activated form, PPIs bind to cysteine residues in a subunit of the proton pump and inhibit acid humor into the canalicular lm.

All four PPIs bind to the cysteine matter, which is crucial for inhibiting the proton pump.
However, omeprazole, lansoprazole, and rabeprazole bind to additional cysteine residues that do not appear to be related to the medicine acid-inhibiting import of these agents. Whether pantoprazole’s selective protection to the acid-inhibiting cysteine residuum is pharmacodynamically important is animate thing investigated.
Omeprazole, lansoprazole, and pantoprazole bind irreversibly to the gastric proton pump, requiring chemical action of new pumps or start of resting pumps. The protective cover of rabeprazole has been shown in vitro to be partially reversible; however, the clinical grandness of this measuring has yet to be determined. Because PPIs inhibit only actively secreting proton pumps, gastric acid ontogeny is optimal when the PPI is taken about 30 minutes before a meal.

All four PPIs, when given orally within the therapeutic dosing parcel, dose-dependently inhibit basal and stimulated acid bodily fluid, resulting in an gain in both the magnitude and time of acid prohibition. No substantial fluctuation is apparent among the four PPIs in increasing gastrin concentrations.
This is a part of article Treatment for Acid-Related Disorders Taken from "Generic Aciphex (Rabeprazole) Review" Information Blog