RetaRick_CA said:Albumin binding above 99% is the whole reason weekly dosing works, and it is also why the trough matters more than the peak.
I will push back on the "any working dose is fine" framing. The maintenance evidence sits overwhelmingly at the top studied dose, and the extension data shows regain tracking dose reduction rather than tracking stopping. Holding low is reasonable; pretending it is evidentially equivalent is not.
Correct me if the detail matters more than I have assumed.
The figures, for anyone assembling their own picture. For anyone assembling their own picture: Tmax is one to three days, terminal half-life about 165 to 170 hours, steady state at four to five weeks, and subcutaneous bioavailability near 89%. Those four numbers explain most of the questions people ask about timing.
Happy to go further on any of that.
DataDave said:I will push back on the "any working dose is fine" framing.
There is a second half to this that has not been said yet. Resolution therefore closed the doors unevenly, and the asymmetry follows from the bulks lists. For 503B the shortage clause was the only route to these molecules, so that route shut completely. A 503A pharmacy can still argue a doorway via "component of an approved drug" — but only for the substance in the form present in the approved product, which is exactly where the base-versus-salt argument lives, and it does nothing about the copy restriction, which came back into force on resolution.
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Browse GL BiochemFollowing on from Dr.BariatricHTX — and this may be the naive question:
What actually distinguishes 503A from 503B, in terms of what each may make and from what starting material?
Reporting back.
Update since I posted: I held at 1.7mg for a further twelve weeks and lost another 4kg slowly, which settles it for me. I was escalating because the number was available, not because I had stopped responding.