From PsychonautWiki
(Redirected from 3fluoroethamphetamine)
Jump to: navigation, search
Summary sheet: 3-FEA
Molecular structure of 3-FEA
Chemical Nomenclature
Common names 3-FEA
Substitutive name 3-Fluoroethamphetamine
Systematic name N-Ethyl-1-(3-fluorophenyl)propan-2-amine
Class Membership
Psychoactive class Entactogen / 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.

Threshold 15 - 20 mg
Light 20 - 30 mg
Common 30 - 70 mg
Strong 70 - 90 mg
Heavy 90 mg +
Total 4 - 6 hours
Onset 20 - 60 minutes
Come up 30 - 60 minutes
Peak 1.5 - 2.5 hours
Offset 2 - 3 hours
After effects 6 - 12 hours

Threshold 15 - 20 mg
Light 20 - 30 mg
Common 30 - 50 mg
Strong 50 - 60 mg
Heavy 60 mg +
Total 1 - 2.5 hours
Onset 5 - 15 minutes
Come up 5 - 10 minutes
Peak 30 - 60 minutes
Offset 30 - 60 minutes
After effects 1 - 3 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.

3-Fluoroethamphetamine (also known as 3-FEA) is a novel ring-substituted amphetamine compound that produces a mixture of entactogenic and stimulant effects when administered. 3-FEA is structurally related to a series of designer fluorinated substituted amphetamines that originally included compounds such as 2-FA, 2-FMA, 3-FA, 4-FMA, 4-FA.[1]

Like its parent compound 3-FA, the pharmacological, toxicological, and subjective effects of 3-FEA in humans have yet to be mapped out in detail. Anecdotal reports have characterised 3-FEA as a moderately potent serotonin-dominant triple monoamine releaser that produces a mixture of entactogenic and mild stimulating effects.[citation needed]

3-FEA has an extremely short history of human recreational use and has not been documented being sold on the streets. It has recently been made available for sale on the grey market as a research chemical by online vendors.[citation needed] Due to its potent psychostimulant effects, likely habit-forming properties, and unknown toxicity profile, it is strongly recommended that one use proper harm reduction practices if using this substance.


Generic structure of an amphetamine molecule

3-FEA, or 3-fluoroethamphetamine, is a synthetic molecule of the amphetamine chemical class. Molecules of the amphetamine class contain a phenethylamine core comprised of a phenyl ring bound to an amino (NH2) group through an ethyl chain substituted with a methyl group at Rα (i.e. amphetamines are alpha-methylated phenethylamines).

3-FEA is the 3-position fluorinated analog of ethylamphetamine (also known as ethamphetamine). It is also an analog of fenfluramine with the 3-trifluoromethyl group replaced with a 3-fluoro substituent.[citation needed]


Although 3-FEA 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 reuptake inhibitor and/or releaser of the monoamine neurotransmitters serotonin, dopamine, and norepinephrine.[2][3]

It has been demonstrated that compared to the unsubstituted ethylamphetamine, 3-fluoroethamphetamine is a weaker releaser of dopamine, but a stronger releaser of both serotonin and norepinephrine, producing the strongest reinforcing effects in animal studies out of a range of 3-substituted amphetamine derivatives tested, despite not being the most potent dopamine releaser.[3][2]

This indicates that 3-FEA effectively increases the levels of all the three major monoamine neurotransmitters dopamine, norepinephrine, and serotonin in the brain by acting as a releasing agent of said neurotransmitters and/or by binding to and partially blocking the transporter proteins that normally clear those molecules from the synaptic cleft after they have fulfilled their function of conducting a neural impulse. This transporter blockade allows these molecules to accumulate within core synaptic regions of the brain to extra-endogenous levels, resulting in a combination of relaxing, stimulating, disinhibiting and euphoric effects associated with entactogenic substituted amphetamines such as MDMA or 4-FA.[citation needed]

Subjective effects

Unlike its close analog 3-FA, which has been reported as being relatively functional and non-recreational, 3-FEA appears to produce effects more similar to another analog 4-FA, which produces notably entactogenic effects. 3-FEA has also been reported to produce less stimulation compared to 4-FA to the degree that some users report it as being primarily sedating. This effect profile likely makes 3-FEA a poor candidate for functional use and better suited for recreational use in a manner similar to MDMA. The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects

Cognitive effects

After effects
Aftereffects (3).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

The toxicity and long-term health effects of recreational 3-FEA use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because 3-FEA has an extremely brief history of human usage, first becoming available in mid-2016. Early anecdotal reports from people within the community who have tried 3-FEA 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 and using it very cautiously sparingly (although nothing can be completely guaranteed).

Potential cardiotoxicity

Due to its serotonin-releasing entactogenic properties, it is possible 3-FEA may display significant affinity and activity at the 5-HT2B receptor, which like 5-HT2B agonists such as MDMA and fenfluramine would make it cardiotoxic with long-term or heavy use.[4]

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

Tolerance and addiction potential

Although it still remains to be seen, the chronic use of 3-FEA will likely come to be considered to be 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-FEA develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. Afterward, it takes about 2 - 3 days for the tolerance to be reduced to half and 3-7 days to be back at baseline (in the absence of further consumption). 3-FEA likely presents cross-tolerance with all dopaminergic and serotonergic stimulants and entactogens, meaning that after the consumption of 3-FEA all stimulants will have a reduced effect (including atypical stimulants one might not expect, such MDMA or amphetamine due to its reliance on robust dopamine and norepinephrine stores to exert its full spectrum of effect).


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.[6][7] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[8] Psychosis very rarely arises from therapeutic use.[9][10]

Dangerous interactions

Although many psychoactive substances are safe on their own, they can become dangerous and even life-threatening when combined with other substances. The list below contains some common potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses of each but still increase the potential risk of death. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

Serotonin syndrome risk

Combinations in the list below may increase the amount of neurotransmitters such as serotonin and dopamine to dangerous or even fatal levels.

Legal status

3-FEA is currently a grey area compound within many 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, individuals may still be charged for its possession under certain circumstances such as under analog laws and with intent to sell or consume.

  • United States: 3-FEA 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.
  • United Kingdom: 3-FEA is considered a Class A drug as a result of the amphetamine analog clause of the Misuse of Drugs Act 1971.[13]
  • Canada: 3-FEA would be considered Schedule I as it is an analog of Amphetamine.[14]
  • New Zealand: 3-FEA is an amphetamine analog, so is a Schedule 3 controlled substance in New Zealand.[15]

See also

External links


  1. Quednow, B., Girreser, U., Junge, T., & Ro, P. (2005). Isomeric Fluoro-methoxy-phenylalkylamines: a new series of controlled-substance analogues (designer drugs), 148, 143–156. https://doi.org/10.1016/j.forsciint.2004.05.003
  2. 2.0 2.1 Tessel RE, Rutledge CO. Specificity of release of biogenic amines from isolated rat brain tissue as a function of the meta substituent of N-ethylamphetamine derivatives. The Journal of Pharmacology and Experimental Therapeutics 1976;15:142.
  3. 3.0 3.1 Tessel RE, Woods JH. Substituted N-ethylamphetamine self injection responding in the rhesus monkey: structure-activity relationships. The Journal of Pharmacology and Experimental Therapeutics 1978; 2: 274–81.
  4. Huang, X. P., Setola, V., Yadav, P. N., Allen, J. A., Rogan, S. C., Hanson, B. J., ... & Roth, B. L. (2009). Parallel functional activity profiling reveals valvulopathogens are potent 5-hydroxytryptamine2B receptor agonists: implications for drug safety assessment. Molecular Pharmacology, 76(4), 710-722. https://doi.org/10.1161/01.CIR.102.23.2836
  5. Treatment for amphetamine psychosis | [1]
  6. Treatment for amphetamine psychosis | [2]
  7. Hofmann FG (1983). A Handbook on Drug and Alcohol Abuse: The Biomedical Aspects (2nd ed.). New York: Oxford University Press. p. 329. ISBN 9780195030570.
  8. Treatment for amphetamine psychosis | [3]
  9. Stimulant Misuse: Strategies to Manage a Growing Problem | http://www.acha.org/prof_dev/ADHD_docs/ADHD_PDprogram_Article2.pdf
  10. http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf
  11. Gillman, P. K. (2005). Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. British Journal of Anaesthesia, 95(4), 434-441. https://doi.org/10.1093/bja/aei210
  12. Gillman, P. K. (2005). Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. British Journal of Anaesthesia, 95(4), 434-441. https://doi.org/10.1093/bja/aei210
  13. Misuse of Drugs Act 1971 (Legislation.gov.uk) |http://www.legislation.gov.uk/ukpga/1971/38/schedule/2/part/I
  14. Controlled Drugs and Substances Act (S.C. 1996, c. 19) |http://laws-lois.justice.gc.ca/eng/acts/C-38.8/page-12.html#h-28
  15. http://www.legislation.govt.nz/act/public/1975/0116/latest/whole.html#DLM436576