|Summary sheet: 3-FMA|
|Routes of Administration|
3-Fluoromethamphetamine (also known as 3-FMA) is a novel synthetic ring-substituted fluorinated amphetamine compound that produces entactogenic and stimulant effects when administered. Following the introduction of 3-FEA, 3-FMA subsequently entered the designer drug market as a compound structurally related to a series of fluorinated substituted amphetamines that originally included compounds such as 2-FMA, 3-FA, 4-FMA, 4-FA.
Like its parent compound 3-FA, the pharmacological, toxicological, and subjective effects of 3-FMA in humans have yet to be mapped out in detail. Early reports have so far characterized 3-FMA as a moderately potent serotonin-dominant triple monoamine releaser (or reuptake inhibitor) that produces a relatively short-lived balance of entactogenic and stimulant effects. Based on related compounds, it is not unreasonable to speculate that this compound possesses neurotoxic, cardiotoxic and other potential to-be-discovered toxic properties, which is why extreme caution is advised.
3-FMA has an extremely short history of recreational use and has yet to be documented being sold on the streets. It has recently been made available for sale on the gray market as a research chemical through online vendors. The appearance of it as well as 3-FEA on the research chemicals market coincides with the increased efforts to control the popular entactogenic stimulant 4-FA.
Due to its potent psychostimulant effect, likely habit-forming properties as well as unknown toxicity profile, it is strongly recommended that one use proper harm reduction practices if choosing to use this substance.
3-FMA, or 3-fluoromethamphetamine, is a synthetic molecule of the amphetamine family. Molecules of the amphetamine family contain a phenethylamine core featuring a phenyl ring bound to an amino (NH2) group through an methyl chain with an additional methyl substitution at Rα (i.e. amphetamines are alpha-methylated phenethylamines). 3-FMA is the 3-position fluorinated analog methamphetamine; however, it is currently speculated to behave more in the manner of shorter-lived entactogenic stimulant. Additionally, is is also a positional isomer of 2-FMA and 4-FMA.
This pharmacology section is incomplete.
You can help by adding to it.
Although 3-FMA has not been formally studied on the same level as traditional amphetamines, it is currently assumed that like other substituted amphetamines with substitutions at similar positions, it most likely acts primarily as a triple releasing agent of serotonin, dopamine, and norepinephrine.
|This subjective effects section is a stub.|
As such, it is still in progress and may contain incomplete or wrong information.
You can help by expanding or correcting it.
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 PsychonautWiki contributors. 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 ☠. Early reports suggest 3-FMA has an effect profile that lies in between that of 4-FMA and 2-FMA, possessing both the functional properties of 2-FMA and the euphoric properties of 4-FMA. At lower doses, it has been reported to lean towards functional and productive use, while as one increases the dose, the euphoria becomes both more prevalent as well as distracting.
- Tactile enhancement - This component primarily tends to occur at higher doses only and is rarely observed lower to medium doses.
- Physical euphoria
- Appetite suppression
- Increased heart rate
- Increased perspiration
- Teeth grinding - This component can be considered to be less intense when compared with that of MDMA as well as 2-FMA.
- 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:
- Cognitive euphoria
- Thought acceleration
- Focus enhancement
- Anxiety suppression
- Analysis enhancement
- Motivation enhancement
- Compulsive redosing
- Increased music appreciation - This component primarily tends to happen at higher doses only, as low to medium doses of 3-FMA are more focused and productivity-oriented.
- Time distortion - This can be described as the experience of time speeding up and passing much quicker than it usually would when sober.
Anecdotal reports which describe the effects of this compound within our experience index include:
Toxicity and harm potential
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.
The toxicity and long-term health effects of human recreational 3-FMA use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because 3-FMA has an extremely short history of human usage, becoming available only in mid-2017. Anecdotal evidence from people who have tried 3-FMA within the community suggests that there do not seem to be any negative health effects attributed to simply trying this drug at low to moderate doses by itself and using it sparingly (but nothing can be completely guaranteed).
Due to its putative serotonin-releasing and entactogenic properties, it is possible that 3-FMA may display excess activity at the 5-HT2b receptor, which, would make it cardiotoxic with long-term use as seen in other 5-HT2b agonists such as fenfluramine and MDMA.
It is perhaps worth noting that in the field of medicinal chemistry, the fluorine substitution is sometimes seen as desirable in central nervous system pharmaceutical agents, and is a common practice due to the corresponding increase in lipophilicity granted by the substitute.
It is strongly recommended that one use harm reduction practices when using this drug.
Tolerance and addiction potential
Although it still remains to be seen, the chronic use of 3-FMA likely can be considered moderately addictive with a high potential for abuse and capable of causing psychological dependence among a certain population of users. When dependence or addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage.
Tolerance to many of the effects of 3-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 - 10 days to be back at baseline (in the absence of further consumption). 3-FMA presents cross-tolerance with all dopaminergic and serotonergic stimulants and entactogens, meaning that after the consumption of 3-FMA all stimulants will have a reduced effect (including atypical stimulants one might not expect, like MDMA or amphetamine due to its reliance on dopamine and norepinephrine to exert its full euphoric effect).
Abuse of compounds within the amphetamine chemical 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). A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely. The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis. Psychosis very rarely arises from therapeutic use.
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 overcome the user and cause respiratory arrest.
- Opioids - Stimulants increase respiration rate allowing a higher dose of opiates. 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.
- 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 psychoses that resemble schizophrenia, but not worse than the psychoses 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.
- PCP - Increases risk of tachycardia, hypertension, and manic states.
- Methoxetamine - Increases risk of tachycardia, hypertension, and manic states.
- Psychedelics (e.g. LSD, mescaline, psilocybin) - Increases risk of anxiety, paranoia, and thought loops.
- 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.
- 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.
This legality section is a stub.
As such, it may contain incomplete or wrong information. You can help by expanding it.
3-FMA is currently a grey area compound within many parts of the world. People may still be charged for its possession under certain circumstances such as under analogue laws and with intent to sell or consume.
- Canada: 3-FMA would be considered Schedule I as it is an analogue of Amphetamine.
- China: As of October 2015 3-FMA is a controlled substance in China.
- Germany: 3-FMA is controlled under Anlage I BtMG (Narcotics Act, Schedule I) as of December 13, 2014. It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.
- New Zealand: 3-FMA is an amphetamine analogue, so is a Schedule 3 controlled substance in New Zealand.
- Switzerland: 3-FMA is a controlled substance specifically named under Verzeichnis E.
- Turkey: 3-FMA is a classed as drug and is illegal to possess, produce, supply, or import. 
- United Kingdom: 3-FMA is considered a Class A drug as a result of the amphetamine analog clause of the Misuse of Drugs Act 1971.
- United States: 3-FMA may be considered an analogue of amphetamine under the Federal Analogue Act. The Federal Analogue Act, 21 U.S.C. § 813, is a section of the United States Controlled Substances Act, allowing any chemical "substantially similar" to an illegal drug (in Schedule I or II) to be treated as if it were also in Schedule I or II, but only if it is intended for human consumption.
- ↑ Rösner, P., Quednow, B., Girreser, U., Junge, T. (March 2005). "Isomeric Fluoro-methoxy-phenylalkylamines: a new series of controlled-substance analogues (designer drugs)". Forensic Science International. 148 (2–3): 143–156. doi:10.1016/j.forsciint.2004.05.003. ISSN 0379-0738.
- ↑ Smart, B. E. (1 June 2001). "Fluorine substituent effects (on bioactivity)". Journal of Fluorine Chemistry. 109 (1): 3–11. doi:10.1016/S0022-1139(01)00375-X. ISSN 0022-1139.
- ↑ 3.0 3.1 3.2 Shoptaw, S. J., Kao, U., Ling, W. (21 January 2009). Cochrane Drugs and Alcohol Group, ed. "Treatment for amphetamine psychosis". Cochrane Database of Systematic Reviews. doi:10.1002/14651858.CD003026.pub3. ISSN 1465-1858.
- ↑ Hofmann, F. G. (1983). A handbook on drug and alcohol abuse: the biomedical aspects (2nd ed ed.). Oxford University Press. ISBN 9780195030563.
- ↑ http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf
- ↑ Greenwald, M. K., Lundahl, L. H., Steinmiller, C. L. (December 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 (13): 2624–2637. doi:10.1038/npp.2010.175. ISSN 0893-133X.
- ↑ Siciliano, C. A., Saha, K., Calipari, E. S., Fordahl, S. C., Chen, R., Khoshbouei, H., Jones, S. R. (10 January 2018). "Amphetamine Reverses Escalated Cocaine Intake via Restoration of Dopamine Transporter Conformation". The Journal of Neuroscience. 38 (2): 484–497. doi:10.1523/JNEUROSCI.2604-17.2017. ISSN 0270-6474.
- ↑ Krystal, J. H., Perry, E. B., Gueorguieva, R., Belger, A., Madonick, S. H., Abi-Dargham, A., Cooper, T. B., MacDougall, L., Abi-Saab, W., D’Souza, D. C. (1 September 2005). "Comparative and Interactive Human Psychopharmacologic Effects of Ketamine and Amphetamine: Implications for Glutamatergic and Dopaminergic Model Psychoses and Cognitive Function". Archives of General Psychiatry. 62 (9): 985. doi:10.1001/archpsyc.62.9.985. ISSN 0003-990X.
- ↑ Branch, L. S. (2022), Consolidated federal laws of Canada, Controlled Drugs and Substances Act
- ↑ 关于印发《非药用类麻醉药品和精神药品列管办法》的通知 | http://www.sfda.gov.cn/WS01/CL0056/130753.html
- ↑ "Anlage I BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 19, 2019.
- ↑ "Achtundzwanzigste Verordnung zur Änderung betäubungsmittelrechtlicher Vorschriften" (in German). Bundesanzeiger Verlag. Retrieved December 19, 2019.
- ↑ "§ 29 BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 19, 2019.
- ↑ Misuse of Drugs Act 1975 No 116 (as at 01 July 2022), Public Act – New Zealand Legislation
- ↑ "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020.
- ↑ Başbakanlık Mevzuatı Geliştirme ve Yayın Genel Müdürlüğü
- ↑ https://resmigazete.gov.tr/eskiler/2014/01/20140125-3-1.pdf
- ↑ Misuse of Drugs Act 1971