2-F(M)A Metabolism

[m060mm]

Any possibility that someone could speculate on the metabolism of 2-FMA?

Should it follow the same possible path of 4-FMA -> 4-FA? What would be the other byproduct of that reduction?

4-FA is also said to be excreted largely unchanged. Can the same be said for 2-FA? What might 2-FA breakdown into?

I'm not exactly sure if this is a tall order - I apologize if it is. I often see those with relevant backgrounds commenting about 'the unlikelihood of the fluorine bond allowing for the breakdown of the phenyl ring' so I figure it's one of those things where experts can take a glance and know a decent amount.

 

[Poodles!]

4-FMA can be a bit of a manic ride that lasts quite a long time, I've often wondered exactly how much could possibly be metabolised to 4-FA, because it seems to maintain it's manic side right the way through rather than taking on the relaxed characteristics of 4-FA. It must be metabolised an excreted pretty slowly since I've felt pretty buzzed upon waking the next day, despite dosing early afternoon. It's definately more of a drain on the body than 4-FA too, so I'd be interested in seeing some toxicity studies on 4-FMA in the future.

As for 2-F(M)A, there's a lot more speculation. Sure, some 2-FMA will be metabolised to 2-FA, but both will likely undergo para-hydroxylation. But to what degree I don't know. I wouldn't be surprised if more 2-FMA was metabolised to 2-FA than Methamp to Amp because of how similar the drugs are in effect, duration and dose and 2-FMA doesn't last nearly as long as Meth (although I've never tried meth) which suggests it is metabolised and/or excreted faster. How the flourine would affect this is beyond my level of knowledge. Hopefully someone with more eduction on the matter could approach it from a more theoretical POV.

You could try taking some 2-F(M)A and then piss into a mass spectrometer? If I were a postgrad, that would definately be at the top of my to-do list.


Edit: I'm not a postgrad, but I'm still putting this on my lifes to-do list... Somewhere above swimming with dolphins but below sex in space. Well there goes my productive day *licks some more spilt 3-MeO-PCP*

EditEdit: CYP3A4 for demethylation, CYP2D6 for hydroxylation (of methamphetamine). Doesn't really add much, but I stumbled across the linked site and thought it was interesting.

 

[sekio]

4-hydroxylation of amphetamine is a rather minor pathway, it probably doesn't contribute to the experience much.

I bet "most" 2-fma will be excreted unchanged, and the primary metabolite will be the deaminated ketone. The metabolic pathway would follow that of amphetamine/meth.

 

[m060mm]

Thanks for the replies!

It must be metabolised an excreted pretty slowly since I've felt pretty buzzed upon waking the next day, despite dosing early afternoon.

This has been my experience as well, especially if I took more than a minor/functional dose. Implies potential zero-order kinetics? It certainly feels like that's how it works, awake or asleep.

both will likely undergo para-hydroxylation.

Ive been trying to learn chem but it's been a slow process. What does that mean as far as (active?) metabolites, safety, etc. - is it possible to guess?

piss into a mass spectrometer

In the name of science!

Interesting site, btw. I'm going to have to browse endlessly some night when sleep just refuses to see me.

And I have to brush up on meth/amphetamine metabolism before I can reply to you Sekio.

 

[sekio]

From memory, less than 5% amphetamine is metabolised to 4-hydroxyamphetamine. It's a really minor process.

 

[Poodles!]

^Same goes for MDMA to MDA and the debate about whether it produces enough MDA to produce the psychedelic effects of high dose MDMA.

My thought process above was how the flourine could affect whether more or less will follow a particular pathway, but if it's not likely to change it much then you're right.

If we assume alpha-methyldopamine is the primary metabolite causing neurotoxicy (or a metabolite of this metabolite). Then it's reasonable to assume that the 2-fluoro analogue could pose a similar threat. This would require hydroxylation. It's only in high/repeated doses that this becomes an issue in the case of amphetamine though. In methamphetamines case, it's mostly the excessive release of dopamine that seems responsible for the neurotoxicity. Again, the military and people with ADHD seem to have no problem using it responsibly.

The moral of the story is to simply be sensible with your stims. If any of the fluoro amphetamines pose any real threat, it will likely come from as-yet unknown binding, such as 5-HT2B affinity which as you probably known can lead to heart valve hypertrophy with prolonged use. I would't be surprised if 4-F(M)A had affinity for these these receptors. 4-FMA certainly seems to fuck with serotonin in large doses... it has an usual dose response curve IME.


Edit:

This has been my experience as well, especially if I took more than a minor/functional dose. Implies potential zero-order kinetics?

I'm not sure if there's any way to find out without a fancy lab. It seems like you need to hit a certain point though. Maybe enzyme saturation ala MDMA has something to do with this?

I mentioned unsusual dose response above. By this I mean it's the opposite from what I've come to expect from 2-F(M)A. the 2-F's seem to have a ceiling on the psychological effects where increasing the dose just increases the physical sides. with 4-FMA though, it's active from around 10mg similarly to the 2-F's (maybe a bit less potent) but the psychological effects just keep going and going. I only discovered this towards the end of my first gram but I ended up plugging what was left and I was FUCKED. I ended up buyinh 5 more grams and it's sitting in my draw next to my bed.

I'm actually quite terrified by it, I'm not sure how i'm managing this much self control to be quite honest.... The thought of combining with IAP which I'll get next week is giving me a fat erection right now. Seriously. I'm thinking of vaping some MDPV just to take my mind of it!

 

[Dmytry]

The moral of the story is to simply be sensible with your stims. If any of the fluoro amphetamines pose any real threat, it will likely come from as-yet unknown binding, such as 5-HT2B affinity which as you probably known can lead to heart valve hypertrophy with prolonged use. I would't be surprised if 4-F(M)A had affinity for these these receptors. 4-FMA certainly seems to fuck with serotonin in large doses... it has an usual dose response curve IME.

Isn't 5-HT2b binding with PEAs mostly dependent on an electron rich area at the 3 position to mimic tryptamines more closely? ex: fenfluoramine, mdma, also 5-MeO-tryptamines

while excess levels of serotonin can over-activate 5-HT2b on its own that does not make the releaser itself an agonist. even taking too much 5-htp is bad for your heart, thats part of the reason why its prescribed with carbidopa.

but im not a pharmacologist yet, so i may be wrong

edit: found this article, the only 5-ht2b diagram i could find

from http://www.sciencedirect.com/science/article/pii/S1093326308000259

i dont really think that the 2-sub and 4-sub amphetamines are anything to worry about in regard to heart valve problems

 

[pofacedhoe]

even taking too much 5-htp is bad for your heart,

is this so?

 

[amanitadine]

Ahhh Sekio my hat goes off to ya, yr patience is incredible, and have done a noble job of picking up the reigns in the great vacating of ADD. So many of these posts possess just enough "knowledge" to get into trouble, or provide a good laugh, and I'm impressed continually with your temerity and restraint, and continued willingness to lay down the accurate information.