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 actually want to know is what the phase 2 dropout pattern implies about how the phase 3 tolerability will read.
Numbers rather than impressions, if you have them.
Short answer first, then the reasoning. 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.
TrialTracker_MD said:It helps to say which part of this you are uncertain about.
TrialTracker_MD 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.PainCLE 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 matches mine closely enough to be worth saying so out loud. I had assumed I was the exception until I read this.
Adding the clinical framing, because it changes how the question reads. Take it one variable at a time. Almost every unanswerable question in these threads is unanswerable because three things changed in the same fortnight, and no amount of subsequent argument can untangle them after the fact.