Trifluoromethyl-tubercidin (TFMT) inhibits host MTr1 and suppresses virus replication. TFMT inhibits MTr1 through interaction at its S-adenosyl-l-methionine binding pocket to restrict influenza virus replication. TFMT was effective in inhibiting viral replication in mice, displayed little toxicity.

The median inhibitory concentration (IC50) for trifluoromethyl-tubercidin against IAV infection was 0.30 μM, and no notable in vitro toxicity was observed in the range of effective concentrations, as measured with water-soluble tetrazolium (WST)–8 cell viability assay. Trifluoromethyl-tubercidin treatment also greatly inhibited IAV replication when administered 3 to 4 hours after infection. Trifluoromethyl-tubercidin showed inhibitory activity in the IAV-infected mouse cell line LA-4, albeit with lower potency (IC50 = 7.7 μM) than in human cells[1].

Trifluoromethyl-tubercidin treatment at 2 days after infection with IAV. At this point, NP and PB2 mRNA levels were significantly reduced by trifluoromethyl-tubercidin treatment in mouse lungs, indicating that the trifluoromethyl substitution of tubercidin reduces in vivo toxicity to levels we could not detect, but retains anti-IAV efficacy[1].