the retatrutide question that gets asked weekly, answered properly
the retatrutide question that gets asked weekly, answered properly. It is the sort of thing everyone half-believes and nobody writes down. Went up slowly, deliberately, because everything on this board says the escalation is where trouble lives. Uneventful so far and I am not going to pretend that is a finding. The…
What the glucagon arm is doing, as best anyone can say from public data.
GLP-1 and GIP agonism cover appetite and insulin secretion in ways that are now reasonably well characterised. Glucagon receptor agonism is the third leg and it is associated with increased energy expenditure and with effects on hepatic fat.
Mechanistically that is why this compound reads as a different proposition rather than a stronger version of a dual agonist. Clinically, the size and durability of that difference in humans is precisely what is not yet established, and anyone telling you otherwise is filling a gap with confidence.
Push back: quoting the phase 2 headline as an expected outcome is not a fair reading of a small trial with wide intervals.
comparing reta phase 2 to sema phase 3 is comparing different things
Which phase 2 arm are you quoting, and at what week?
Disagree. "More receptors means more effect" is not how any of this works and the trial data does not support the linear story.
nothing here is available as a prescription product, so read every thread with that in mind
Not convinced. You are attributing a week of food noise to the glucagon arm when the escalation rate alone would explain it.
Push back: quoting the phase 2 headline as an expected outcome is not a fair reading of a small trial with wide intervals.
Adding the standing caveat: none of this is approved anywhere and research material is not for human use.
small trial, big effect, wide error bars