This is an unofficial archive of PsychonautWiki as of 2025-08-08T03:33:20Z. Content on this page may be outdated, incomplete, or inaccurate. Please refer to the original page for the most up-to-date information.
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.
3-FA, or 3-Fluoroamphetamine, is a synthetic molecule of the 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). 3-FA does not contain a methyl group bound to the terminal amine RN of the amphetamine core, which renders it structurally and functionally similar to amphetamine. 3-FA is the 3-fluorinated analogue of amphetamine.
Pharmacology
Although 3-FA has not been formally studied on the same level as traditional amphetamines, it is not unreasonable to assume that just like other substituted amphetamines with substitutions at similar positions (with the notable exception of 4-FA), it most likely acts primarily as both a dopamine and norepinephrinereleasing agent, with modest selectivity for serotonin. This means it effectively increases the levels of the norepinephrine and dopamine neurotransmitters in the brain by binding to and partially blocking the transporter proteins that normally clear and reuptake those molecules from the synaptic cleft for future reuse. This allows dopamine and norepinephrine to accumulate within the brain to extra-endogenous degrees, which is known to produce stimulating, motivatory and euphoric effects in humans.
Subjective effects
3-FA is considered to be a potent and complex stimulant with mild entactogenic undertones when compared to other substances its class, like 4-FA. However, it does not have the productivity and focus-enhancing effects often claimed by users of 2-FA or 2-FMA which has had the effect of limiting its appeal.
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 ☠.
Teeth grinding - This component can be considered to be less intense when compared with that of MDMA as well as 2-FMA.
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:
Increased music appreciation - This component primarily tends to happen at higher doses only, as low to medium doses of 3-FA 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.
Experience reports
Anecdotal reports which describe the effects of this compound within our experience index include:
The toxicity and long-term health effects of recreational 3-FA use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because 3-FA has an extremely short history of human usage. Anecdotal evidence from people who have tried 3-FA 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).
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.[4]
Regardless, due to its novelty and unstudied nature, it is strongly recommended that one use harm reduction practices if experimenting with this substance.
Tolerance and addiction potential
As with other stimulants, the chronic use of 3-FA can be considered moderately addictive with a high potential for abuse and is 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-FA 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-FA presents cross-tolerance with [[Cross-tolerance::all dopaminergicstimulants]], meaning that after the consumption of 3-FA all stimulants will have a reduced effect (especially including atypical stimulants one might not expect, like MDMA due to its reliance on dopamine and norepinephrine to exert its full euphoric effect).
Given its claimed equipotency to methamphetamine it may be similarly difficult to dose. 3-FA has not been studied to the same degree as other amphetamines, so its toxicity profile in humans is subject to speculation and has yet to be scientifically validated. Thus, it is strongly recommended that one use harm reduction practices when using this substance.
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).[5] A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[5][6] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[5] Psychosis very rarely arises from therapeutic use.[7]
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.[8] 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.[9][10]
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.[11]
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.
3-FA is currently a grey area compound within all parts of the world, meaning its regulation lies in a legal grey 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 intent to sell or consume.
China: As of October 2015 3-FA is a controlled substance in China.[12]
France: As of december 2024, 3-FA is not explicitly scheduled. It is thus legal to possess, although in a grey area.[13]
Germany: 3-FA is controlled under the NpSG (New Psychoactive Substances Act)[14] as of November 26, 2016.[15] Production and import with the aim to place it on the market, administration to another person and trading is punishable. Possession is illegal but not penalized.[16]
New Zealand: 3-FA is an amphetamine analogue, so is a Schedule 3 controlled substance in New Zealand.[17]
Switzerland: 3-FA is a controlled substance specifically named under Verzeichnis E.[18]
The Netherlands: 3-FA is a controlled substance as of July 1, 2025. [19]
Turkey: 3-FA is classed as a drug and is illegal to possess, produce, supply, or import.[20][21]
United Kingdom: 3-FA is considered a Class A drug as a result of the amphetamine analogue clause of the Misuse of Drugs Act 1971.[22]
United States: 3-FA may be considered to be an analog of amphetamine, thus falling 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.[citation needed]
↑Rösner, P., Quednow, B., Girreser, U., Junge, T. (10 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. ISSN0379-0738.
↑Camilleri, A., Johnston, M. R., Brennan, M., Davis, S., Caldicott, D. G. E. (15 April 2010). "Chemical analysis of four capsules containing the controlled substance analogues 4-methylmethcathinone, 2-fluoromethamphetamine, alpha-phthalimidopropiophenone and N-ethylcathinone". Forensic Science International. 197 (1–3): 59–66. doi:10.1016/j.forsciint.2009.12.048. ISSN1872-6283.
↑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)
