On an unrelated and annoyingly semantic note, the abbreviation "M1" kind of erks me. The "-one" in methylone is indicative of the ketone, its not pronounced like the numeral.
Yeah if that bothers you we can continue nitpicking for a while, many trivial drug names are inaccurate or misleading, we all got opinions on it.
bk-MDMA is better for methylone, but not very short and compact. I never had misunderstandings with the name M1 even though it could be misinterpreted as primary metabolite. The only thing that would irk me is if people would be saying methylone as [meth-ill-'wan] instead of [meth-il-lone].
I was going to close the thread because the question is answered, but maybe there is an issue left. Methylone is quite dopaminergic compared to MDMA, and as a monoamine releaser it mainly shows cross-tolerance with other monoamine releasers, the more their pharmacological profile (SE : DA : NE ratio) would overlap the more cross-tolerance I suppose you would expect.
The question I would raise as a hijacked topic for this thread is: what kind of change in effect might be seen with a serotonergic agonist effect like with a psychedelic such as 2C-I after the brain's serotonin has been depleted say with large and repeated dosis of MDAI?
Also, 2C-I is fairly stimulating. The reason for that would be expected to be dopaminergic agonism, right?
So perhaps after having taken methylone a lot, taking 2C-I could produce dirtier kinds of dopaminergic effect than normally? I mean after depleting your dopamine I would personally expect many drugs acting on the same system to be dirtier as well, because maybe the efficacy of the whole dopaminergic system is changed, there might be an imbalance between the CNS and PNS?
