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.
So the question, as narrowly as I can put it: what the phase 2 dropout pattern implies about how the phase 3 tolerability will read.
Practical detail welcome, however dull — the duller the better.
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.
LabKate said:It is worth asking what the claim would look like if it were false.
Agreeing with LabKate, and the qualification matters more than the agreement. 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 Biochemjason_sac26 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…
This matches mine closely enough to be worth saying so out loud. I had assumed I was the exception until I read this.
Adding the clinical framing, because it changes how the question reads. 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.