why does nobody talk about biopsy
Slightly embarrassed to be asking this, but: why does nobody talk about biopsy. Bought small because the evidence base is early. That is the only defensible position I could construct. The honest evidence position, written out so this board does not drift. Phase 2 data exists in a specific, biopsy-characterised…
Histological endpoints in this field are scored on biopsy: resolution of steatohepatitis without worsening of fibrosis, or improvement in fibrosis without worsening of steatohepatitis. Both are harder to achieve and to interpret than an imaging surrogate.
It is a dual agonist at the GLP-1 and glucagon receptors. The glucagon arm is associated with increased energy expenditure and with effects on hepatic fat, which is why the development programme is oriented towards liver disease.
Which endpoint — histological response, fibrosis improvement, or fat fraction?
Went slowly because everything published describes a deliberate escalation. That is the extent of what I will say about it.
the hepatic data is what makes this compound different from the others
Which phase and which arm are you quoting?