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T 705 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. IC50 & Target: IC50: 341 nM (RdRP)[1]In Vitro: T 705 (Favipiravir) is an antiviral drug that selectively inhibits the RNA-dependent RNA polymerase of influenza virus. 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 alpha, beta or gamma with IC50>1 mM. The IC50 for the human RNA polymerase II is 905 uM, T 705 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]. T 705 (T-705) acts as a pro-drug, its cytotoxicity is expected to be cell-line dependent. T 705 inhibits in a dose-dependent manner MNV-induced CPE (EC50: 250+/-11 uM) and MNV RNA synthesis in cell culture (EC50:124+/-42 uM). Despite this rather modest antiviral activity, T 705 is able to completely inhibit norovirus replication at a concentration of 100 ug/mL, which is a concentration that has little or no adverse effect on the host cell (cell viability >80%)[2].In Vivo: T 705 (30 mg/kg/day, orally) improves survival compare to placebo. T 705 (Favipiravir) 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].
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