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3-FEA

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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.



⇣ Oral
Dosage
Threshold 15 mg
Light 20 - 35 mg
Common 35 - 70 mg
Strong 70 - 90 mg
Heavy 90 mg +
Duration
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



⇣ Insufflated
Dosage
Threshold 15 mg
Light 20 - 35 mg
Common 35 - 60 mg
Strong 50 - 60 mg
Heavy 60 mg +
Duration
Total 1 - 2 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.

Interactions
Alcohol
GHB
GBL
Opioids
Cannabis
Caffeine
Ketamine
Methoxetamine
Psychedelics
Cocaine
DXM
PCP
25x-NBOMe
2C-T-x
5-MeO-xxT
DOx
Tramadol
aMT
MAOIs
Summary sheet: 3-FEA

3-Fluoroethamphetamine (abbreviated 3-FEA and also known as PAL-353) is a synthetic ring-substituted fluorinated amphetamine that produces a combination of entactogenic and stimulant effects. It is part of a series of designer fluorinated amphetamines such as 2-FA, 3-FA and 4-FA. Due to its ethyl N-side chain however, it would be more accurate to refer to this compound as an aphaethylamine. It is the first if not one of the few substituted aephetamines to have ever been made available on the consumer drug market. Yet, like its parent compound [[3-FA], its pharmacological, toxicological and subjective effects profile have yet to be mapped out in detail.

3-FEA has an extremely short history of recreational use and is almost never found on the streets. It has recently been made available for sale as a gray market research chemical through online vendors.[citation needed]

Chemistry

3-FEA, also known as 3-fluoroethamphetamine, is a synthetic molecule of the aephetamine family. Molecules of the aephetamine class contain a phenethylamine core featuring a phenyl ring bound to an amino (NH2) group through an ethyl chain with an additional ethyl substitution at Rα (i.e. aephetamines are alpha-ethylated phenethylamines). Unlike its close analog 3-FA, 3-FEA contain an additional ethyl group bound to the terminal amine RN of the amphetamine core, which renders it structurally and functionally similar to other fluoroinated amphetamine. 3-FA is the 3-fluorinated analog of "aephetamine".

Pharmacology

Although 3-FEA 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. Notably, however, it has been demonstrated that "compared to the unsubstituted ethylamphetamine, 3-fluoroethamphetamine is a weaker releaser of noradrenaline, but a stronger releaser of both dopamine and serotonin, and produced the strongest reinforcing effects in animal studies out of a range of 3-substituted aephetamine derivatives tested, despite not being the most potent dopamine releaser"[1][2][3][4] This means it effectively increases the levels of all three major monoamine neurotransmitters like dopamine, norepinephrine and serotonin in the brain by binding to and partially blocking the transporter proteins that normally clear those molecules from the synaptic cleft after they have carried the neural impulse. This allows dopamine, serotonin and norepinephrine to accumulate within core regions of the brain to extra-endogenous levels, resulting in both relaxing, stimulating, motivatory and euphoric effects associated with serotonin-releasing substituted amphetamines like MDMA or other fluorinated amphetamines like 4-FA.

Additionally, studies have demonstrated that 2-flourine amphetamine substitutions serve to limit the activity of the compound at the alpha-1 adrenergic receptor with an over 200-fold increased selectivity for A2 receptors over A1 receptors.[5] It has also been demonstrated that 2-substitution of a hydrogen with fluorine on the aromatic ring of norepinephrine produces a beta-adrenergic agonist with little alpha activity.[6] This has led the online community to speculate that the milder uncomfortable cognitive and/or physical side effects and the greater efficacy as a nootropic associated with 2-FA are at least partially due to decreased activity at the alpha-1 adrenergic receptors, resulting in significantly less norepinephrine reuptake inhibition and thus a "ceiling" to the amount of the recreational effects it can induce. It is unknown to what extent this applies to 3-FEA's pharmacology given its incredibly short period of human use.

Subjective effects

 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.

Unlike its analogs 2-FA and 2-FMA, both of which have been recognized for being very functional and moderated stimulants with dose-ceilings that made it harder to abuse, it is likely 3-FEA leans more in the direction of the euphoric entactogenic stimulant 4-FA. It is likely a poor candidate for functional use and is likely to be better suited for recreational outings. As a result, it is recommended that one use this substance very sparingly and cautiously.

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

Cognitive effects

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:

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

Main article: Research chemicals § 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 short history of human usage, becoming available only in mid-2016. Anecdotal evidence from people who have tried 3-FEA 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).

Due to its putative serotonin-releasing and entactogenic properties, it is likely that 3-FEA may display excess activity at the 5-HT2b receptor, which like MDMA and fenfluramine would make it would be 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.[7]

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-FEA 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-FEA 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-FEA presents cross-tolerance with [[Cross-tolerance::all dopaminergic and serotonergic stimulants]] and entactogens, meaning that after the consumption of 3FEA 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).

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).[8] A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[9][10] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[11] Psychosis very rarely arises from therapeutic use.[12][13]

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.

  • "[[DangerousInteraction" contains a listed "[" character as part of the property label and has therefore been classified as invalid.]] - This combination may increase the amount of neurotransmitters such as dopamine to dangerous or even fatal levels. Examples include syrian rue, banisteriopsis caapi, and some antidepressants.[14]
  • Stimulants - 3-FEA can be potentially dangerous in combination with other stimulants as it can increase one's heart rate and blood pressure to dangerous levels.
  • "[[DangerousInteraction" contains a listed "[" character as part of the property label and has therefore been classified as invalid.]] & "[[DangerousInteraction" contains a listed "[" character as part of the property label and has therefore been classified as invalid.]] - 25x compounds are highly stimulating and physically straining. Combinations with 3-FEA should be strictly avoided due to the risk of excessive stimulation and heart strain. This can result in increased blood pressure, vasoconstriction, panic attacks, thought loops, seizures, and heart failure in extreme cases.
  • "[[UncertainInteraction" contains a listed "[" character as part of the property label and has therefore been classified as invalid.]] - Combining alcohol with stimulants can be dangerous due to the risk of accidental over-intoxication. Stimulants mask alcohol's depressant effects, which is what most people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects will be left unopposed, which can result in blackouts and severe respiratory depression. If mixing, the user should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • "[[UnsafeInteraction" contains a listed "[" character as part of the property label and has therefore been classified as invalid.]] - Combinations with DXM should be avoided due to its inhibiting effects on serotonin and norepinephrine reuptake. There is an increased risk of panic attacks and hypertensive crisis, or serotonin syndrome with serotonin releasers (MDMA, methylone, mephedrone, etc.). Monitor blood pressure carefully and avoid strenuous physical activity.
  • "[[UnsafeInteraction" contains a listed "[" character as part of the property label and has therefore been classified as invalid.]] - Any neurotoxic effects of MDMA are likely to be increased when other stimulants are present. There is also a risk of excessive blood pressure and heart strain (cardiotoxicity).
  • "[[UncertainInteraction" contains a listed "[" character as part of the property label and has therefore been classified as invalid.]] - Some reports suggest combinations with MXE may dangerously increase blood pressure and increase the risk of mania and psychosis.
  • "[[UncertainInteraction" contains a listed "[" character as part of the property label and has therefore been classified as invalid.]] - Both classes carry a risk of delusions, mania and psychosis, and these risk may be multiplied when combined.
  • "[[UnsafeInteraction" contains a listed "[" character as part of the property label and has therefore been classified as invalid.]] - 3-FEA may be dangerous to combine with other stimulants like cocaine as they can increase one's heart rate and blood pressure to dangerous levels.
  • "[[DangerousInteraction" contains a listed "[" character as part of the property label and has therefore been classified as invalid.]] - Tramadol is known to lower the seizure threshold[15] and combinations with stimulants may further increase this risk.
  • MDMA - The neurotoxic effects of MDMA may be increased when combined with amphetamines.
  • Cocaine - This combination may increase strain on the heart to dangerous levels.

This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

3-FEA 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.

  • United States: 3-FEA may be considered to be an analog of amphetamine, thus falling under the Federal Analog Act. The Federal Analog 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: It is illegal to produce, supply, or import this drug under the Psychoactive Substance Act, which came into effect on May 26th, 2016.[16]

See also

References

  1. ↑ Tessel RE, Woods JH. Structural relationship between meta-substituted N-ethylamphetamines and self-administration in rhesus monkeys. Pharmacologist 1974;16:142.
  2. ↑ 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. ↑ 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. ↑ pmid=417172
  5. ↑ 2-(Arylalkylamino)adenosin-5'-uronamides: a new class of highly selective adenosine A2 receptor ligands | http://pubs.acs.org/doi/abs/10.1021/jm00169a015
  6. ↑ Effect of fluorine substitution on the agonist specificity of norepinephrine | http://www.sciencemag.org/content/204/4398/1217.short
  7. ↑ Fluorine substituent effects (on bioactivity) | http://www.sciencedirect.com/science/article/pii/S002211390100375X
  8. ↑ Treatment for amphetamine psychosis | [1]
  9. ↑ Treatment for amphetamine psychosis | [2]
  10. ↑ Hofmann FG (1983). A Handbook on Drug and Alcohol Abuse: The Biomedical Aspects (2nd ed.). New York: Oxford University Press. p. 329. ISBN 9780195030570.
  11. ↑ Treatment for amphetamine psychosis | [3]
  12. ↑ Stimulant Misuse: Strategies to Manage a Growing Problem | http://www.acha.org/prof_dev/ADHD_docs/ADHD_PDprogram_Article2.pdf
  13. ↑ http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf
  14. ↑ Gillman, P. K. (2005). "Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity". British Journal of Anaesthesia. 95 (4): 434–441. doi:10.1093/bja/aei210 Freely accessible. eISSN 1471-6771. ISSN 0007-0912. OCLC 01537271. PMID 16051647. 
  15. ↑ Talaie, H.; Panahandeh, R.; Fayaznouri, M. R.; Asadi, Z.; Abdollahi, M. (2009). "Dose-independent occurrence of seizure with tramadol". Journal of Medical Toxicology. 5 (2): 63–67. doi:10.1007/BF03161089. eISSN 1937-6995. ISSN 1556-9039. OCLC 163567183. 
  16. ↑ Psychoactive Substances Act 2016 (Legislation.gov.uk) | http://www.legislation.gov.uk/ukpga/2016/2/contents/enacted
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