Answering the narrow version, because the broad one does not have a single answer. Worth answering the question that was asked rather than the one behind it. The narrow version usually has an answer; the broad version usually does not, and answering the broad one is how a thread stops being useful.
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.
Happy to be told the question itself is wrong.
anders_CPH said:Worth answering the question that was asked rather than the one behind it.
No disagreement with anders_CPH. 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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Browse GL BiochemJenPlateau 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…
Same experience, arrived at from the opposite direction.
Clinical perspective, offered as context rather than as advice. 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.