Fig 1. Diltiazem inhibits SARS-CoV-2 infection in cells.

(A) Vero-E6 cells were treated with DMSO or inhibitors at the indicated concentrations for 1 h, and then infected with HRB25 (M.O.I. = 0.01). The supernatants were harvested at 24 h post-infection for plaque assays. PFU, plaque-forming units. (B) The viability of Vero-E6 cells was determined in the presence of inhibitors at the indicated concentrations. (C) Vero-E6 cells were treated with diltiazem at different concentrations or vehicle to determine the CC₅₀. CC₅₀: 50% cytotoxic concentration. (D and E) IC₅₀ of diltiazem to HRB25 infectivity. Vero-E6 cells were treated with vehicle or diltiazem at the indicated concentrations for 1 h, and then infected with HRB25 (M.O.I. = 0.01); the supernatants were harvested at 24 h post-infection to determine viral RNA copy numbers (D) and virus titers (E) by use of qPCR and plaque assays, respectively. IC₅₀: 50% inhibitory concentration. (F and G) Vero-E6 cells were treated with diltiazem for 1 h, and then infected with HRB25 at an M.O.I. of 0.01 (F) or 5 (G); the supernatants were harvested at the indicated timepoints for plaque assays. (H and I) BEAS-2B cells (H) and Calu-3 cells (I) were treated with diltiazem for 1 h, and then infected with HRB25 (M.O.I. = 5). At 24 h post-infection, the viral RNA level in the cell lysate was measured by qPCR. The data shown are the means ± SDs of three independent experiments or replicates. The two-tailed unpaired Student’s t-test was used for the statistical analysis. *p < 0.05, **p < 0.01, ***p < 0.001.