In VeroE6 cells, the antiviral activity of CQ/HCQ against SARS-CoV had an EC50 of 4.1 (±1.0) μM and 34(±5) μM, CC50 of >128 μM and CC50 > 100 and SI of >31 and SI>3, respectively [10,11]. SARS-CoV replication was inhibited by 99% at 16 μM CQ 3 days post-infection [12]. The data indicates that CQ has stronger anti-SARS-CoV activity than HCQ. In addition, CQ has both a prophylactic and a therapeutic advantage. Vincent et al. tested various concentrations of CQ (0.1–10 µM) added 20–24 h prior to SARS-CoV infection and found that 0.1, 1, and 10 µM CQ reduced infectivity by 28%, 53%, and 100%, respectively; when CQ was added immediately after virus adsorption, 0.1–1 µM and 33–100 µM reduced the infection by 50% up to 90–94%; addition of CQ 3 and 5 h after virus adsorption was still significantly effective, yet to achieve equivalent antiviral effect, a higher concentration of CQ was needed [13]. In HRT-18 cells, the antiviral activity of CQ against HCoV-OC43 had an EC50 of 0.306 (±0.091) μM, CC50 of 419.0 (±192.5) μM, and SI of 1.369 [14].