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Posted On: 10/11/2023 1:10:26 AM
Post# of 155794
The FDA wants to see either stopping fat induced liver inflammation and no worsening of fibrosis or improvement of fibrosis by one stage and no worsening of liver inflammation.
Akero's drug was specifically targeted at reducing fibroblast growth factor that was hoped to stop fibrosis. But it would do little to nothing for the underlying inflammation driving that fibrosis. So of course they chose reduced fibrosis as their primary endpoint.
Leronlimab on the other hand blocks the chemokines that cause the inflammation and fibrosis and preferentially creates brown (good) fat over white (bad) fat. That's the problem with almost all of the NASH drugs I've seen so far. They try to take care of a small piece of the puzzle instead of hitting the root causes.
Akero's drug was specifically targeted at reducing fibroblast growth factor that was hoped to stop fibrosis. But it would do little to nothing for the underlying inflammation driving that fibrosis. So of course they chose reduced fibrosis as their primary endpoint.
Leronlimab on the other hand blocks the chemokines that cause the inflammation and fibrosis and preferentially creates brown (good) fat over white (bad) fat. That's the problem with almost all of the NASH drugs I've seen so far. They try to take care of a small piece of the puzzle instead of hitting the root causes.
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