FGEN (and AKBA) - Thanks for the feedback/dialog. Comments below (FWIW):
Why? It isn't like we are particularly good at knowing what is due to off target interactions, what is due to downstream ramifications, ... . Even for drugs that are decades old (e.g. statins - where we don't know why they work, or, therefore, how to minimize AE while maximizing benefit). And this class of drugs (PHIs) is undoubtedly wildly less well understood and HIF is a nexus of interactions (i.e. wildly complex).
FWIW, as you probably remember, you and I disagree on this. I understand the theory, but as a practical reality it does not actually seem to be a particularly good predictor of AE. See our previous thread on this at #msg-96549701 (the link in that post is key for anyone else following this thread. Hope it still works).
I agree this is one possible story. Of many. But when it comes to the liver... it seems, broadly, that interaction with it is more likely to have negative consequences than positive. All that said, my point in the post at the start of this thread wasn't that they positively have liver issues. Nor was it that if they did have negative interactions it kills the drug. (e.g. random example - if it were to have a Hy's Law issue of 1 in 1000 more than placebo, but also did nothing more than create the same boost in OS that EPO does, but for the EPO non-responders... then it is a drug with a lot of potential.) It was, like many of my posts, just listing things that are worth thinking about and looking for in future results or data releases.
I generally agree (e.g. my comments on the odd distribution of CV events in 041), but still will be looking at/for liver issues.
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