What the GLP-1 receptor actually does when exenatide binds it
The receptor is expressed in more tissues than the popular account allows, and that is the whole story.
Cagrilintide
Page 3 of 4 of this archive, newest first.
Dual, triple, co-formulated: a taxonomy the coverage keeps collapsing
The glucagon arm raises energy expenditure and also raises hepatic glucose output. Balancing those is the whole engineering problem.
What we would need to measure to explain the response distribution
The mechanism is well described. The variance is not.
Why a drug that acts on the pancreas changes what food tastes like
A tour of the tissues where the receptor is expressed, and what happens in each.
The kidney, the heart and the receptor nobody was looking for
The same receptor population that produces the therapeutic effect produces the commonest adverse one.
Why a drug that acts on the pancreas changes what food tastes like
A tour of the tissues where the receptor is expressed, and what happens in each.
Why the fifth week of a dulaglutide dose feels different from the first
An accumulation model, drawn from published parameters, with its assumptions stated.
Why receptor selectivity is the least discussed number in incretin pharmacology
The class is described as though every molecule in it did the same thing. At the receptor, they demonstrably do not.
What we would need to measure to explain the response distribution
A catalogue of open questions, with an assessment of how likely each is to be resolved.
GIP was a failed target for thirty years. Then it was not.
The glucagon arm raises energy expenditure and also raises hepatic glucose output. Balancing those is the whole engineering problem.
The GLP-1 receptor is not a switch, and retatrutide is not a key
Receptor pharmacology explains more of the clinical picture than the dose does — and almost none of it appears in the material patients are given.
Where the receptor is: a tissue-by-tissue account of tirzepatide’s reach
The same receptor population that produces the therapeutic effect produces the commonest adverse one.
From cell to clinic: where the extrapolation stops being safe
Receptor pharmacology is strong on average effects and almost silent on individual variation. That gap is where most reader questions live.
Amylin is not an incretin, and cagrilintide is not a GLP-1 agonist
The glucagon arm raises energy expenditure and also raises hepatic glucose output. Balancing those is the whole engineering problem.
Where the receptor is: a tissue-by-tissue account of tirzepatide’s reach
The same receptor population that produces the therapeutic effect produces the commonest adverse one.
The incretin receptors, ranked by how much we actually know about them
The class is described as though every molecule in it did the same thing. At the receptor, they demonstrably do not.
Six things incretin pharmacology cannot currently predict
The mechanism is well described. The variance is not.
The limits of mechanism: why receptor data will not tell you who responds
The mechanism is well described. The variance is not.
The incretin receptors, ranked by how much we actually know about them
The receptor is expressed in more tissues than the popular account allows, and that is the whole story.
The limits of mechanism: why receptor data will not tell you who responds
A catalogue of open questions, with an assessment of how likely each is to be resolved.