2-FA

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Summary sheet: 2-FA
2-FA
2-FA.svg
Chemical Nomenclature
Common names 2-FA
Substitutive name 2-Fluoroamphetamine
Systematic name 1-(2-Fluorophenyl)propan-2-amine
Class Membership
Psychoactive class Stimulant
Chemical class Amphetamine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.



⇣ Oral
Dosage
Threshold 5 mg
Light 15 - 30 mg
Common 30 - 50 mg
Strong 50 - 60 mg
Heavy 60 mg +
Duration
Total 2 - 4 hours
Onset 15 - 30 minutes
Come up 15 - 30 minutes
Peak 1 - 2 hours
Offset 1 - 1.5 hours









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.

Interactions
Alcohol
GHB
GBL
Opioids
Cocaine
Cannabis
Caffeine
Ketamine
Methoxetamine
Psychedelics
DXM
PCP
25x-NBOMe
2C-T-x
5-MeO-xxT
DOx
Tramadol
aMT
MAOIs


2-Fluoroamphetamine (also known as 2-FA) is a novel stimulant substance of the amphetamine class. It is a structural analog of amphetamine and is presumed to possess a similar mechanism of action, promoting the release of dopamine and norepinephrine in the brain.

2-FA is part of a series of amphetamine analogs that first appeared on the online research chemical market in the 2010s.[1][2] These compounds include 2-FMA, 3-FA, 3-FEA and 4-FA and are reported to produce a range of stimulating and euphoric effects, many of which have been used as research chemical substitutes for classical street stimulants and entactogens.[citation needed] Of these, 2-FA is considered to be most amphetamine-like in its subjective effects. It is commonly compared to the d-isomer of amphetamine (dexedrine).

2-FA is commonly taken orally. While capable of being taken via insufflation or vaporization, this has been reported to be highly unpleasant and noxious compared to its parent compound. Despite some users reporting efficacy as an alternative to prescription stimulants for ADHD, little is known about the potential toxicological effects that accompany its long-term use as a substitute for prescribed stimulants.

Very little data exists about the pharmacological properties, metabolism, and toxicity of 2-FA. It is highly advised to use harm reduction practices if using this substance.

Chemistry

Generic structure of a amphetamine molecule

2-FA, or 2-Fluoroamphetamine, is a synthetic molecule of the amphetamine family. 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). Unlike its close analogue 2-FMA, 2-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. 2-FA is the 2-position fluorinated analogue of amphetamine.

Pharmacology

Although 2-FA has not been formally studied on the same level as traditional amphetamines, it is safe 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 norepinephrine releasing agent. 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 those monoamines from the synaptic cleft. This allows dopamine and norepinephrine to accumulate within the brain to extra-endogenous levels, resulting in stimulating, motivating and euphoric effects.

Subjective effects

In comparison to other substituted amphetamines, 2-FA 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 and effective psychoactive substance for performing general productivity tasks in a manner that is similar to dextroamphetamine. However, at higher doses, it reportedly loses its productivity and attention-enhancing effects and begins to take on a recreational character due to the distracting euphoria and overstimulation that can result. However, it is often said that it possesses a "ceiling dose" that purportedly lowers the abuse threshold relative to methamphetamine, although this has yet to be scientifically demonstrated.

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 ☠.

Physical effects
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Cognitive effects
User.svg

After effects
Aftereffects (3).svg


Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

Further information: Research chemicals § Toxicity and harm potential

The toxicity and long-term health effects of recreational 2-FA use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because 2-FA has very little history of human usage. Anecdotal evidence from people who have tried 2-FA within the community suggest 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). Others have commented that its d-isomer form is virtually similar to the effects of d-amphetamine, and thus far little has been shown to give reason to suspect that its toxicity is radically different (though future evidence to the contrary may prove otherwise).

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.[3]

It is strongly recommended that one use harm reduction practices when using this drug.

Tolerance and addiction potential

As with other stimulants, the chronic use of 2-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 2-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). 2-FA presents cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of 2-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).

In a analogous way tolerance to amphetamine relates to tolerance on methamphetamine, 2-FA has been observed to have a similar relationship to its more popular relative, 2-FMA.

Psychosis

Main article: Stimulant psychosis

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).[4] A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[4][5] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.Cite error: Closing </ref> missing for <ref> tag[6]

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 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.[7][8]
  • 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.[9]
  • 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.
    • 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.

Legal status

2-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.

  • Canada: 2-FA would be considered Schedule I as it is an analogue of Amphetamine.[10]
  • China: As of October 2015 2-FA is a controlled substance in China.[11]
  • Germany: 2-FA is controlled under the NpSG (New Psychoactive Substances Act)[12] as of November 26, 2016.[13] 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.[14]
  • New Zealand: 2-FA is an amphetamine analogue, so is a Schedule 3 controlled substance in New Zealand.[15]
  • Switzerland: 2-FA is a controlled substance specifically named under Verzeichnis E.[16]
  • Turkey: 2-FA is a classed as drug and is illegal to possess, produce, supply, or import.[17] [18]
  • The Netherlands: 2-FA is currently legal, but it is part of a substance group that may be banned soon as part of a recently passed law on New Psychoactive Substances (NPS). [19]
  • United Kingdom: 2-FA is considered a Class A drug as a result of the amphetamine analog clause of the Misuse of Drugs Act 1971.[20]
  • United States: 2-FA may be considered to be an analogue of amphetamine under the Federal Analogue Act and thus a Schedule II drug. 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.

See also

External links

References

  1. ↑ 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. ISSN 0379-0738. 
  2. ↑ 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. ISSN 1872-6283. 
  3. ↑ 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. 
  4. ↑ 4.0 4.1 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. 
  5. ↑ Hofmann, F. G. (1983). A handbook on drug and alcohol abuse: the biomedical aspects (2nd ed ed.). Oxford University Press. ISBN 9780195030563. 
  6. ↑ http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf
  7. ↑ 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. 
  8. ↑ 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. 
  9. ↑ 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. 
  10. ↑ Branch, L. S. (2022), Consolidated federal laws of Canada, Controlled Drugs and Substances Act 
  11. ↑ "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. 
  12. ↑ "Anlage NpSG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 19, 2019. 
  13. ↑ "Gesetz zur Bekämpfung der Verbreitung neuer psychoaktiver Stoffe" (PDF) (in German). Bundesanzeiger Verlag. Retrieved December 19, 2019. 
  14. ↑ "§ 4 NpSG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 19, 2019. 
  15. ↑ Misuse of Drugs Act 1975 No 116 (as at 01 July 2022), Public Act – New Zealand Legislation 
  16. ↑ "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  17. ↑ Başbakanlık Mevzuatı Geliştirme ve Yayın Genel Müdürlüğü 
  18. ↑ https://resmigazete.gov.tr/eskiler/2014/01/20140125-3-1.pdf
  19. ↑ Wijziging van de Opiumwet in verband met het toevoegen van een derde lijst met als doel het tegengaan van de productie van en de handel in nieuwe psychoactieve stoffen en enkele andere wijzigingen (Dutch), 2024 
  20. ↑ Misuse of Drugs Act 1971 


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