Remdesivir, approved for the treatment of coronavirus disease (COVID-19), has been associated with QTc interval prolongation and torsade de pointes (TdP) in case reports. However, data are conflicting regarding the ability of remdesivir to inhibit the human ether-a-go-go-related (hERG)-related current. The objective of this study was to investigate the effects remdesivir and its primary metabolite, GS-441524, on hERG-related currents. Human embryonic kidney (HEK 293) cells stably expressing hERG were treated with various concentrations of remdesivir and GS-441524. The effects of acute and prolonged exposure on hERG-related current was assessed using whole cell configuration of voltage-clamp protocols. Acute exposure to remdesivir and GS-441524 had no effect on hERG currents and the half-activation voltage (V1/2). Prolonged treatment with 100 nM and 1 µM remdesivir significantly reduced peak tail currents and hERG current density. The propensity for remdesivir to prolong QTc intervals and induce TdP in predisposed patients warrants further investigation.