stalled for 8 weeks at 1.7mg and I refuse to panic this time
stalled for 8 weeks at 1.7mg and I refuse to panic this time. Making the case below, and I expect to lose some of it in the comments.
Since the title puts numbers in the shop window: 8 weeks and 1.7mg.
Asked here what the difference was between the imaging and biopsy endpoints and got a genuinely excellent answer.
Looked for independent results across this whole site and found almost none. Worth knowing before forming an opinion.
Not medical advice, obviously, and nothing here is approved for human use. One person with a spreadsheet.
best — the order this archive was captured in
Independent purity results for this compound are very sparse across the whole site, which means any impression about consistency is built on almost nothing.
Read the phase 2 hepatic paper properly and the endpoint definitions were more interesting than the headline response rate.
independent testing on this compound is very thin
Yes — nothing containing this is approved anywhere, which is the first fact and usually the last one mentioned.
Which phase and which arm are you quoting?
research material is not approved for human use, which is why the clinical record here is thin
Cosigning on the glucagon arm. It is the mechanistic thread that connects the hepatic and the metabolic effects.
Yes — histological endpoints are a far harder bar than the surrogate measures people are used to quoting.
Yes — histological endpoints are a far harder bar than the surrogate measures people are used to quoting.
Agreed — and the endpoint definitions are where the actual claim lives.
Correction: that is the imaging endpoint, not the histological one. The paper reports both and they differ substantially.
That figure is from the obesity programme, and this thread is about the hepatic one.
Right, and the trial titration was slow for reasons that are visible in the tolerability tables.
Assumed the weight numbers were the point and was corrected. They are secondary to what this is being developed for.
a liver endpoint is not a weight endpoint with better marketing
Sent a vial to VendorInvestigate because there was nothing on file. 97.9% against a claimed 97.0%. First entry for this compound in my own log.
Histological endpoints in this field are scored on biopsy: resolution of steatohepatitis without worsening of fibrosis, or improvement in fibrosis without worsening of steatohepatitis. Both are harder to achieve and to interpret than an imaging surrogate.
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Push back: the evidence here is phase 2, in a specific population, and it does not support a general ranking.
Push back: the evidence here is phase 2, in a specific population, and it does not support a general ranking.
This is the framing the board needs. It is a hepatic programme first.
Same. Very thin independent data on this one, which should make everybody here more tentative than they are.
Histological endpoints in this field are scored on biopsy: resolution of steatohepatitis without worsening of fibrosis, or improvement in fibrosis wit
Disagreeing with this bit: that number comes from a different programme with a different population.
read the histology endpoint definitions before quoting a response rate
I would not read across from the obesity programmes. Different population, different endpoint, different question.
What this compound is actually being developed for, since the boards treat it as a weight-loss molecule with a footnote.
It is a dual GLP-1 and glucagon receptor agonist, and the glucagon arm links to hepatic fat and energy expenditure. The headline programme is metabolic liver disease, with endpoints scored on biopsy rather than on a scale.
That matters for how the data should be read. A histological response rate in a biopsy-confirmed population answers a very different question from a mean weight change in an obesity trial, and quoting one in place of the other — which happens in nearly every thread here — is not a comparison.
Disagree — that is a weight endpoint from a different programme and you are quoting it in a hepatic context.
Bought small because the evidence base is early. That is the only defensible position I could construct.
Imaging-derived liver fat fraction is a surrogate. It correlates with histology imperfectly, and a trial reporting one is not reporting the other.
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