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.
The question I want answered 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.
Answering the narrow version, because the broad one does not have a single answer. There is a difference between no evidence and evidence of no effect, and this subject is one where the two get swapped freely in both directions.
LipidDoc_ATL said:There is a difference between no evidence and evidence of no effect, and this subject is one where the two get swapped freely in both directions.
Agreeing with LipidDoc_ATL, and the qualification matters more than the agreement. 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.RheumBOS 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 pattern here, and in the same order. I had assumed I was the exception until I read this.
Clinical perspective, offered as context rather than as advice. 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.