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 actually want to know is what the phase 2 dropout pattern implies about how the phase 3 tolerability will read.
Tell me what I have not thought of.
This one has a reasonably settled answer, so here it is. The mechanism and the magnitude are separate questions. Agreeing that something happens says nothing about whether it happens enough to act on.
FDA_TrackerJim said:The mechanism and the magnitude are separate questions.
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 Biochemandrew_nyc 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…
Second this. Nothing to add that would improve it.
Adding the clinical framing, because it changes how the question reads. It helps to say which part of this you are uncertain about. A precise question gets a precise answer; a general one gets everybody’s favourite anecdote.