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. 2020 Nov 12;117(48):30687–30698. doi: 10.1073/pnas.2012939117

Fig. 7.

Fig. 7.

UMB18-2 inhibits all highly pathogenic human coronaviruses in multiple cell lines. (A) A549-ACE2 cells were infected with SARS-CoV at MOI 0.1 and treated with UMB18-2 at 50 µM or 10 µM (with 0.5% or 0.1% DMSO being the appropriate negative controls) for 48 h. Supernatant was collected and used for TCID50 assay to determine viral titer. Mean TCID50/mL and SD are displayed from three independent experiments performed in triplicate. (B) As in A but infection at MOI 0.01. (C) Huh7-ACE2 cells were infected with SARS-CoV at MOI 0.1 and treated with UMB18-2. Viral production was analyzed as in A but after 24 h of infection. (D) Vero E6 cells were infected with SARS-CoV-2 at MOI 0.1 and treated with UMB18-2 as in A. Viral production was analyzed as in A, but after 24 h of infection. (E and F) As described in A and B, but with SARS-CoV-2 infection. (G and H) Cells that were infected in E and F were collected in TRIzol and used for qRT-PCR analysis. Primers targeting RdRp were used. Input levels were normalized to GAPDH RNA and fold change of transcript levels was determined relative to DMSO control for each concentration of compound. Data are from a representative experiment. (I and J) A549-DPP4 cells were infected with MERS-CoV in the same way as described for A and B. (K and L) MERS-CoV RNA analysis as described for G and H. In all cases t tests were performed for vehicle control vs. drug treated samples; *P < 0.05, **P < 0.01, ****P < 0.0001.