TirzTom said:If two explanations both fit, the useful question is which one predicts something the other does not.
I would rather people stopped quoting the 24% as if it were a licensed outcome. It is a phase 2 result in a few hundred participants with no cardiovascular endpoint and no long-term safety data, and this board has a habit of treating pipeline numbers as settled.
Adding the numbers, since they settle part of this. For anyone reading later: the numbers in this thread are worth checking against a primary source before you act on them, including mine. Half the figures circulating in this community trace back to a secondary summary that dropped a qualifier.
Dr.CardioMD said:I would rather people stopped quoting the 24% as if it were a licensed outcome.
Adding the part of the answer the thread has not reached. 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.
Happy to go further on any of that.
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Browse GL BiochemA narrower follow-up, since the general answer is now clear:
Why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose?
OP back with an update, since a thread like this is useless without one.
Rereading it with the dropout table open changed my view. I still think it is the most interesting molecule in the pipeline; I no longer think the 24% is the number that will end up on a label.