Biotech Values

[mcbio]

(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.

Thanks for the comments. Agreed, a very consequential distinction for ENTA vs. other RSV treatment MoAs. I guess the one thing I will ask on from the Reviral PR is they do claim their fusion inhibitor rapidly reduced viral load to undetectable levels. Is the expectation that this will not hold up over time because it leaves a residual disease burden? At least on the surface, rapidly reducing viral loads to undetectable levels would seem to be what you would want in such a trial.