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.
For anyone tracking the class: GLP-1 alone gets you appetite, GLP-1 plus GIP adds tolerability and lipid handling, and adding glucagon adds expenditure and liver-fat reduction. Each addition also adds a receptor system that can generate side effects.
What I am trying to establish is what the phase 2 dropout pattern implies about how the phase 3 tolerability will read.
Happy to be told the question itself is wrong.
Answering the narrow version, because the broad one does not have a single answer. The distinction that resolves most of these threads is between what is true on average and what is true for one person. Both are real; they answer different questions and get quoted as if they were the same one.
Dr.MetabolicMD said:The distinction that resolves most of these threads is between what is true on average and what is true for one person.
That is correct as far as it goes, and here is where it stops going. 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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Browse GL Biochemlisa_labSD 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.
From the other side of the consultation, briefly. The version of this that has an answer is narrower than the version being asked. Narrow it and it becomes tractable; leave it broad and the thread will produce nine confident and incompatible replies.