Here, we performed an in vitro toxicity assessment for remdesivir at clinically relevant concentrations around the cmax of 9 µM using H9c2 rat cardiomyoblasts and neonatal mouse cardiomyocytes (NMCM) as heart models and rat NRK-52E cells and human RPTEC/TERT1 cells as kidney models. Due to the tendency of nucleoside analogs for mitochondrial toxicity, we focused on metabolic changes and mitochondrial function. Additionally, we analyzed the functionality of NMCM and determined early proteomic changes.