DFBTA is a highly effective and orally active inhibitor of ANO1, specifically the calcium-activated chloride channel anoctamin-1. It exhibits potent inhibitory activity, with an IC 50 of 24 nM. Notably, DFBTA demonstrates significant analgesic efficacy in treating inflammatory pain [1].

DFBTA exhibits minimal cytotoxicity and cardiotoxicity, as indicated by its weak impact on HEK293 proliferation and hERG activity, both with IC50 values exceeding 30 μM [1].

DFBTA, administered to C57BL/6 mice in doses ranging from 40-80 mg/kg orally (IG) and 40 mg/kg intravenously (IV), exhibits low acute toxicity as evidenced by a minimum lethal dosage (MLD) exceeding 1000 mg/kg. When given orally at a dose of 1000 mg/kg, DFBTA demonstrates superior pharmacokinetic properties, including an oral bioavailability greater than 75% and minimal brain penetration (less than 1.5% brain/plasma ratio) [1].