Biological Activity
Favipiravir is a novel viral RNA polymerase inhibitor, it is phosphoribosylated by cellular enzymes to its active form, Favipiravir-ribofuranosyl-5′-triphosphate (RTP). Favipiravir-RTP inhibits the influenza viral RNA-dependent RNA polymerase (RdRP) activity with IC50 of 341 nM.
In Vitro
Favipiravir (T 705) is an antiviral drug that selectively inhibits the RNA-dependent RNA polymerase of influenza virus. Favipiravir (T 705) is a novel antiviral compound that selectively and potently inhibits the RNA-dependent RNA polymerase (RdRP) of influenza and many other RNA viruses. Favipiravir-RTP does not inhibit the human DNA polymerase α, β or γ with IC50>1 mM. The IC50 for the human RNA polymerase II is 905 μM; Favipiravir is therefore 2,650 times more selective for the influenza virus RdRP, consistent with the lack of inhibition of host-cell DNA and RNA synthesis[1]. Favipiravir (T 705) acts as a pro-drug, its cytotoxicity is expected to be cell-line dependent. Favipiravir inhibits in a dose-dependent manner MNV-induced CPE (EC50: 250±11 μM) and MNV RNA synthesis in cell culture (EC50:124±42 μM). Despite this rather modest antiviral activity, Favipiravir (T 705) is able to completely inhibit norovirus replication at a concentration of 100 μg/mL, which is a concentration that has little or no adverse effect on the host cell (cell viability >80%)[2].
In Vivo
Favipiravir (T 705) (30 mg/kg/day, orally) improves survival compare to placebo. Favipiravir (T 705) also provides significant protection against the A/Duck/MN/1525/81(H5N1) virus at a dose of 33 mg/kg/day or more, regardless of the number of daily doses. When given 4 times a day, all mice survive[1].
References & source
Published experimental findings depend on the model and assay conditions. They do not guarantee equivalent performance in every application. For laboratory research use only.