PMC:7321036 / 47326-48392 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7321036","sourcedb":"PMC","sourceid":"7321036","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7321036","text":"We found pharmacological inhibitors of CK2, p38 MAPK signaling, PIKFYVE, and CDKs to possess strong antiviral efficacy. Cells were pre-treated with inhibitor molecules, followed by SARS-CoV-2 infection (STAR Methods), and virus quantity (anti-NP antibody against SARS-CoV-2) and cell viability were quantified 48 h after infection. As a positive control and for comparison, remdesivir was tested, and the expected favorable antiviral activity was observed (half maximal inhibitory concentration [IC50 ] = 1.28 μM; Figure 7B). Silmitasertib, an inhibitor of CSNK2A1 and CSNK2A2, was found to possess antiviral activity (IC50 = 2.34 μM; Figures 7C and S5). In conjunction with data supporting physical interaction (Gordon et al., 2020) and co-localization with N protein (Figure 5F), as well as a potential role in remodeling extracellular matrix upon infection (Figures 5 and S3), CK2 signaling appears to be an important pathway hijacked by SARS-CoV-2. Furthermore, silmitasertib is currently being considered for human testing as a potential treatment for 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