Vonoprazan hydrochloride, a proton pump inhibitor (PPI), effectively functions as a potassium-competitive acid blocker (P-CAB) with potent antisecretory properties. It significantly inhibits H+,K+-ATPase activity in porcine gastric microsomes, displaying an IC50 of 19 nM at pH 6.5. Developed primarily for researching acid-related conditions such as gastroesophageal reflux disease and peptic ulcer disease, vonoprazan hydrochloride also aids in the eradication of Helicobacter pylori [1] [2] [3].

Vonoprazan demonstrates concentration-dependent activity on porcine gastric H+, K+-ATPase, ranging from 0.1 nM to 10 μM over 30 minutes, without affecting Na+, K+-ATPase activity, even at concentrations up to 500 times its IC 50 against gastric H+, K+-ATPase [2].

Vonoprazan (1-4 mg/kg; p.o.) effectively inhibits both basal and 2-deoxy-D-glucose (200 mg/kg; s.c.)-induced gastric acid secretion in a dose-dependent manner, with complete inhibition observed at the 4 mg/kg dosage in male 7- or 8-week-old Sprague-Dawley rats [2]. This outcome suggests a proportional relationship between the administered dose of vonoprazan and its efficacy in reducing gastric acid secretion, highlighting its potential therapeutic role in conditions requiring gastric acid suppression.