PedsEndoPhilly said:

The mechanism that matters here is not stomach emptying, it is central.

That holds for the injectable. The oral formulation has different absorption behaviour and the dose numbers are not interchangeable, which is worth saying out loud because people quote them as if they were.

MounjBrad said:

The mechanism is more central than most summaries suggest.

This is exactly what I could not find anywhere else.

PedsEndoPhilly said:

The mechanism that matters here is not stomach emptying, it is central.

This is where I part company with the consensus forming above. The trial means are being read too generously in this thread. STEP populations were selected, supported, and titrated by protocol, and the real-world curves are consistently a few points worse. That difference is not noise, it is what happens when you remove the study infrastructure.

emily_PDX said:

Reading about receptor desensitisation and trying to work out which of the effects adapt over time and which do not, because people clearly experience…

Receptor pharmacology relevant to the pharmacology: semaglutide is a GLP-1R agonist with a C-18 fatty acid chain that enables albumin binding (>99%), creating a depot effect with a ~168-hour half-life enabling weekly dosing[1].

Tirzepatide is a dual GIP/GLP-1R agonist with higher GIP affinity (5:1 GIP:GLP-1 potency ratio). The GIP component may enhance beta-cell function and adipocyte lipid metabolism beyond what GLP-1 alone achieves.

For the pharmacology, the pharmacology explains the clinical differences between these agents.

Moderator note: reminder that nothing in this thread is medical advice, and that clinical claims need a source. Carry on.