Cloperastine hydrochloride inhibits the hERG K⁺ currents in a concentration-dependent manner with an IC₅₀ value of 27 nM. IC50 & Target: 27 nM (K⁺ currents)^[1] In Vitro: Cloperastine inhibits the hERG K⁺ currents in a concentrationdependent manner with IC₅₀ value of 27±3 nM^[1]. Among the antitussive agents, Cloperastine, which possesses antitussive and antiedemic activity, also relaxes the bronchial musculature. Cloperastine is a drug with a central antitussive effect, and is also endowed with an antihistaminic and papaverine-like activity similar to codeine but without its narcotic effects^[2]. In Vivo: In the anesthetized guinea pigs, Cloperastine at a therapeutic dose of 1 mg/kg prolonged the QT interval and monophasic action potential (MAP) duration without affecting PR interval or QRS width^[1]. Cloperastine hydrochloride shows relatively low acute toxicity when administered by the intraperitoneal route in rats and mice, and shows minor toxicity by the oral route when administered as Cloperastine fendizoate, the LD₅₀ in rats and mice for the two administration routes exceeds 1000 and 2000 mg/kg, respectively^[2].