It sounds like this is another MOA that could get at cccDNA formation, but I don't really understand it well. I am intrigued still by the IMCR MOA to destroy infected hepatocytes which could cause must faster elimination of HBV reservoir (hepatocytes have a long life span so inhibiting formation of cccDNA without directly targeting the reservoir may take a long time). However, even if IMCR is successful it will most likely need to be used w other drugs (like those being developed by ENTA) to directly target the viral life cycle.
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