Pharmacokinetics and absolute bioavailability of lansoprazole

Abstract

The total clearance was 517 ml.min-1, and the absolute bioavailability was 91% for the 30-mg and 81% for the 15-mg enteric-coated formulation. The elimination half-life was about 1 h. No correlation of the plasma levels to the sparteine metabolic ratio was found, and no correlation to the mephenytoin type could be established, since all volunteers of the mephenytoin type were extensive metabolizers. Although considerable variation, inter- and intraindividually, was observed, the increase in Cmax and AUC did not deviate from dose proportionality. The present galenic formulation ensures a high bioavailability after a single dose.

Evaluation of Six Proton Pump Inhibitors As Inhibitors of Various Human Cytochromes P450: Focus on Cytochrome P450 2C19

“…The C max and C max,portal were corrected for plasma f u to generate C max,u and C max,portal,u , respectively. For each PPI, the estimated k a (deconvoluted oral data based on published IV data) was obtained from the literature as follows: 0.037 (omeprazole), 0.178 (esomeprazole), 0.013 (lansoprazole), 0.011 (pantoprazole), and 0.005 (rabeprazole) min Ϫ1 (Landahl et al, 1992;Pue et al, 1993;Gerloff et al, 1996;Andersson et al, 2001;Setoyama et al, 2005). Unfortunately, in the absence of published IV data, it was not possible to obtain estimates of C max,portal for dexlansoprazole.…”

“…For omeprazole and esomeprazole, the experimentally derived parameters for metabolism-dependent inhibition (K I,u and k inact ) were also considered. Where possible, the k a for each individual PPI was calculated by leveraging published human oral and IV pharmacokinetic data (Landahl et al, 1992;Pue et al, 1993;Gerloff et al, 1996;Andersson et al, 2001;Setoyama et al, 2005). With the exception of dexlansoprazole, it was possible to calculate C max,portal and C max,portal,u (see Materials and Methods).…”

Enhanced Dissolution and Stability of Lansoprazole by Cyclodextrin Inclusion Complexation: Preparation, Characterization, and Molecular Modeling

“…1) and selectively inhibits the H + /K + -ATPase of the parietal cell of the stomach (1). As a representative proton pump inhibitor, LSP has been clinically used in the therapy of gastric and duodenal ulcerative disease with a superior or equivalent clinical efficacy to H 2 receptor antagonist (2,3).…”

“…As a representative proton pump inhibitor, LSP has been clinically used in the therapy of gastric and duodenal ulcerative disease with a superior or equivalent clinical efficacy to H 2 receptor antagonist (2,3). However, the bioavailability of LSP was not consistent with wide intersubject variation (1,4), which is ascribed to the variation in the genotype of CYP2C19, possible degradation by the gastric acid, and limited water solubility (4)(5)(6). Besides, LSP, as presented in formulations, suffer from chemical degradation due to its sensitivity to low pH and light (7).…”

Determination of Pantoprazole Sodium and Lansoprazole in Individual Tablet Dosage Forms by RP‐HPLC Using Single Mobile Phase

“…It has an empirical formula of C 16 H 14 F 3 N 3 O 2 S and a molecular weight of 369.36. Literature survey revealed HPTLC, spectrophotometric and spectrofluorometric methods for determination of lansoprazole in bulk, dosage forms, biological fluids and acid-induced degradation studies [14][15][16][17] Experimental A High Performance Liquid Chromatograph system, with LC solutions data handling system (Shimadzu-LC 2010) with an auto sampler was used for the analysis. The data was recorded using LC 2010 solutions software.…”