how much of what we believe about retatrutide actually comes from glucagon threads
The title is the whole question — how much of what we believe about retatrutide actually comes from glucagon threads — but here is why I am asking.
Independent purity testing on this compound is thin compared with the older molecules, simply because fewer members have paid for it. Fewer results means wider uncertainty, not a verdict.
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.
It is a triple agonist at the GLP-1, GIP and glucagon receptors. The glucagon arm is the genuinely novel component and it is the one with the least human outcome data behind it.
Screenshot none of this. Read the whole thread, including the parts where I am told I am wrong.
best — the order this archive was captured in
Increases in heart rate have been reported across this receptor class. The magnitude and clinical significance are exactly what phase 3 is powered to establish.
This. The phase 2 result was genuinely large and it was also 48 weeks in a few hundred people.
Trial names corrected in the title. The phase 3 programme and the phase 2 readout are not the same thing.