switched from 10mg to 15mg and nausea got better, not worse
switched from 10mg to 15mg and nausea got better, not worse, which sounds obvious until you try to state the evidence for it.
Numbers, in the order they matter: 10mg and 15mg.
Sent a vial to VendorInvestigate out of curiosity. Result was 98.5% against a claimed 98.0%, which is the first independent number I had seen for this compound anywhere.
The thing that surprised me was how much of the discussion here is inference rather than measurement.
That is everything I have. The rest is opinion and I have tried to keep it out.
best — the order this archive was captured in
Where the evidence actually stands, since every thread here assumes a different answer.
Phase 2 reported a large mean body weight change at 48 weeks across a few hundred participants with a slow, protocol-driven escalation. The effect size was striking. The confidence intervals were wide, the population was small, and the duration was under a year.
Phase 3 is running. Until it reports, everything else — including the ranking arguments this board loves — is extrapolation from a small study. That is not a criticism of the compound; it is a description of the evidence.
That is body weight change, not fat mass. The trials report the first and people quote it as the second.
Correction: TRIUMPH is the phase 3 programme. The number you are quoting is from the phase 2 readout, which is a different trial.
Small fix — three receptors, not two. GLP-1, GIP and glucagon, and the third one is the reason this compound gets its own board.
Left up. It reads the phase 2 paper carefully and it is honest about the intervals.
What is the source for that figure — the published paper or a summary of it?
triple agonist — GLP-1, GIP and glucagon, and the glucagon arm is the new part
Push back: quoting the phase 2 headline as an expected outcome is not a fair reading of a small trial with wide intervals.
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.
research-use-only material is not approved for human use, full stop
the glucagon component is why the metabolic story reads differently
Read the phase 2 paper twice before ordering anything. Recommend that to anyone in this board: the error bars are the interesting part.
Agreed, and the framing that helps is: this is a phase 2 compound with phase 3 running. Everything else is inference.
Sceptical of the extrapolation. Forty-eight weeks does not tell you about seventy-two, and the curve shape is exactly what is unknown.
Which phase 2 arm are you quoting, and at what week?
the escalation is where most of the reported trouble sits
the escalation is where most of the reported trouble sits
Adding the standing caveat: none of this is approved anywhere and research material is not for human use.
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.
That reads as a titration plan for an unapproved compound. This board cannot host that and it should not want to.
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.
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.
nothing here is available as a prescription product, so read every thread with that in mind
heart rate is the thing people report watching
phase 2 data only, and people quote it like it is a label
Stopped at a low step because there was no reason to go further and no data to tell me what further would do.
Not convinced. You are attributing a week of reflux to the glucagon arm when the escalation rate alone would explain it.
comparing reta phase 2 to sema phase 3 is comparing different things
The injection-site soreness profile felt different rather than worse. Hard to describe and impossible to quantify, so take it as an impression.
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.
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