Pharmacology: Pharmacodynamics: Mode of Action: Lansoprazole belongs to a class of anti secretory compounds, the substituted benzimidazoles, 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 regarded as the acid (proton) pump within the parietal cell, lansoprazole has been characterized as a gastric acid-pump inhibitor, in that it blocks the final step of acid production. The effect is dose-related and leads to inhibition of both basal and stimulated gastric acid secretion irrespective of the stimulus. Lansoprazole does not exhibit anticholinergic or histamine type-2 antagonist activity.
Pharmacokinetics: Lanpac capsules contain an enteric-coated granule formulation of lansoprazole. Absorption of lansoprazole begins only after the granules leave the stomach. Absorption is rapid, with mean peak plasma levels of lansoprazole occurring after approximately 1.7 hours. After a single-dose administration of 15mg to 60mg of oral lansoprazole, the peak plasma concentrations (Cmax) of lansoprazole and the area under the plasma concentration curves (AUCs) of lansoprazole were approximately proportional to the administrated dose.
Absorption: The absorption of lansoprazole is rapid, with the mean Cmax occurring approximately 1.7 hours after oral dosing, and the absolute bioavailability is over 80%. In healthy subjects, the mean (±SD) plasma half-life was 1.5 (±1.0) hours. Both the Cmax and AUCs are diminished by about 50% to 70% if lansoprazole is given 30 minutes after food, compared to the fasting condition. There is no significant food effect if lansoprazole is given before meals.
Distribution: Lansoprazole is 97% bound to plasma proteins. Plasma protein binding is constant over the concentration range of 0.5 to 5.0 µg/mL.
Metabolism: Lansoprazole is extensively metabolized in the liver. Two metabolites have been identified in measurable quantities in plasma (the hydroxylated sulfinyl and sulfone derivatives of lansoprazole). These metabolites have very little or no antisecretory activity. Lansoprazole is thought to be transformed into two active species which inhibit acid secretion by blocking the proton pump [(H', K')-ATPase enzyme system] at the secretory surface of the gastric parietal cell. The two active species are not present in the systemic circulation. The plasma elimination half-life of lansoprazole is less than 2 hours while the acid inhibitory effect lasts more than 24 hours. Therefore, the plasma elimination half-life of lansoprazole does not reflect its duration of suppression of gastric acid secretion.
Elimination: Following single-dose oral administration of LANPAC, virtually no unchanged lansoprazole was excreted in the urine. In one study, after a single oral dose of C-lansoprazole, approximately one-third of the administered radiation was excreted in the urine and two-thirds was recovered in the feces. This implies a significant biliary excretion of the lansoprazole metabolites.
Gastro Esophageal Reflux Disease (GERD); Benign peptic ulcer (Both duodenal and gastric ulcer); NSAID-associated gastric and duodenal ulcer; Pathological hyper-secretory condition e.g. Zollinger-Ellison syndrome; Adjuvant therapy with amoxicillin or clarithromycin to eradicate H. pylori infection.
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LANPAC is available as a capsule in 30mg strength. Both directions for use specific to the route and available methods of administration for each of these dosage forms are presented in the table. LANPAC should be taken BEFORE EATING. LANPAC products SHOULD NOT BE CRUSHED OR CHEWED. Renal insufficiency patients and geriatric patients do not require dosage adjustment. However, dosage adjustment should be considered in patients with severe liver disease.
A02BC03 - lansoprazole ; Belongs to the class of proton pump inhibitors. Used in the treatment of peptic ulcer and gastro-oesophageal reflux disease (GERD).