why does nobody talk about dual agonist
why does nobody talk about dual agonist, and I want the answer with the reasoning attached rather than just the conclusion. Assumed the weight numbers were the point and was corrected. They are secondary to what this is being developed for. Independent purity results for this compound are very sparse across the whole…
phase 2 in liver disease is a different evidence question from weight
The escalation schedules in the published protocols are slow and deliberate, and the tolerability tables show why. That is a description of the trials rather than a suggestion for anybody.
Correction: that is the imaging endpoint, not the histological one. The paper reports both and they differ substantially.
do not import intuitions from the obesity programmes
That figure is from the obesity programme, and this thread is about the hepatic one.
Correcting myself: the readout I quoted was the 42-week interim rather than the endpoint.
read the histology endpoint definitions before quoting a response rate
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.
the titration in the trials was slow and deliberate
Imaging-derived liver fat fraction is a surrogate. It correlates with histology imperfectly, and a trial reporting one is not reporting the other.
this board is small because the compound is early
That is an escalation schedule for an unapproved compound and this board does not host those.
That is an escalation schedule for an unapproved compound and this board does not host those.
Adding the standing caveat — unapproved compound, research material is not for human use.
independent testing on this compound is very thin