Praze Mechanism of Action

Pharmacology: Pharmacodynamics: Lansoprazole is a substituted benzimidazoles which is anti-secretory compound that suppress gastric acid secretion by specific inhibition of the H⁺, K⁺-ATPase enzyme system at the secretory surface of the gastric parietal cell. Because this enzyme system is the "acid (proton) pump" within the gastric mucosa, Lansoprazole has been characterized as a gastric acid pump inhibitor. Lansoprazole blocks the final step of the acid production. This effect is dose related and inhibits basal and stimulated acid secretion regardless of the stimulus.
It has been reported that blood coagulation and platelet aggregation capacities are severely impaired under acidic conditions and that fibrin formed as a result of blood coagulation is dissolved by pepsin under acidic conditions. Lansoprazole is considered to increase gastric pH, thereby improving blood coagulation and platelet aggregation capacities and inhibiting pepsin activity, resulting in suppression of bleeding. Also, lansoprazole is considered to increase gastric pH by inhibiting acid secretion, thereby promoting repair of injured mucosa, which is inhibited under acidic conditions.
Pharmacokinetics: Lansoprazole can be administered intravenously (IV). The degree of inhibition of gastric acid secretion is similar following oral or IV administration. Lansoprazole is 97% bound to plasma proteins. Lansoprazole is extensively metabolized by the liver via CYP2C19 and CYP3A4 to inactive metabolites. Lansoprazole is metabolized in parietal cells to two active metabolites that are not present in systemic circulation. The plasma elimination half-life is less than 2 hours which does not reflect duration of suppression of gastric acid secretion that last more than 24 hours, apparently because of prolonged binding to the parietal H⁺, K⁺-ATPase enzyme. The metabolites are excreted in feces (67%) and urine (33%).
Lansoprazole is not removed by hemodialysis.