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.
What I am trying to establish is what the phase 2 dropout pattern implies about how the phase 3 tolerability will read.
I would rather have one careful answer than five confident ones.
Answering the narrow version, because the broad one does not have a single answer. 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.
TirzTom said: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…
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 BiochemDr.SportsMedIN 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.
Adding the clinical framing, because it changes how the question reads. The useful move here is to separate what is established from what is widely repeated. Those two sets overlap less than the confident tone of most write-ups suggests, and the second set is where nearly all the disagreement on this board comes from.