Talk:Eutylone

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Summary sheet: Eutylone

Template:SubstanceBox/Eutyulone

Eutylone β-Keto-1,3-benzodioxolyl-N-ethylbutanamine ('Eutylone, bk-EBDB, N-Ethylbutylone) is a stimulant compound developed in the 1960s which has been reported as a novel designer drug and has appeared recently (2019) being sold as a designer drug. As a designer drug, it is commonly sold on the street along with ethylone as a substitute or counterfeit for NEP and methylone (all of which have collectively come to be referred to as "stimulating with low serotonergic activity") due to methylone's declining availability on the research chemical market. However, in spite of behavioral and pharmacological similarities between eutylone and MDMA, the observed subjective effects of both substances are not completely identical, eutylone has some of the euphoria which can remind of that of MDMA, but with a shorter duration and weaker effects. . [1]

Subjective effects include stimulation, thought acceleration, motivation enhancement, increased libido, appetite suppression dehydration, dry mouth , and euphoria, Euthylone is reported to be less potent than its relatives butylone, methylone and ethylone as well as possessing more classic stimulant as opposed to entactogenic effects.

Euthylone has an extremely short history of human use and very little data exists about its pharmacological properties, metabolism, and toxicity. It is highly advised to use harm reduction practices if using this substance.

Chemistry

Eutylone or β-Keto-1,3-benzodioxolyl-N-ethylbutanamine , is a synthetic molecule of the cathinone family. Cathinones are structurally similar to amphetamines in that they 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. Cathinones such as eutylone are alpha-methylated phenethylamines (i.e. amphetamines) but differ from them with the addition of a ketone functional group (a carbonyl group at Rβ).

Pharmacology

Eutylone acts as a mixed reuptake inhibitor/releasing agent of serotonin, norepinephrine, and dopamine.[2][3] These are the neurotransmitters in charge of pleasure, reward, motivation and focus. This is done by inhibiting the reuptake and reabsorption of the neurotransmitters after they have performed their function of transmitting a neural impulse, essentially allowing them to accumulate and be reused, causing physically stimulating and euphoric effects.

In comparison to methylone, it has much lower affinity for the norepinephrine transporter, while its affinity for the serotonin and dopamine transporters is similar.[4][5] The results of these differences in pharmacology relative to MDMA is that butylone, like its close analog ethylone is less potent in terms of dose, has more balanced catecholaminergic effects relative to serotonergic, and behaves more like a reuptake inhibitor like methylphenidate than a releaser like amphetamine; however, eutyulonestill has relatively robust releasing capabilities.[6]

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), a literature which relies on collected anecdotal reports and the personal experiences of PsychonautWiki contributors. As a result, they should be taken with a healthy amount of skepticism. It is worth noting that these effects will not necessarily occur in a consistent or reliable manner, although higher doses (common+) are more likely to induce the full spectrum of reported effects. Likewise, adverse effects become much more likely with higher doses and may include serious injury or death.

Physical effects
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Cognitive effects
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After effects
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Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found on the subreddit /r/researchchemicals

Toxicity and harm potential

The toxicity and long-term health effects of recreational Eutylone use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because Eutylone has very little history of human usage. Anecdotal evidence from people who have tried Eutylone within the community suggests that there do not seem to be strong adverse effects attributed to using this substance at low to moderate doses and sparingly.

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 Eutylone 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 eutyulone 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). Eutyulone presents cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of Eutyulone 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., paranoia, hallucinations, or delusions).[7] A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[8][9] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[10] Psychosis very rarely arises from therapeutic use.[11][12]

Dangerous interactions

Although many psychoactive substances are reasonably safe to use on their own, they can quickly become dangerous or even life-threatening when combined with other substances. The list below includes some known dangerous combinations (although it cannot be guaranteed to include all of them). Independent research (e.g. Google, DuckDuckGo) should always be conducted to ensure that a combination of two or more substances is safe to consume. Some interactions listed have been sourced from TripSit.

  • 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 handled with extreme care due to DXM's effects on serotonin and norepinephrine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome with stimulants that increase levels of serotonin (MDMA, methylone, mephedrone, etc.). Monitor blood pressure carefully and avoid strenuous physical activity.
  • MDMA - The neurotoxic effects of MDMA may be increased when combined with other stimulants. There is also a risk of excessive heart strain.
  • MXE - Combinations with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • Stimulants - Eutylone can be potentially dangerous in combination with other stimulants as they can increase one's heart rate and blood pressure to dangerous levels.
  • Cocaine - This combination may increase strain on the heart.
  • Tramadol - Tramadol lowers the seizure threshold.[13] Combinations with stimulants may further increase this risk.

Serotonin syndrome risk

Combinations with the following substances can cause dangerously high serotonin levels. Serotonin syndrome requires immediate medical attention and can be fatal if left untreated.

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.


See also

External links

References

  1. "Cathinone | Ask Dr. Shulgin Online". 
  2. Inhibition of plasma membrane monoamine transporters by beta-ketoamphetamines (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/10528135
  3. The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain (ScienceDirect) | http://www.sciencedirect.com/science/article/pii/S0014299906013811
  4. "Pharmacological characterization of designer cathinones in vitro" | http://onlinelibrary.wiley.com/doi/10.1111/j.1476-5381.2012.02145.x/pdf
  5. The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain (ScienceDirect) | http://www.sciencedirect.com/science/article/pii/S0014299906013811
  6. "Pharmacological characterization of designer cathinones in vitro" | http://onlinelibrary.wiley.com/doi/10.1111/j.1476-5381.2012.02145.x/pdf
  7. Treatment for amphetamine psychosis | [1]
  8. Treatment for amphetamine psychosis | [2]
  9. Hofmann FG (1983). A Handbook on Drug and Alcohol Abuse: The Biomedical Aspects (2nd ed.). New York: Oxford University Press. p. 329. ISBN 9780195030570.
  10. Treatment for amphetamine psychosis | [3]
  11. Stimulant Misuse: Strategies to Manage a Growing Problem | http://www.acha.org/prof_dev/ADHD_docs/ADHD_PDprogram_Article2.pdf
  12. http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf
  13. 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
  14. 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