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 am after is what the phase 2 dropout pattern implies about how the phase 3 tolerability will read.
If the honest answer is that nobody knows, that is a useful answer and I would rather have it.
Taking the question as asked, rather than the general version of it. The version of this that has an answer is narrower than the version being asked. Narrow it and it becomes tractable; leave it broad and the thread will produce nine confident and incompatible replies.
PeptideChemSF said:The version of this that has an answer is narrower than the version being asked.
No disagreement with PeptideChemSF. 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 Biochemhannah_MT 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.
Same experience, arrived at from the opposite direction. Nothing to add that would improve it.
Clinical perspective, offered as context rather than as advice. Order of operations matters more than any single choice here: establish a baseline, change one thing, wait long enough for it to express itself, then measure again under the same conditions.