dose escalation — my 16-week log, condensed into one table
The title is the argument: dose escalation — my 16-week log, condensed into one table. Here is the rest of it.
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.
The standing caveat, written out properly because it keeps getting compressed into a footnote.
Nothing containing this compound is approved by any regulator. Research-use-only material is not approved for human use. That is not a legal formality on this board — it is why there is so little independent data, why the escalation schedules people post are invented, and why nobody here can answer a dosing question.
What this board can usefully do is read the published trials carefully, log independent purity results, and be honest about how thin the evidence base is. Everything else belongs somewhere with a clinician in it.
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.
Happy to answer the boring questions. Those are usually the ones worth asking.
best — the order this archive was captured in
The phase 2 readout ran to 48 weeks in a few hundred participants with a slow escalation. Both the size and the duration matter when people quote the headline number.
Trial names corrected in the title. The phase 3 programme and the phase 2 readout are not the same thing.
research-use-only material is not approved for human use, full stop
Phase 2 estimates effect and finds a dose range. Phase 3 estimates it precisely in a bigger population and catches what phase 2 was too small to see. Treating them as the same tier of evidence is the recurring error here.
That is body weight change, not fat mass. The trials report the first and people quote it as the second.
the phase 2 numbers were striking and they were also 48 weeks in a small population
Nothing containing this compound is approved anywhere. Research-use-only material is not approved for human use, and that is a statement of fact rather than a disclaimer.
Agreed on the heart-rate reports. They are consistent enough across the threads to be worth noting, not enough to be a finding.
The sulphur burps profile felt different rather than worse. Hard to describe and impossible to quantify, so take it as an impression.
How fast was the escalation? That is usually the variable that explains the reports.
What do you think the glucagon component is adding, specifically?
wait for phase 3 before you argue about rankings
the TRIUMPH programme is still running, so anything definitive is premature
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.
The thing that surprised me was how much of the discussion here is inference rather than measurement.
the TRIUMPH programme is still running, so anything definitive is premature
Disagree with this specific inference. A 48-week readout does not tell you the shape of the curve after it.
the glucagon component is why the metabolic story reads differently
triple agonist — GLP-1, GIP and glucagon, and the glucagon arm is the new part
small trial, big effect, wide error bars
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.
Small fix — three receptors, not two. GLP-1, GIP and glucagon, and the third one is the reason this compound gets its own board.
Are you tracking heart rate at all?
dose escalation in the trials was slow for a reason
Which phase 2 arm are you quoting, and at what week?
comparing reta phase 2 to sema phase 3 is comparing different things
Careful with the rankings. A phase 2 result and a phase 3 result are not on the same evidential footing and cannot be listed in one table.
heart rate is the thing people report watching
the energy-expenditure story is mechanistically interesting and clinically unproven
- 1the TRIUMPH programme is still running, so anything definitive is premature7 comments in this branch · started by u/hugo_pires
- 2The phase 2 readout ran to 48 weeks in a few hundred participants with a…6 comments in this branch · started by u/niels_lindqvist