{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["16"],"submitter":["Lu M"],"pubmed_abstract":["Introduction
The aim of this study is to characterize the pharmacology of linaprazan glurate (X842), an ethyl ester prodrug of linaprazan (a novel potassium-competitive acid blocker), in animal species in vitro and in vivo to achieve a better pharmacological profile.Methods
Pharmacokinetic profiling, hydrogen (H+)/potassium (K+)-ATPase inhibition, and gastric acid inhibition experiments were performed.Results
X842 was rapidly absorbed with a very low plasma concentration. X842 was rapidly transformed by enzymatic cleavage into its active metabolite, linaprazan, as shown by the half-life, maximum concentration, and area under the concentration-time curve of the two substances. Selective inhibition of the gastric H+/KIntroductionThe aim of this study is to characterize the pharmacology of linaprazan glurate (X842), an ethyl ester prodrug of linaprazan (a novel potassium-competitive acid blocker), in animal species in vitro and in vivo to achieve a better pharmacological profile.Methods
Pharmacokinetic profiling, hydrogen (H+)/potassium (K+)-ATPase inhibition, and gastric acid inhibition experiments were performed.Results
X842 was rapidly absorbed with a very low plasma concentration. X842 was rapidly transformed by enzymatic cleavage into its active metabolite, linaprazan, as shown by the half-life, maximum concentration, and area under the concentration-time curve of the two substances. Selective inhibition of the gastric H+/K