We used remdesivir as point of reference, which allowed us to validate the predictions of our multi-scale assessment, but also allowed us to explore the underlying process that might lead to limited clinical effect of remdesivir itself against COVID-19. Our findings show that similar intracellular concentrations of remdesivir relative to dATP can effectively inhibit SARS-CoV2 replication, aligned with previous studies [29,30] and experimental evidence [31]. Further, our findings suggest that the limited clinical effectiveness observed for remdesivir [32] might rely on unstudied pharmacokinetic properties and/or time to treatment relative to viral replication rather than drug limited inhibition capacity.