N-Ethylhexedrone

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Summary sheet: N-Ethylhexedrone
N-Ethylhexedrone
N-ethyl-nor-hexedrone.svg
Chemical Nomenclature
Common names Hexen, Hex-en, NEH, Ethyl-Hexedrone
Substitutive name N-Ethylhexedrone, N-Ethyl-nor-hexedrone
Systematic name 2-(ethylamino)-1-phenylhexan-1-one
Class Membership
Psychoactive class Stimulant
Chemical class Cathinone
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.


Smoked
Dosage
Threshold 1 - 2 mg
Light 2 - 5 mg
Common 5 - 10 mg
Strong 10 - 20 mg
Heavy 20 mg +
Duration
Total 1 - 4 hours
Onset 2 - 10 minutes
Peak 10 - 30 minutes
Offset 15 - 30 minutes
After effects 2 - 4 hours




Insufflated
Dosage
Threshold 5 - 15 mg
Light 15 - 30 mg
Common 30 - 40 mg
Strong 40 - 50 mg
Heavy 50 mg +
Duration
Total 2 - 5 hours
Onset 2 - 8 minutes
Peak 30 - 90 minutes
Offset 1 - 4 hours
After effects 1 - 8 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.

N-Ethylhexedrone (also known as NEH and hexen) is a lesser-known novel stimulant substance of the cathinone class. N-Ethylhexedrone is a derivative of hexedrone and is part of a diverse group of compounds called the substituted cathinones. Little is known about its pharmacology, although it likely acts by increasing levels of norepinephrine and dopamine in the brain.

The original synthesis date of N-ethylhexedrone is unknown. It appears to have emerged on the online research chemical market in late 2015. It is an example of a novel psychoactive substance specifically chosen to mimic the features of prohibited substances and bypass drug laws. It is one of a number of substances collectively referred to in popular culture as "bath salts".[citation needed]

User reports characterize N-ethylhexedrone as having euphoric stimulant effects comparable to those of crack-cocaine and α-PVP-type compounds, particularly when they insufflated or vaporized. Like other substituted cathinones, N-ethylhexedrone has gained notoriety for its association with compulsive redosing and addictive behaviors when abused.

Very little is known about the pharmacology, metabolism, and toxicity of N-ethylhexedrone. Due to this, it is highly advised to use harm reduction practices if using this substance.

History and culture

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N-Ethylhexedrone was first identified in a sample from the Belgian Customs laboratory which was received at the JRC on November 2015. In January 2016, it was identified at the JRC in a sample provided by French Customs. Subsequently, in February 2016, the EMCDDA received notifications of the identification of this substance from other countries, such as Sweden, The Netherlands, France, Belgium and Slovenia.[1]

Chemistry

N-ethylhexedrone is a molecule of the cathinone chemical class. The term "substituted cathinone" refers to a broad array of substances based on cathinone, the principally active constituent of the khat plant. Cathinone is principally constituted of a amphetamine core (a phenethylamine core with an alkyl group attached to the alpha carbon) and an oxygen group attached to the beta carbon. Cathinones are also known as the beta-ketone (βk) (double-bonded oxygen to the β-carbon) analogs of amphetamines.

Notably, the cathinone backbone can be modified in three different places to create hundreds of possible compounds, which include substituents such as on the aromatic ring, the alpha carbon, or the amine group.[2]

Pharmacology

Very little data exists on the human pharmacokinetics and pharmacodynamics of N-ethylhexedrone and other substituted cathinones. Like amphetamines, synthetic cathinones exert their stimulating and sympathomimetic effects via increasing synaptic concentration of catecholamines such as dopamine, serotonin and norepinephrine. These molecules are able to inhibit monoamine reuptake transporters producing a decreased clearance of the neurotransmitters from the synapse. Furthermore, they may cause release of biogenic amines from intracellular stores.[3]

Synthetic cathinones are generally less able than amphetamines to cross the blood–brain barrier because the beta-keto group causes an increase in polarity. Unlike other synthetic cathinones, pyrrolidine derivatives have a higher ability to cross the blood–brain barrier because the pyrrolidine ring confers a low polarity to these molecules. The studies on the metabolism of synthetic cathinones have shown that they are N-demethylated, the keto group is reduced to hydroxyl and ring alkyl groups are oxidised.[4]

Subjective effects

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User reports suggests that N-ethylhexedrone has more side effects compared to other stimulants like mephedrone or NEP. This can to excessive redosing, sobriety delusions and toxicity, which can eventually lead to highly uncomfortable experiences. The effects of vaporized N-ethylhexedrone are reported to be much stronger and more euphoric with less side effects than when insufflated or taken orally, but extreme care should be taken with this route of administration due to the degree it promotes compulsive and reckless use.

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. These 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 of inducing 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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Cognitive effects
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Auditory 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:

Additional experience reports can be found here:

Toxicity and harm potential

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

Early anecdotal reports from those who have tried N-ethylhexedrone suggests that there do not seem to be any negative health effects attributed to simply trying it at low to moderate doses by itself and using it in a sparing and controlled fashion (but nothing can be completely guaranteed).

Some users have reported N-ethylhexedrone to be caustic to the nasal membrane when it is insufflated.[citation needed]

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 N-ethylhexedrone can be considered moderately addictive with a high potential for abuse and seems to be readily liable 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 N-ethylhexedrone 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 total absence of further consumption). N-ethylhexedrone presents cross-tolerance with all noradrenergic and dopaminergic stimulants, meaning that after the consumption of N-ethylhexedrone all stimulants will have a reduced effect.

Psychosis

Main article: Stimulant psychosis

Abuse of compounds within the stimulant 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., anxiety and paranoia, hallucinations, or delusions).[5] A review on treatment for (dextro)amphetamine, 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]

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/25x-NBOH - Members of the 25x family are highly stimulating and physically straining. Combinations with stimulants should be avoided 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 - Combinations with DXM should be strictly avoided due to DXM's effects on serotonin and dopamine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome.
  • MXE - Combinations with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • Tramadol - Tramadol lowers the seizure threshold.[9] Combinations with stimulants may further increase this risk.
  • MDMA - The neurotoxic effects of MDMA are generally thought to increase when combined with amphetamine and other stimulants.[citation needed]
  • 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.[10]
  • Cocaine - This combination may increase strain on the heart to dangerous levels.[citation needed]

Legal status

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

  • Brazil: Possession, production and sale is illegal as it is listed on Portaria SVS/MS nº 344.[11]
  • Sweden: N-Ethylhexedrone was classified as an illegal narcotic in Sweden on June 21st, 2016.[12]
  • United Kingdom: N-Ethylhexedrone is a Class B drug in the United Kingdom as a result of the cathinone catch-all clause.[13]

See also

External links

References

  1. Guillou, C., Reniero, F., Vicente, J. L., Holland, M., Kolar, K., Chassaigne, H., ... & Schepers, H. (2018). Collaboration of the Joint Research Centre and European Customs Laboratories for the Identification of New Psychoactive Substances. Current pharmaceutical biotechnology, 19(2), 91-98. https://doi.org/10.2174/1389201019666180523122717
  2. Liu, C., Jia, W., Li, T., Hua, Z., & Qian, Z. (n.d.). Identification and analytical characterization of nine synthetic cathinone derivatives N-ethylhexedrone, 4-Cl-pentedrone, 4-Cl--EAPP, propylone, N-ethylnorpentylone, 6-MeO-bk-MDMA, -PiHP, 4-Cl--PHP, and 4-F--PHP. https://doi.org/10.1002/dta.2136
  3. Cozzi, N.V., Sievert, M.K., Shulgin, A.T., Jaco 3rd., P., Ruoho, A.E., 1999. Inhibition of plasma membrane monoamine transporters by beta-ketoamphetamines. Eur. J. Pharmacol. 381, 63–69.
  4. Meyer, M.R., Maurer, H.H., 2010. Metabolism of designer drugs of abuse: an updated review. Curr. Drug Metab. 11, 468–482
  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. 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. https://doi.org/10.1007/BF03161089
  10. 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
  11. http://portal.anvisa.gov.br/documents/33868/3233596/56+-+RDC+N%C2%BA+159-2017-DOU.pdf/27be30ee-3884-46fe-b7ba-ae2f94b74693
  12. 31 nya ämnen kan klassas som narkotika eller hälsofarlig vara | https://www.folkhalsomyndigheten.se/nyheter-och-press/nyhetsarkiv/2016/juni/31-nya-amnen-kan-klassas-som-narkotika-eller-halsofarlig-vara/
  13. United Kingdom. (2010). Misuse of Drugs Act 1971 (S.I. 2010/1207). London: The Stationery Office Limited. Retrieved February 9, 2018, from https://www.legislation.gov.uk/uksi/2010/1207/made