three years of TRIUMPH threads, summarised so you do not have to read them
three years of TRIUMPH threads, summarised so you do not have to read them — a position I have arrived at slowly and would like tested.
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.
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.
If somebody has the same thing measured a different way, post it next to mine and we will see whether they agree.
best — the order this archive was captured in
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.
Is that the 48-week figure or an earlier readout?
Standing reminder in every thread here: unapproved compound, research material is not for human use, nothing on this board is medical advice.
phase 2 data only, and people quote it like it is a label
not approved anywhere, which is the single most important fact in this board