u/hana_pereira

Disagree — you are quoting a combination arm as though it were monotherapy.

Agreed, and the combination arms are where the interesting numbers actually live.

nausea profile in the combination trials is the thing to read carefully

Agreed, and the trial number is a mean of a very wide distribution — the tails are enormous and nobody posts from the middle.

a lot of people plateau nicely at 10mg and never need 15

That is preclinical work and the thread is treating it as a human finding.

Small fix: SURMOUNT is the obesity programme, SURPASS is the type-2 programme. They are different endpoints and the numbers do not transfer.

What is the waist doing? That is usually the number still moving during a scale stall.

Not sure that follows. You went up a step and changed your training in the same fortnight.

I would separate the two claims. That the GIP arm exists is uncontroversial; that it explains your muscle cramps pattern is a guess.

hold the dose that works, the ladder is not a leaderboard

Push back: "gentler than sema" is a population statement. Plenty of people on this board have the opposite experience and they are not doing it wrong.

Same experience with the appetite effect being flatter across the week rather than front-loaded.

Agreed, and the trial number is a mean of a very wide distribution — the tails are enormous and nobody posts from the middle.

Correction to my own post above — I said 15mg and I have been on 7.5mg since the spring. Same argument, wrong number.

2.5mg is a four-week starting dose, not a maintenance dose. Worth being precise since people search these threads.

Not convinced. Amylin signalling is not a GLP-1 pathway and the mechanism you are proposing conflates them.

Independent purity results for this compound are very sparse across the whole site, which means any impression about consistency is built on almost nothing.

Correcting myself upthread: I gave the 22-week figure and the paper reports 89 weeks.

long-acting amylin is the whole point of the molecule

the hepatic data is what makes this compound different from the others

amylin analogue, different receptor family, different story

Not convinced. Imaging-based fat fraction is not the same as a histological response and the paper is explicit about that.

phase 3 data will change most of what gets said here

That is preclinical work and the thread is treating it as a human finding.

Is there any independent purity data on this compound that you have seen?

This is the distinction that keeps this board honest — different axis, not a stronger version of the same one.

Which phase and which arm are you quoting?

Small fix — dual agonist, GLP-1 and glucagon. No GIP arm in this molecule.

Yes.

Agreed, with one qualifier: that is the mean of the top arm and the spread around it was enormous.

SURMOUNT-1 landed around 21% at 72 weeks on the top arm

This. Biopsy-confirmed and imaging-suggested are different evidentiary categories and get run together constantly.

SURMOUNT-1 ran 72 weeks with the top arm around 21% mean body weight change. SURPASS is the diabetes programme and reports glycaemic endpoints, so quoting the two interchangeably is a category error.

This.

amara_kuipers is right that the evidence base here is thin. Conclusions should be held loosely.

switching from sema is not a dose conversion, there is no clean equivalence

Nothing containing this compound is approved anywhere. Research-use-only material is not approved for human use.

Held 7.5 for five months. Everyone kept asking when I was going to 10. The answer was never, because 7.5 was working.

This matches mine. Milder early fullness than I expected, and what there was settled inside a fortnight of each step.