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RCs 2-FMA (2-Fluoromethamphetamine) - Megathread

Task-starting and sustained attention are different beasts for sure. When I was finishing my dissertation, dextroamphetamine definitely provided both, along with some of the mood lift, bordering on euphoria. The mood lift makes starting tasks less daunting, and the tunnel vision/hyperfocus help keep effort consistent.

Are you saying you think 2-FMA is worse for you because it's a stronger dopamine releaser? My understanding has been, lacking actual binding profile studies, racemic 2-FMA is probably actually a stronger NE releaser than d-amph, which in turn is stronger than d-meth. I haven't seen anyone even speculate as to enantiomer-specific activity of 2-FMA, but pulling things out of thin air, I would guess, as with meth, the l-enantiomer of 2-FMA is extremely biased towards NE, and the d-enantiomer is more balanced. This would explain the apparent ceiling effect of 2-FMA. Since reports are that high doses increase vasoconstriction and tachycardia without more central stimulation, it would make sense that racemic 2-FMA, which as far as I know is all anyone has ever taken (correct me if I'm wrong), would be NE biased as a single drug. 2-FMA is also less associated with psychosis and mania in user reports, which suggests less dopamine bias. This could all be complicated by metabolism—there's a paper on plausible metabolites of 2-FMA, but as with its binding potency, the literature is sparse.

I do agree that dopamine release is not strictly better for ADHD pharmacotherapeutics. Most anecdotes I've read about attempts to use d-meth for ADHD suggest that it can be counterproductive, but more so because of the heightened euphoria. I view mood lift as something that needs to be optimized: enough to overcome task anxiety and increase task enjoyment, but not so much you stop worrying at all about the actual life obligation ADHD is interfering with. I also personally wonder if the apparent anxiolysis along with more subtle stimulation of 2-FMA might be due to interactions with sigma receptors, or maybe a relative lack thereof compared to meth. Since 2-FMA is unlikely to be enough of a cash cow to merit clinical trials, and hasn't been the subject of alarmist media reporting, I think the motivation to do binding assays on it is weak, and so insight about its pharmacology is likely to continue only at a trickle.

Good luck in any case with your research and writing. It's not the easiest thing for those of us with ADHD diagnoses, and optimizing medication goes a long way to help with that.
My problem is task-starting, much more than sustained attention, except for super boring tasks like studying or reading/doing something I hate (like paperwork)
I guess that I don't respond well to NE releasers, but that's not the case with NE reuptake inhibitors... for me yohimbe feels pretty nice, I feel very motivated while on yohimbe, but I'm totally unfocused, same with NEP which seems to be pretty potent on NE ...
I do consider 2-fma useless but I remember that my first batch was pretty nice, and it worked nicely, but it was much more euphoric.... So, what was that? who knows, I guess we are receiving poison from China/India and not actually any pure racemic anything, let alone pure l-/d-enantiomers...
I also think you're right about euphoria and mood lift, too much is too distracting, but not enough makes everything robotic and boring, and 4f-mph and specially late batches of 2-fma feel too robotic for me , boring as fuck (but I much prefer 4f-mph as functional adhd medication).
3-mmc after peak effects would be the perfect adhd medication for me but obviously it's too much serotonin to waste daily...
The problem is that any dopamine releasers that create serious task-starting inducing euphoria doesn't seem sustainable long term in terms of subjective effects... for example kratom could be euphoric for a bit more than a year, taking daily, but after that... it's "something" but not enough to induce starting tasks....

In anycase, I subjectively feel 2-fma more much dopamine dominant than 2-FA or 4f-mph, but yeah, you could be right and perhaps it's the sigma fuckery what feels so zombieish, I don't like that feeling to be honest, I only enjoy the 2-fma "rush", if we can call it that way..., the comeup, maybe?
 
My problem is task-starting, much more than sustained attention, except for super boring tasks like studying or reading/doing something I hate (like paperwork)
I guess that I don't respond well to NE releasers, but that's not the case with NE reuptake inhibitors... for me yohimbe feels pretty nice, I feel very motivated while on yohimbe, but I'm totally unfocused, same with NEP which seems to be pretty potent on NE ...
I do consider 2-fma useless but I remember that my first batch was pretty nice, and it worked nicely, but it was much more euphoric.... So, what was that? who knows, I guess we are receiving poison from China/India and not actually any pure racemic anything, let alone pure l-/d-enantiomers...
I also think you're right about euphoria and mood lift, too much is too distracting, but not enough makes everything robotic and boring, and 4f-mph and specially late batches of 2-fma feel too robotic for me , boring as fuck (but I much prefer 4f-mph as functional adhd medication).
3-mmc after peak effects would be the perfect adhd medication for me but obviously it's too much serotonin to waste daily...
The problem is that any dopamine releasers that create serious task-starting inducing euphoria doesn't seem sustainable long term in terms of subjective effects... for example kratom could be euphoric for a bit more than a year, taking daily, but after that... it's "something" but not enough to induce starting tasks....

In anycase, I subjectively feel 2-fma more much dopamine dominant than 2-FA or 4f-mph, but yeah, you could be right and perhaps it's the sigma fuckery what feels so zombieish, I don't like that feeling to be honest, I only enjoy the 2-fma "rush", if we can call it that way..., the comeup, maybe?
Grading papers, for me, was always hell on Earth, partially because of the classes I had to teach, and for that, BOTH initiation and attention were problems. Sometimes, psychostimulants alone won't do it, and the fear and dread of missing an obligation has to be added on top...

Aside from testing what you have, it's hard to say what you're getting. That's a problem with RCs, but also a problem, obviously, with medical and pharmaceutical regulation since it is hard in most countries to get affordable, convenient treatment and in sufficient doses of the right agents to effectively treat symptoms. In America, for dextroamphetamine prescription, I have to pick it up at the pharmacy on the exact right day, or else have to schedule an appointment with the physician a month early, and it is difficult to manage obligations and trips to the pharmacy during the day sometimes. The alternative is unfortunately not always being sure ahead of time what you're getting. Impurities, like unreacted reagents, leftover solvent, and so on, can definitely be in RCs, but obviously the worst case is that the substance is incorrectly or fraudulently identified. Government agencies, sometimes foreign ones (foreign to the sellers), have a habit of crashing the parties of RC sellers, which I'm sure makes the reliability of the sellers lower given they're playing a cat-and-mouse game at the same time as they're trying to offer grey-market retail services. This reliability problem happens with street drugs too, as in the case of PMA being sold as "ecstasy," which to normal people means MDMA. If the effects really feel different, testing might be a good idea, either with common reagents, or a friend in the chemistry department... That said, if other agents work better than 2-FMA, or "2-FMA," for you, I hope your loss is at least limited to the money invested in it.

I'm just speculating on (making up) the pharmacology. The 2-fluoro substitution in the ring theoretically, I'm not sure if it's been measured specifically for 2-FMA but the models are pretty well characterized, increases lipophilicity, but if that were the only relevant action, the 2-FMA would just be "more lipophilic meth," and yet the 4-fluoro substitution also increases lipophilicity, and yet 4-FMA is a much less potent compound with stronger entactogenic properties (so also not "more lipophilic meth"); calculated logP for 2-FMA is 2.3, and for 4-FMA is 2.2, which is consistent with the greater potency of 2-FMA, but is 2.1 for meth (it's a logarithmic scale, so 2-FMA is about 50% more lipophilic than meth). Another reason lipophilicity can't be the entire story is because 4-FMA intermediate in lipophilicity, but lowest in potency, and highest in entactogenic effects, there is a clearly not a linear relationship in all properties from meth -> 4-FMA -> 2-FMA. So the fluoro- ring substitution is affecting some combination of metabolism and binding properties. Non-psychedelic substituted phenethylamine tend to not bind to NE and DA receptors directly, but α2 binding could be another mechanism of anxiolysis, for example. I doubt 2-FMA is an α2 ligand, though, given it's apparent effects on vascular tone. NE release will increase α2 activation (via NE itself), but any agent that causes NE release would do so. Lipophilicity could, however, alter tissue volume distribution, even in the brain, so the biasedness towards certain NE/DA pathways might be altered, changing effects. d-meth and d-amph are already anxiolytic for most people at low doses, but also anxiogenic in higher doses (I would guess 2-FMA would become anxiogenic too, if your heart were racing and fingertips blue from >100 mg or etc.). All of this, of course, is caveated by the fact that even this rampant speculation requires that the agent in question is actually 2-FMA.

A lot of drugs, approved pharmaceuticals, plant compounds, and RCs alike, do have "rush"-like properties. And yes, subjective rushes are great for getting going, but sustained mood lift and enthusiasm is better for focus. Drugs can be tremendously beneficial in ADHD, as with many other conditions, but none are miracles, at least not yet, and at least not after tolerance and adaptation to their subjective effects. It's certainly worthwhile to get one's treatment regimen in order, but sometimes the best point of view is "I have to do this work that sucks, and I'll do it, and drug therapy will help it only suck two-thirds to three-quarters as much." Of course the more optimistic view is that medication can make already gratifying things incredibly sublime.
 
Well I decided to buy a gram of 2-fma. Been years since I’ve tried it and I think the last batch was a bad synth. Been overdoing the 4f-Mph and it’s starting to turn on me. Need something for school that doesn’t make me feel like my heart is about to explode
 
Hello guys, I have a question regarding 2-FMA, after reading psychonautwiki's guide on volumetric liquid dosing.

What solvent should I use? I've heard 2-FMA is soluble in Distilled Water, but I've seen threads of bacteria forming in users mixtures. Should I instead use Alcohol, or a mix of both?
Additionally, what mg/ml would be stable? I plan on using anywhere from 15-30mg per dose.

I've already purchased an MG scale to weigh my powder, along with 1g calibration weights, and have all the consumables such as syringes, Distilled Water and various Alcohols including Vodka.

Sorry for the barrage of questions, I'm new to this, having only dabbled in Modafinil. I'm studying a competitive course in University and have a busy lifestyle, which when compounded with the fact that I have undiagnosed ADHD (I'm currently in the process of getting a diagnosis, but the process here is extremely drawn out) makes it extremely hard for me to perform until I can get a proper prescription.

Thanks for any clarifications you guys can provide <3!
 
Hello guys, I have a question regarding 2-FMA, after reading psychonautwiki's guide on volumetric liquid dosing.

What solvent should I use? I've heard 2-FMA is soluble in Distilled Water, but I've seen threads of bacteria forming in users mixtures. Should I instead use Alcohol, or a mix of both?
Additionally, what mg/ml would be stable? I plan on using anywhere from 15-30mg per dose.

I've already purchased an MG scale to weigh my powder, along with 1g calibration weights, and have all the consumables such as syringes, Distilled Water and various Alcohols including Vodka.

Sorry for the barrage of questions, I'm new to this, having only dabbled in Modafinil. I'm studying a competitive course in University and have a busy lifestyle, which when compounded with the fact that I have undiagnosed ADHD (I'm currently in the process of getting a diagnosis, but the process here is extremely drawn out) makes it extremely hard for me to perform until I can get a proper prescription.

Thanks for any clarifications you guys can provide <3!
2-fma is not that potent. Just weight out powder. Assuming your scale is few mg +/- that’s totally fine with it.
 
Just bombed 50mg of 2-fma. From what I recall it’s a bit weaker per mg than adderall IR. With adderall I usually take 22.5mg which is followed by a 15mg redose approximately 3-4 hours later. I prefer less serotonergic activity as my sole intent with this compound is to be utilized as a study aid. I’ll report back later with an update.
 
Well 1 1/2 hour later and it lines up with my previous experiences I’ve had with it in the past so I’m glad this batch is on par, if not even better, than the stuff I had years ago. Provides a sense of alertness and clean energy without the nasty peripheral side effects that adderall can lead to. Definitely less “euphoric” than adderall, but for my purposes as a study aid it makes it even more effective. So far so good.
 
What are the major differences between BromoAmphetamine, ChloroAmphetamine, FlouroAmphetamine and IodoAmphetamine ?
 
2-fma is not that potent. Just weight out powder. Assuming your scale is few mg +/- that’s totally fine with it.
Thanks for the reply mate! Actually, I was thinking for convenience sake it would be easier to create a solution as I plan on using it 3-5 days a week for the next month or two, to get me through this busy period.

If I do follow your suggestion though, would placing a 1g calibration weight first THEN adding the powder lead to better accuracy? I forgot the source, but I read it helps.
 
Has anyone confirmed what compound they are actually consuming?

Both para and meta mon-substitutions of the amphetamines with halogens is well researched and most tended to be toxic in one way or another (neurotoxic or cardiotoxic) but I don't believe anyone expected ortho substitution to significantly alter affinity, merely alter the MW, LogP and (I would assume) pKa.

I should add that the fluorines were magnitudes less toxic - virtually the same as unsubstituted amphetamine

Unexpectedly, 4-flouro derivative of aminorex was > x4 the potency of aminorex in animal models. In that case it will certainly slow down metabolism (and the few reports mention 16 hours plus) and possibly it improves VMAT-2 transport but nobody ever asked WHY it was so significantly more potent.

Does anyone have any references for ANY ortho monosubstituted amphetamines? Everywhere I look are papers on the 'designer drug' but nothing on actual activity.

It's going to increase steric bulk and slightly move the aromatic but it's just so... unanticipated. 2-methyl amphetamine is well explored.
 
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Thanks for the reply mate! Actually, I was thinking for convenience sake it would be easier to create a solution as I plan on using it 3-5 days a week for the next month or two, to get me through this busy period.

If I do follow your suggestion though, would placing a 1g calibration weight first THEN adding the powder lead to better accuracy? I forgot the source, but I read it helps.
Well it depends on how good/cheap is your scale. Some cheapish scales tend to be less accurate when weighting out very small amounts. So check it for yourself, measure 1g + 30mg and 30mg alone.

And use your calibration weight to calibrate it from time to time. Be sure surface you measure on is perfectly leveled. Don’t measure where there are air currents.

Put to capsules for convenience rather than making solution.

Expect tolerance and some level of addictivity even with your intended dosing schedule.
 
To clarify just in case, measure 1g and add what it shows to be 30mg and than weight out that alone and see how/if it’s showing different result.
 
To clarify just in case, measure 1g and add what it shows to be 30mg and than weight out that alone and see how/if it’s showing different result.
Well it depends on how good/cheap is your scale. Some cheapish scales tend to be less accurate when weighting out very small amounts. So check it for yourself, measure 1g + 30mg and 30mg alone.

And use your calibration weight to calibrate it from time to time. Be sure surface you measure on is perfectly leveled. Don’t measure where there are air currents.

Put to capsules for convenience rather than making solution.

Expect tolerance and some level of addictivity even with your intended dosing schedule.
Got it! Also, the scale I got has this thing called a wind shelter, which should prevent the environment from skewing the results.

And absolutely, I know the nature of what I'm going to take, and will try my best to control myself.
Then again, its easy to say the above when I'm not actually on 2-FMA (still on the way), so I guess we'll see.
 
Today, purchasing RC's on the internet is a russian roulette. No trust vendors at all.
no, no trust vendors or trust anything...
now I'm so reluctant to try anything, even tryptamines and phenethylamines...
 

My German is poor but the 2,4,5-trifluoroamphetamine is mentioned.

But beware, fenfluramine is an example of how toxicity of ring-substituted amphetamines may be chronic rather than acute.

I don't think you're implying they are similar, but obviously, fenfluramine vs. a monosubstituted, especially ortho- monosubstituted, analog is not very similar, even if "fluorine is involved." Also, the n-ethyl substitution on fen makes is different. But let alone the meta- position, obviously, a carbon-carbon bond ring substitution is very different from ring halogenation. Again, I know you understand... I'm not a chemist anyway. Obviously caution is warranted no matter what, because you're right: the pharmacology of 2-FMA is not well characterized. However, cardiac valve leaflet pathology also seems poorly understood from what I can tell—guanfacine is a putative 5-HT2B agonist, but is used, if uncommonly, to treat hypertension, so it seems that post-trial evidence doesn't indicate a valvulopathy risk. Nevertheless, there might be such a risk, and others, from 2-FMA. Edit: just because it seems obviously to have, as expected, pro-hypertensive and a positive chronotrope, as could be explained by NE release/reuptake inhibition, the usual chronic risks, like cardiomyopathy, caution is obviously warranted even w/ out knowledge of novel ways it might cause harms. Some are clear!

I've found 2-FMA mentioned in patent apps (US 2022/0152088 A1) and patents (11,045,465 B2), but certainly not relating to its potential legitimate application as a pharmaceutical.
 
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No - I'm not suggesting that. But aminorex was another stimulant that proved to have 5HT2b activity proved to be chronically cardiotoxic. It's just one of those things that medicinal chemists are wary of. Any new medicine would specifically be tested for such activity.

The N substitution was not involved in the 5HT2b affinity of fenfluramine. N-dealkylation occurs and the primary amine actually had MORE 5HT2b affinity.

I was merely reminding people that ring-substituted amphetamines have a pretty bad record. Sibutramine (look closely, it's got the p-Cl amphetamine scaffold within it) and phentermine are two more examples that proved to be cardiotoxic.

Put simply, such simple molecules don't tend to be especially selective BUT ring-substitution can produce unsought selectivity.

I posted that German patent merely because it was the only related compound I could find and if you read it, it does actually cover a number of different ring-substitutions. Sadly my German isn't good enough for me to draw much inference from it and hoped that someone else might be able to shed some more light on the topic.

As previously stated, I think medicinal chemists presumed that an ortho substitution wouldn't make much of a difference BUT ortetamine shows that certain ortho substitutions can make a big difference. I'm speculating that the increased steric bulk means that VMAT2 cannot actively transport.
 
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