Reading the phase 2 write-up next to the injectable trials, and the comparison people keep making does not survive putting the two protocols side by side.
Phase 2: about 14.7% at 36 weeks on 45mg, GI adverse events broadly in line with the injectables, no food-timing requirement.
What I am trying to establish is whether a non-peptide oral agonist can match injectable exposure in practice, or whether the convenience is bought with a lower ceiling.
Tell me what I have not thought of.
This one has a reasonably settled answer, so here it is. The mechanism and the magnitude are separate questions. Agreeing that something happens says nothing about whether it happens enough to act on.
FDA_TrackerJim said:The mechanism and the magnitude are separate questions.
FDA_TrackerJim has the substance of this right. The condition it depends on is worth stating. The manufacturing argument is the underrated one. Peptide synthesis capacity has been the binding constraint on this entire class, and a small molecule is made in ordinary chemical plants. If it holds up in phase 3, the supply and price picture changes more than the efficacy picture does.
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Browse GL BiochemVanRx_Mike said:Reading the phase 2 write-up next to the injectable trials, and the comparison people keep making does not survive putting the two protocols side by…
Same pattern here, and in the same order. Nothing to add that would improve it.
Adding the clinical framing, because it changes how the question reads. It helps to say which part of this you are uncertain about. A precise question gets a precise answer; a general one gets everybody’s favourite anecdote.