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 after is what the phase 2 dropout pattern implies about how the phase 3 tolerability will read.
Not looking for reassurance. Looking for the part I have got wrong.
Short answer first, then the reasoning. Worth answering the question that was asked rather than the one behind it. The narrow version usually has an answer; the broad version usually does not, and answering the broad one is how a thread stops being useful.
JennaRN said:Worth answering the question that was asked rather than the one behind it.
JennaRN has the substance of this right. The condition it depends on is worth stating. 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.BariatricHTX 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.
Adding the clinical framing, because it changes how the question reads. It is worth asking what the claim would look like if it were false. If nothing would look different, it is not a claim about the world and no amount of discussion will settle it.