Sceptical rather than excited about the triple agonist, and I would like somebody to talk me out of the scepticism with data rather than enthusiasm.
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 actually want to know 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.
Short answer first, then the reasoning. If two explanations both fit, the useful question is which one predicts something the other does not. That is answerable; arguing about which sounds more plausible is not.
TirzTom said:If two explanations both fit, the useful question is which one predicts something the other does not.
No disagreement with TirzTom. 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 Biochemandrew_nyc said:Sceptical rather than excited about the triple agonist, and I would like somebody to talk me out of the scepticism with data rather than enthusiasm.
This is my experience too, for whatever a second data point is worth. Nothing to add that would improve it.
Clinical perspective, offered as context rather than as advice. Most of what circulates confidently in this community traces back to one summary of one study, and the qualifier was dropped somewhere in the third retelling.