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2-Fluoromethamphetamine (also known as 2-FMA) is a novel stimulant substance of the amphetamine class. It is a structural analog of methamphetamine and is related to 2-FA, 3-FA, and 4-FMA. 2-FMA produces its stimulant effects through action at dopamine and norepinephrine receptors in the brain.
WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.
DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.
The sale of 2-FMA on the online research chemical market was first reported in August 2007.[1]. It appeared alongside other fluorinated amphetamines like 2-FA and 4-FA. It appears to be unknown in the clinical and research literature.
Very little data exists about the pharmacological properties, metabolism, and toxicity of 2-FMA. It is strongly advised to use harm reduction practices if using this substance.
2-Fluoromethamphetamine (2-FMA) is a synthetic molecule of the substituted amphetamine class. Molecules of the amphetamine class contain a phenethylamine core featuring a phenyl ring bound to an amino (NH2) group through an ethyl chain with an additional methyl substitution at Rα (i.e., amphetamines are alpha-methylated phenethylamines). 2-FMA contains a methyl group bound to the terminal amine RN of the amphetamine core, a substitution it shares with methamphetamine.
2-FMA is the 2-position fluorinated analog of methamphetamine and the N-methylated homolog of 2-FA (2-fluoroamphetamine).
Although 2-FMA has not been formally studied on the same level as traditional amphetamines, it is thought that it acts as both a dopamine and norepinephrinereleasing agent. This means it effectively increases the levels of the norepinephrine and dopamine in the brain by binding to and partially blocking the transporter proteins that normally remove them from the synaptic cleft. This allows dopamine and norepinephrine to accumulate within the brain, resulting in stimulating and euphoric effects.
Subjective effects
In comparison to other substituted amphetamines, 2-FMA is reported to be relatively free of side effects such as nausea, high blood pressure, anxiety and an uncomfortable offset ("comedown"). It is considered to be a functional stimulant for performing general productivity tasks in a manner similar to amphetamine or lisdexamfetamine (Vyvanse). However, at higher doses, it typically loses its productivity and focus-enhancing effects and begins to take on a recreational character due to the distracting euphoria that it can produce. Majority of users report through anecdotal reports that this has a ceiling effect with high dose (Heavy+) ranges where many report of the uncomfortable effects from stimulants when passing or entering the strong-heavy dose range.
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWikicontributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
Physical effects
Stimulation - In terms of its effects on the physical energy levels of the user, 2-FMA is usually considered to be very energetic and stimulating in a fashion that is slightly weaker to that of methamphetamine, but stronger than that of modafinil, caffeine, and methylphenidate. The particular style of stimulation which 2-FMA presents can be described as forced, but compared to many other stimulants such as amphetamine many describe it as a very "clean" stimulation. This means that, at higher dosages, it becomes difficult or impossible to keep still as jaw clenching, involuntary bodily shakes and vibrations become present, resulting in extreme shaking of the entire body, unsteadiness of the hands, and a general loss of fine motor control.
The visual effects of 2-FMA are usually less consistent and only mildly noticeable at higher dosages. They are somewhat comparable to deliriants and occur more readily in darker areas.
Distortions
Drifting(breathing and morphing) - This effect is usually subtle and barely noticeable and only occurs at higher dosages or when combined with cannabis.
Brightness alteration - 2-FMA can make spaces seem brighter as a result of its pupil dilating effects.
Hallucinatory states
Transformations - This effect occurs very rarely, and typically only when the user has taken high doses, is coming down, or has been awake for unusually long periods. It is usually very mild when it does occur.
Time distortion - This can be described as the experience of time speeding up and passing much quicker than it usually would when sober.
After effects
The effects which occur during the offset of a stimulant experience generally feel negative and uncomfortable in comparison to the effects which occurred during its peak. This is often referred to as a "comedown" and occurs because of neurotransmitter depletion. Its effects commonly include:
This toxicity and harm potential section is a stub.
As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it. Note: Always conduct independent research and use harm reduction practices if using this substance.
The toxicity and long-term health effects of recreational 2-FMA use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because 2-FMA has a very limited history of human usage.
Anecdotal reports from those who have tried 2-FMA suggest that there do not seem to be any negative health effects attributed to simply trying this substance at low to moderate doses by itself or using it sparingly (but nothing can be completely guaranteed).
As with other stimulants, the chronic use of 2-FMA can be considered moderately addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage.
Tolerance to many of the effects of 2-FMA develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). 2-FMA presents cross-tolerance with [[Cross-tolerance::all dopaminergicstimulants]], meaning that after the consumption of 2-FMA all stimulants will have a reduced effect.
The use of compounds in the amphetamine class at high dosages for prolonged periods of time can potentially result in a stimulant psychosis that may present with a variety of symptoms (e.g., paranoia, hallucinations, or delusions).[2][3] A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[3][4] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[3]
Dangerous interactions
Warning:Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
Alcohol - Drinking alcohol on stimulants is considered risky because it reduces the sedative effects of the alcohol that the body uses to gauge drunkenness. This often leads to excessive drinking with greatly reduced inhibitions, increasing the risk of liver damage and increased dehydration. The effects of stimulants will also allow one to drink past a point where they might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel the alcohol and the stimulant less.
GHB/GBL - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the depressant effects of the GHB/GBL may over come the user and cause respiratory arrest.
Benzodiazepines - These substances can strongly mitigate the comedown of Stimulants and allow higher doses of them, which is a dangerous combination. And through the habit-forming properties, these substances should be consumed with extreme caution.
Opioids - Opioids combined with amphetamines have been found to potentially synergize unpredictably, increasing the chance of overdose.[5] Stimulants also increase respiration rate allowing a higher dose of opioids. If the stimulant wears off first, then the opiate may overcome the patient and cause respiratory arrest.
Cocaine - The rewarding effects of cocaine are mediated by DAT inhibition, and an increase of exocytosis of dopamine through the cell membrane. Amphetamine reverses the direction of DAT and the direction vesicular transports within the cell by a pH mediated mechanism of displacement, thus excludes the regular mechanism of dopamine release through means of exocytosis because the effects Na+/K+ ATPase are inhibited. You will find cardiac effects with the combination of cocaine and amphetamine due to a SERT mediated mechanism from the subsequent activation of 5-HT2B, which is an effect of serotonin-related valvulopathy. Amphetamines generally cause hypertension in models of abuse, and this combination can increase the chances of syncope due to turbulent blood flow during valve operation. The rewarding mechanisms of cocaine are reversed by administration of amphetamine.[6][7]
Cannabis - Stimulants increase anxiety levels and the risk of thought loops and paranoia, which can lead to negative experiences.
Caffeine - This combination of stimulants is generally considered unnecessary and may increase strain on the heart, as well as potentially causing anxiety and physical discomfort.
Tramadol - Tramadol and stimulants both increase the risk of seizures.
DXM - Both substances raise heart rate; in extreme cases, panic attacks caused by these substances have led to more serious heart issues.
Ketamine - Combining amphetamine and ketamine may result in psychosis that resembles schizophrenia, but not worse than the psychosis produced by either substance alone, but this is debatable. This is due to amphetamines ability to attenuated the disruption of working memory caused by ketamine. Amphetamine alone may result in grandiosity, paranoia, or somatic delusions with little to no effect on negative symptoms. Ketamine, however, will result in thought disorders, disruption of executive functioning, and delusions due to a modification of conception. These mechanisms are due to an increase of dopaminergic activity in the mesolimbic pathway caused by amphetamine due to its pharmacology effecting dopamine, and due to a disruption of dopaminergic functioning in the mesocortical pathways via NMDA antagonism effects of ketamine. Combining the two, you may expect mainly thought disorder along with positive symptoms.[8]
PCP - Increases risk of tachycardia, hypertension, and manic states.
Methoxetamine - Increases risk of tachycardia, hypertension, and manic states.
Gabapentinoids - Gabapentinoids like Pregabalin or Gabapentin can mitigate the comedown of Stimulants, but through the very fast tolerance development the effects will become less after a few days
25x-NBOMe - Amphetamines and NBOMes both provide considerable stimulation that when combined they can result in tachycardia, hypertension, vasoconstriction and, in extreme cases, heart failure. The anxiogenic and focusing effects of stimulants are also not good in combination with psychedelics, as they can lead to unpleasant thought loops. NBOMes are known to cause seizures, and stimulants can increase this risk.
2C-T-x - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
5-MeO-xxT - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
DOx
aMT - aMT has MAOI properties which may interact unfavorably with amphetamines.
MAOIs - MAO-B inhibitors can increase the potency and duration of phenethylamines unpredictably. MAO-A inhibitors with amphetamine can lead to hypertensive crises.
Acetazolamide - Administration may increase serum concentration of amphetamine.
Ascorbic acid - Lowers urinary pH; may enhance amphetamine excretion.
Furazolidone - Amphetamines may induce a hypertensive response in patients taking furazolidone.
Guanethidine - Amphetamine inhibits the antihypertensive response to guanethidine.
Haloperidol - Limited evidence indicates that haloperidol may inhibit the effects of amphetamine but the clinical importance of this interaction is not established.
Lithium carbonate - Isolated case reports indicate that lithium may inhibit the effects of amphetamine.
Norepinephrine - Amphetamine abuse may enhance the pressor response to norepinephrine.
Phenothiazines - Amphetamine may inhibit the antipsychotic effect of phenothiazines, and phenothiazines may inhibit the anorectic effect of amphetamines.
Sodium bicarbonate - Large doses of sodium bicarbonate inhibit the elimination of amphetamine, thus increasing the amphetamine effect.
TCAs - Theoretically increases the effect of amphetamine, but clinical evidence is lacking.
As such, it may contain incomplete or wrong information. You can help by expanding it.
2-FMA is currently a gray area compound within all parts of the world, meaning its regulation lies in a legal gray area and that it is not known to be specifically illegal ("scheduled") within any country. However, people may still be charged for its possession under certain circumstances such as under analogue laws and with the intent to sell or consume.
Canada: 2-FMA would be considered Schedule I as it is an analogue of Amphetamine.[9]
China: As of October 2015 2-FMA is a controlled substance in China.[10]
France: As of december 2024, 2-FMA is not explicitly scheduled. It is thus legal to possess, although in a grey area.[11]
Germany: 2-FMA is controlled under Anlage I BtMG (Narcotics Act, Schedule I)[12] as of December 13, 2014.[13] It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.[14]
New Zealand: 2-FMA is an amphetamine analogue, so is a Schedule 3 controlled substance in New Zealand.[15]
Switzerland: 2-FMA is a controlled substance specifically named under Verzeichnis E.[16]
Turkey: 2-FMA is a classed as drug and is illegal to possess, produce, supply, or import.[17][18]
The Netherlands: 2-FMA is a controlled substance as of July 1, 2025. [19]
United Kingdom: 2-FMA is considered a Class A drug as a result of the amphetamine analogue clause of the Misuse of Drugs Act 1971.[20]
Ukraine: 2-FMA is considered a narcotic and is illegal.[21]
↑Hofmann, F. G. (1983). A handbook on drug and alcohol abuse: the biomedical aspects (2nd ed ed.). Oxford University Press. ISBN9780195030563.CS1 maint: Extra text (link)
↑Greenwald, M. K., Lundahl, L. H., & Steinmiller, C. L. (2010). "Sustained release d-amphetamine reduces cocaine but not 'speedball'-seeking in buprenorphine-maintained volunteers: A test of dual-agonist pharmacotherapy for cocaine/heroin polydrug abusers". Neuropsychopharmacology. 35: 2624–2637. doi:10.1038/npp.2010.175.
↑"关于印发《非药用类麻醉药品和精神药品列管办法》的通知" (in Chinese). China Food and Drug Administration. 27 September 2015. Retrieved 1 October 2015.CS1 maint: Unrecognized language (link)
