Taking the question as asked, rather than the general version of it. It is worth asking what the claim would look like if it were false. If nothing would look different, it is not a claim about the world and no amount of discussion will settle it.
Reading the retatrutide phase 2 data properly rather than the headline, and the 24% figure is doing a lot of work that the confidence interval does not support as firmly as people think.
What I am after is what the phase 2 dropout pattern implies about how the phase 3 tolerability will read.
Numbers rather than impressions, if you have them.
CarlaRPh_TPA said:It is worth asking what the claim would look like if it were false.
No disagreement with CarlaRPh_TPA. One condition attached. The glucagon component looks paradoxical and is not. Glucagon receptor agonism raises energy expenditure and drives hepatic fatty-acid oxidation, and its hyperglycaemic tendency is offset by the GLP-1 arm's insulin secretagogue effect. Net result: intake down from GLP-1/GIP, expenditure up from glucagon, glycaemia neutral or improved. It is a balancing act, and it is why the liver-fat results are the most interesting part of the dataset.
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View ResultsBenResearch_OR said:Reading the retatrutide phase 2 data properly rather than the headline, and the 24% figure is doing a lot of work that the confidence interval does…
Can confirm. Same sequence, different timescale. Posting only so the count is not one.
From the other side of the consultation, briefly. Start from the measurement rather than the conclusion. Almost every disagreement here turns out to be two people measuring different things and comparing the numbers anyway.