Good question. Radiopharmaceuticals like this one is produced at the hospital by use of a “cold kit” which is then tested and released for use shortly before the patient is injected and scanned. Page 3-5 in this https://www-pub.iaea.org/mtcd/publications/pdf/trs466_web.pdf explains it well.

Clerks

It looks like the mode of action of botox is a bit more complex (here’s from one of my favorite webpages drugs@fda)

12.1 Mechanism of Action BOTOX blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings. When injected intramuscularly at therapeutic doses, BOTOX produces partial chemical denervation of the muscle resulting in a localized reduction in muscle activity. In addition, the muscle may atrophy, axonal sprouting may occur, and extrajunctional acetylcholine receptors may develop. There is evidence that reinnervation of the muscle may occur, thus slowly reversing muscle denervation produced by BOTOX.

https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/103000s5236lbl.pdf#page13

Good point.

AcCh turnover increase means more is degraded by the enzyme, decrease the opposite.

Depending on the location of the turnover (central nervous system or e.g. In skeletal muscles) this could lead to prolonged or shorter duration of AcCh.

One cool example of a drug working by decreasing AcCh effect (ultimately) is botox, leading to temperary paralysis on the injection site.