Phenotypic screening approaches led to the identification of several viral entry inhibitors. This approach has the advantage of finding cellular‐active compounds, providing information on drug solubility and cell uptake. 117  On the other hand, it is limited in terms of capacity compared to in silico target‐based screening. Hsiang et al. identified emodin (24; Figure 9), the active component from Polygonum multiflorum and Rheum officinale, could block the interaction of S protein with ACE2, with an IC50 value of 10 µM and an EC50 value of 200 µM in an S protein‐pseudotyped retrovirus assay using Vero E6 cells. However, the mechanism of action of this compound still needs to be determined. 118  Sarafianos et al. 48  found that SSAA09E3 (25), a benzamide derivative of 24, could prevent virus‐cell membrane fusion in pseudotype‐based and antiviral‐based assays, with an EC50 value of 9.7 µM, but a CC50 value of 20 µM indicates additional unknown cellular targets.