(ENTA) Re: MoAs of RSV treatments in development
Most RSV treatments in development, including the one about which you posted, are fusion inhibitors. RSV fusion inhibitors work by preventing viral entry into a host cell, but they don’t work on every at-risk cell. Once a given cell is infected with RSV, a fusion inhibitor cannot stifle the viral activity in that cell, which leaves a residual disease burden that may compromise the overall efficacy of the drug.
ENTA’s EDP-938 is not a fusion inhibitor, but rather an N-protein inhibitor. An N-protein inhibitor disrupts RSV’s viral-replication machinery inside an infected cell in an analogous way to the MoAs of HCV DAAs.
The above is a consequential distinction for ENTA’s RSV program, IMO.
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