someone explain phase 2 to me like I have not read a paper in years
Genuine question, and the title is the question: someone explain phase 2 to me like I have not read a paper in years. Stopped at a low step because there was no reason to go further and no data to tell me what further would do. The thing that surprised me was how much of the discussion here is inference rather than…
Glucagon receptor agonism is associated with increased energy expenditure and with hepatic effects. That is a mechanistic story with strong preclinical support and limited phase 2 human data.
the glucagon component is why the metabolic story reads differently
Yes — the comparison threads are apples to oranges and they generate more heat than anything else here.
dose escalation in the trials was slow for a reason
Sent a vial to VendorInvestigate out of curiosity. Result was 99.1% against a claimed 98.5%, which is the first independent number I had seen for this compound anywhere.
the TRIUMPH programme is still running, so anything definitive is premature
Sent a vial to VendorInvestigate out of curiosity.
yara_lindholm is right about the escalation being the variable. It explains most of the difficult reports here.