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 after is why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
Happy to be told the question itself is wrong.
Taking the question as asked, rather than the general version of it. The mechanism and the magnitude are separate questions. Agreeing that something happens says nothing about whether it happens enough to act on.
Dr.GastroMayo said:The mechanism and the magnitude are separate questions.
Dr.GastroMayo has the substance of this right. The condition it depends on is worth stating. The phase 2 numbers were about 24% mean weight loss at 48 weeks on the top dose, with the curve still descending at the end of the study. A curve that has not flattened is a real finding, but it also means the true plateau is unknown, and phase 2 populations are small and selected.
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Browse GL Biochemamsterdam_pete 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…
Adding a me-too, because a thread of one person's experience is not much use. I had assumed I was the exception until I read this.
Clinical perspective, offered as context rather than as advice. 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.