2-FEA

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Summary sheet: 2-FEA
2-FEA
2-FEA.svg
Chemical Nomenclature
Common names 2-FEA
Substitutive name 2-Fluormethamphetamine
Systematic name N-Ethyl-1-(2-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.






Insufflated
Dosage
Threshold Common Heavy
15 - 20 - 30 - 40 - 60 mg
Light Strong
Threshold 15 - 20 mg
Light 20 - 30 mg
Common 30 - 40 mg
Strong 40 - 60 mg
Heavy 60 mg +
Duration
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.

2-Fluoroethamphetamine (2-FEA) is a novel stimulant substance of the amphetamine class that produces classical stimulant effects such as stimulation, enhanced focus and euphoria when administered.

Anecdotal reports suggest that 2-FEA has been compared with 3-FEA, which it is thought to share many of its effects with.

2-FEA is sold on the online research chemical market. It is strongly advised to use harm reduction practices if using this substance.

Chemistry

2-Fluoroethamphetamine (2-FEA) is a synthetic molecule of the substituted 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). 2-FEA contains an ethyl group bound to the terminal amine RN of the amphetamine core.

2-FEA is the N-ethylated homolog of 2-FA (2-fluoroamphetamine).

Pharmacology

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This pharmacology section is incomplete.

You can help by adding to it.

Although 2-FEA has not been formally studied on the same level as traditional amphetamines, it is roughly assumed that it most likely acts primarily as a triple reuptake inhibitor and/or releaser of the monoamine neurotransmitters serotonin, dopamine, and norepinephrine.

This indicates that 2-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

2-FEA is reported to be less stimulating and more euphoric in a fashion that is more compareable to 3-FEA, whilst also having fewer side effects at lower dosages, such as anxiety, nausea and high blood pressure, which it shares with 2-FMA.

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
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Visual effects
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Cognitive effects
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After effects
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Experience reports

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


Toxicity and harm potential

The toxicity and long-term health effects of recreational 2-FEA use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because 2-FEA has a very limited history of human usage.

Anecdotal reports from those who have tried 2-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 or using it sparingly (but nothing can be completely guaranteed).

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

Tolerance and addiction potential

As with other stimulants, the chronic use of 2-FEA can be considered moderately addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage.

Tolerance to many of the effects of 2-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 - 2 weeks to be back at baseline (in the absence of further consumption). 2-FEA presents cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of 2-FEA all stimulants will have a reduced effect.

Dangerous interactions

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

  • 25x-NBOMe - Members of the 25x-NBOMe family are very stimulating and should not be combined with stimulants due to the risk of excessive stimulation. This can result in panic attacks, thought loops, seizures, increased blood pressure, vasoconstriction, and heart failure in extreme cases.
  • Alcohol - Alcohol can be dangerous to combine with stimulants due to the risk of accidental over-intoxication. Stimulants mask the sedative effects of alcohol, which is the main factor people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects of alcohol are left unopposed, which can result in blackouts and respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - DXM should not be combined with stimulants due to its effects on serotonin and dopamine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome.
  • MXE - Combining stimulants with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • Tramadol - Combining stimulants with tramadol increases the risk of seizures.
  • MDMA - The neurotoxic effects of MDMA may be increased when combined with amphetamines.
  • MAOIs - This combination may increase the amount of neurotransmitters such as dopamine to dangerous or even fatal levels. Examples include syrian rue, banisteriopsis caapi, 2C-T-2, 2C-T-7, αMT, and some antidepressants.[1]
  • Cocaine - This combination may increase strain on the heart.

Legal status

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This legality section is a stub.

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

2-FEA is currently a gray area compound within all parts of the world, meaning its regulation lies in a legal gray 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 the intent to sell or consume.

  • Canada: 2-FEA would be considered Schedule I as it is an analogue of Amphetamine.[2]
  • New Zealand: 2-FEA is an amphetamine analogue, so is a Schedule 3 controlled substance in New Zealand.[3]
  • United Kingdom: 2-FEA is considered a Class A drug as a result of the amphetamine analogue clause of the Misuse of Drugs Act 1971.[4]

See also

References

  1. 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
  2. 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
  3. http://www.legislation.govt.nz/act/public/1975/0116/latest/whole.html#DLM436576
  4. Misuse of Drugs Act 1971 (Legislation.gov.uk) |http://www.legislation.gov.uk/ukpga/1971/38/schedule/2/part/I