Favipiravir (T-705) (T-705), an effective and selective RNA-dependent RNA polymerase inhibitor, are applied to treat influenza virus infections.

Favipiravir shows anti-influenza virus activities with IC50 ranged from 0.013 to 0.48 μg/ml for the influenza A viruses, from 0.039 to 0.089 μg/ml for the influenza B viruses, and from 0.030 to 0.057 μg/ml for the influenza C viruses. In mammalian cell lines (MDCK cells, Vero cells, HEL cells, A549 cells, HeLa cells, and HEp-2 cells), Favipiravir shows no cytotoxicity at concentrations up to 1,000 μg/ml. [1] In MDCK cells inoculated with seasonal influenza A (H1N1) viruses, Favipiravir induces lethal mutagenesis. [2]

In influenza virus-infected mice, Favipiravir (200 mg/kg/day, p.o.) protects the mice from death from influenza virus infection. [1] In mice experimentally infected with Ebola virus, Favipiravir efficiently blocks viral production, reaching an antiviral effectiveness of 95% and 99.6% at 2 and 6days after initiation of treatment, respectively. [3]

The cytotoxicity of T-705 is evaluated by an assay with XTT. XTT is converted to aqueous formazan by an enzyme in MDCK cells, Vero cells, HEL cells, A549 cells, HeLa cells, and HEp-2 cells. The compounds are diluted to the appropriate concentrations (volume, 100 μl) with test medium (EMEM containing 10% FCS) in 96-well culture plates in which each well contains a concentration of 2 × 103 cells/100 μL. The test plates are incubated for 3 days at 37°C in 100% humidity and 5% CO2. After 3 days, 50 μl of the XTT reagent (1 mg/ml in FCS-free EMEM containing 5 mM phenazine methosulfate) is added, and the reaction product is assayed by measurement of the absorbance at 450 nm with a microplate reader. Cytotoxicity is expressed as the 50% cell-inhibitory concentration (CC50).(Only for Reference)