3-FA

From PsychonautWiki
Jump to navigation Jump to search
Summary sheet: 3-FA
3-FA
3-FA.svg
Chemical Nomenclature
Common names 3-FA, PAL-353
Substitutive name 3-Fluoroamphetamine
Systematic name 1-(3-Fluorophenyl)-2-propanamine
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 10 mg
Light 20 - 30 mg
Common 30 - 50 mg
Strong 50 - 70 mg
Heavy 70 mg +
Duration
Total 4 - 6 hours
Onset 20 - 60 minutes
Come up 30 - 60 minutes
Peak 2 - 3 hours
Offset 1 - 1.5 hours
After effects 2 - 6 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


3-Fluoroamphetamine (3-FA) is a synthetic ring-substituted fluorinated amphetamine compound that produces potent classical stimulant effects that has been claimed to be "almost equipotent" with methamphetamine.[1] It is one part of a series of designer fluorinated amphetamine analogs such as 2-FA, 2-FMA, 3-FEA, and 4-FA that are known for their euphoric and stimulating effects and growing popularity as research chemical substitutes for classical street stimulants.

3-FA is rarely found on the streets, and only sometimes sold as a grey market research chemical through online vendors.[2][3]

Chemistry

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 norepinephrine releasing 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 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
Child.svg

After effects
Aftereffects (3).svg

Cognitive effects
User.svg


Experience reports

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

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 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 all dopaminergic stimulants, 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.

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).[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 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.[8][9]
  • 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.[10]
  • 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

Handcuffs-300px.png

This legality section is a stub.

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.[11]
  • Germany: 3-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: 3-FA is an amphetamine analogue, so is a Schedule 3 controlled substance in New Zealand.[15]
  • Switzerland: 3-FA is a controlled substance specifically named under Verzeichnis E.[16]
  • Turkey: 3-FA is classed as a drug and is illegal to possess, produce, supply, or import.[17] [18]
  • 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.[19]
  • 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]

See also

External links

References

  1. ↑ Negus, S. S., Mello, N. K., Blough, B. E., Baumann, M. H., Rothman, R. B. (February 2007). "Monoamine Releasers with Varying Selectivity for Dopamine/Norepinephrine versus Serotonin Release as Candidate "Agonist" Medications for Cocaine Dependence: Studies in Assays of Cocaine Discrimination and Cocaine Self-Administration in Rhesus Monkeys". Journal of Pharmacology and Experimental Therapeutics. 320 (2): 627–636. doi:10.1124/jpet.106.107383. ISSN 0022-3565. 
  2. ↑ 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. 
  3. ↑ 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. 
  4. ↑ 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. 
  5. ↑ 5.0 5.1 5.2 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. 
  6. ↑ Hofmann, F. G. (1983). A handbook on drug and alcohol abuse: the biomedical aspects (2nd ed ed.). Oxford University Press. ISBN 9780195030563. 
  7. ↑ http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf
  8. ↑ 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. 
  9. ↑ 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. 
  10. ↑ 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. 
  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. ↑ Misuse of Drugs Act 1971 


Retrieved from ‘https://psychonautwiki.org/w/index.php?title=3-FA&oldid=162169’