In VeroE6 cells, the EC50, CC50 and SI of CQ against SARS-CoV-2 were 1.13 μM, >100 and >88.50, respectively. CQ functioned at the entry, and post-entry stages of SARS-CoV-2 infected cells [16]. In the same cell line, at different multiplicities of infection (MOIs, 0.01, 0.02, 0.2, and 0.8) of SARS-CoV-2, the EC50 for CQ (2.71, 3.81, 7.14, and 7.36 μM) was slightly lower than that of HCQ (4.51, 4.06, 17.31, and 12.96 μM). Consequently, the SI of CQ (100.81, 71.71, 38.26, and 37.12) was slightly higher than that of HCQ (55.32, 61.45, 14.41, 19.25) [17]. These results indicate that the anti-SARS-CoV-2 activity of CQ seems to be more potent than HCQ in vitro. However, another in vitro cell experiment showed that after SARS-CoV-2 infection of VeroE6 cells, the EC50 values for CQ were 23.90 μM and 5.47 μM, and EC50 values for HCQ were 6.14 μM and 0.72 μM, at 24 and 48 h, respectively; When administered prior to SARS-CoV-2 infection of VeroE6 cells, EC50 values for CQ were >100 μM and 18.01 μM, and the EC50 values for HCQ were 6.14 μM and 0.72 μM, at 24 and 48 h, respectively [18]. These results showed that the anti-SARS-CoV-2 activity of CQ was worse than HCQ in vitro. The conflicting results of these two studies may be related to different cell culture methods and experimental conditions. In short, these in vitro studies show that CQ/HCQ have strong anti-SARS-CoV-2 activity.