Seven days, four weeks, one number: how liraglutide exposure actually accumulates
Half-life, accumulation ratio and time to steady state are three separate quantities, and confusing them produces most of the bad advice in circulation.
Cagrilintide
A long-acting amylin analogue, studied alone and co-formulated with semaglutide.
Steady state is not a metaphor — it is an arithmetic fact about exenatide
What the pharmacokinetic data supports about dose timing, missed doses and interruption.
What the GIP receptor adds: reading cagrilintide as two drugs in one sequence
Head-to-head data exists for some of these comparisons and not for others. This piece says which.
Gastric emptying is a mechanism, not a side effect
The central effects are not a bonus. On the current evidence they are the principal mechanism of weight loss.
What we would need to measure to explain the response distribution
The mechanism is well described. The variance is not.
GIP was a failed target for thirty years. Then it was not.
A dual agonist is one molecule with two receptor activities. A co-formulation is two molecules in one pen. The coverage treats them as synonyms.
One receptor, several signals: the case for reading semaglutide as a biased agonist
A tour of what happens in the thirty seconds after binding, and why it matters at week thirty.
How a peptide that lasts seven days binds a receptor that recycles in minutes
What the in-vitro data supports, what it does not, and where the extrapolation to a person begins.
The limits of mechanism: why receptor data will not tell you who responds
Receptor pharmacology is strong on average effects and almost silent on individual variation. That gap is where most reader questions live.
Reading the receptor: what distinguishes survodutide from liraglutide at the molecular level
Receptor pharmacology explains more of the clinical picture than the dose does — and almost none of it appears in the material patients are given.
The brainstem does most of the work
A tour of the tissues where the receptor is expressed, and what happens in each.
Beta-arrestin, cAMP, and the part of dulaglutide’s mechanism nobody quotes
The receptor is expressed in more tissues than the popular account allows, and that is the whole story.
What changing your injection day does to retatrutide exposure, and what it does not
What the pharmacokinetic data supports about dose timing, missed doses and interruption.
Reading the receptor: what distinguishes cagrilintide from survodutide at the molecular level
A tour of what happens in the thirty seconds after binding, and why it matters at week thirty.
GIP was a failed target for thirty years. Then it was not.
A dual agonist is one molecule with two receptor activities. A co-formulation is two molecules in one pen. The coverage treats them as synonyms.
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.
The glucagon receptor arm, and why it is the hardest to reason about
A dual agonist is one molecule with two receptor activities. A co-formulation is two molecules in one pen. The coverage treats them as synonyms.
Non-responders, and the honest state of the evidence about them
The mechanism is well described. The variance is not.
Dual, triple, co-formulated: a taxonomy the coverage keeps collapsing
Head-to-head data exists for some of these comparisons and not for others. This piece says which.
Why the fifth week of a mazdutide dose feels different from the first
The exposure curve explains the timing of both the benefit and the side effects. It is almost never shown to the person injecting.