For antiviral activity, 2fTGH cells were treated with idarubicin along with or without IFN-b and then assessed for control of encephalomyocarditis virus (EMCV) levels and virus-induced cytopathic effect. We selected EMCV since it was previously found to be sensitive to STAT1-CC-dependent improvement in IFN signaling [13] . In the present experiments, we found that idarubicin treatment (at a relatively low concentration of 25 nM) caused a significant decrease in EMCV titer at baseline and with IFN-b treatment (at a relatively low concentration of 5 U/ml) ( Figure 8A ). In addition, we observed that idarubicin-dependent improvement in viral control translates into a significant decrease in viral cytopathic effect under those same treatment conditions ( Figure 8B ). Higher concentrations of idarubicin in combination with IFN-b treatment caused a significant cytotoxic effect (data not shown), consistent with the antineoplastic properties of the drug. Nonetheless, the results with a relatively low concentration of idarubicin provide proof-of-concept that a small molecule activator of the ISRE component of the IFN signaling pathway will allow for increased ISG expression and improved control of viral level.