>>I interpret this to mean that the FXR target of ENTA’s preclinical drug has been “validated” by ICPT’s OCA; hence, if ENTA’s drug is somehow better than OCA, it could end up being a significant asset.
They have more potent agents, but are there good preclinical models to assess efficacy for NASH?
an interesting development would be a cylophilin inhibitor for liver fibrosis that could potentially be used with an FXR - now that would give them a real edge
Has ENTA given guidance as to when they expect their NASH drug(s) to hit the clinic? Also, just curious if they've given any early inkling as to how they could be differentiated from the ICPT drug.