(R)-ランソプラゾール

Pharmaceuticals -> Alimentary tract and metabolism -> Drugs for acid related disorders

Pharmaceuticals -> Listed in ZINC15

Pharmaceuticals -> Used in Switzerland

Breast Feeding; Lactation; Milk, Human; Anti-Ulcer Agents; Gastrointestinal Agents; Proton Pump Inhibitors

Breast Feeding; Lactation; Milk, Human; Anti-Ulcer Agents; Gastrointestinal Agents; Proton Pump Inhibitors

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Warning

H315 (33.3%): Causes skin irritation [Warning Skin corrosion/irritation]

P203, P260, P261, P264, P264+P265, P271, P272, P280, P302+P352, P304+P340, P305+P351+P338, P318, P319, P321, P332+P317, P333+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 3 reports by companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Drug Induced Liver Injury Rank (DILIrank 2.0)

Dexlansoprazole

vLess-DILI-concern

4

Adverse reactions

DOI:10.1016/j.drudis.2016.02.015

◉ Summary of Use during Lactation

◉ Summary of Use during Lactation

A - Alimentary tract and metabolism

QA - Alimentary tract and metabolism

Dexlansoprazole is a proton pump inhibitor (PPI) that suppresses both basal and stimulated gastric acid secretion. PPIs are associated with a risk for a rebound effect and a short-term increase in hypersecretion; thus, such risk cannot be excluded with dexlansoprazole. With long-term use, PPIs are also associated with a risk of increased susceptibility to bacterial infections, vitamin B12 and iron deficiency, and hypomagnesemia and hypocalcemia, possibly leading to osteoporosis and bone fractures. Dexlansoprazole is reported to interfere with the secretin stimulation test and create false positive urine screening tests for tetrahydrocannabinol. Dexlansoprazole can increase gastrin levels, which can cause enterochromaffin-like cell hyperplasia and increase serum CgA levels. Increased CgA levels may cause false positive results in diagnostic investigations for neuroendocrine tumours.

Dexlansoprazole suppresses gastric acid secretion by blocking the final step of acid production. It inhibits the H/K ATPase at the secretory surface of the gastric parietal cell, which is involved in the secretion of hydrochloric acid. H/K ATPase is a proton pump responsible for hydrolyzing ATP and exchanging H⁺ ions from the cytoplasm for K⁺ ions in the secretory canaliculus: this action results in hydrochloric acid secretion into the gastric lumen.

Dexlansoprazole is extensively metabolized in the liver. It undergoes oxidation and reduction, followed by subsequent sulfation, glucuronidation, and glutathione conjugation to form inactive metabolites. Oxidative metabolites are formed from CYP2C19-mediated hydroxylation and CYP3A4-mediated oxidation to the sulfone. CYP2C19 is a polymorphic liver enzyme which exhibits three phenotypes in the metabolism of CYP2C19 substrates: extensive metabolizers (*1/*1), intermediate metabolizers (*1/mutant) and poor metabolizers (mutant/mutant). Dexlansoprazole is the major circulating component in plasma regardless of CYP2C19 metabolizer status. In CYP2C19 intermediate and extensive metabolizers, the major plasma metabolites are 5-hydroxy dexlansoprazole and its glucuronide conjugate, while in CYP2C19 poor metabolizers dexlansoprazole sulfone is the major plasma metabolite.