Butylone

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Summary sheet: Butylone
Butylone
Butylone.svg
Chemical Nomenclature
Common names Butylone, bk-MBDB, B1
Substitutive name β-keto-N-methylbenzodioxolylbutanamine
Systematic name 1-(1,3-benzodioxol-5-yl)-2-(methylamino)butan-1-one
Class Membership
Psychoactive class Stimulant / Entactogen
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.



Oral
Dosage
Threshold Common Heavy
20 - 40 - 80 - 125 - 225 mg
Light Strong
Threshold 20 - 40 mg
Light 40 - 80 mg
Common 80 - 125 mg
Strong 125 - 225 mg
Heavy 225 mg +
Duration
Total 3 - 5 hours
Onset 15 - 60 minutes
Peak 60 - 120 minutes
Offset 60 - 120 minutes
After effects 4 - 12 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.

Butylone (also known as β-keto-N-methylbenzodioxolylbutanamine, βk-MBDB, or B1) is a synthetic entactogen and stimulant of the phenethylamine and cathinone classes. Butylone is the β-keto analog of MBDB and the substituted methylenedioxy analogue of buphedrone.

As a designer drug, it is commonly sold on the street along with ethylone as a substitute or counterfeit for MDMA and methylone (all of which have collectively come to be referred to as "Molly") due to methylone's declining availability on the research chemical market.

However, in spite of behavioral and pharmacological similarities between butylone and MDMA, the observed subjective effects of both substances are not completely identical. [1]

Butylone has only a short history of human use and is reported to be less potent than its relatives methylone and ethylone as well as possessing more classic stimulant as opposed to entactogenic effects.

Chemistry

Butylone, or β-keto-N-methylbenzodioxolylbutanamine, 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 butylone are alpha-methylated phenethylamines (i.e. amphetamines) but differ from them with the addition of a ketone functional group (a carbonyl group at Rβ). Butylone contains a methyl substitution at RN, a substitution which is shared with MDEA, ethylone, 4-MEC, and certain other stimulants and entactogens. Additionally, butylone contains substitutions at R3 and R4 of the phenyl ring with oxygen groups. These oxygen groups are incorporated into a methylenedioxy ring through a methylene chain. Butylone shares this methylenedioxy ring with MDA, MDAI and MDMA.

Pharmacology

Butylone 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 approximately over 4x 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, butylone still has relatively robust releasing capabilities.[6]

Subjective effects

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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After effects
Aftereffects (3).svg

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 here:

Toxicity and harm potential

The toxicity and long-term health effects of recreational butylone use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because butylone has very little history of human usage. Anecdotal evidence from people who have tried butylone 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 butylone 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 butylone 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). Butylone presents cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of butylone 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 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.[13] Combinations with stimulants may further increase this risk.
  • Cocaine - This combination may increase strain on the heart.

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

  • Austria: Butylone is illegal to possess, produce and sell under the NPSG (Neue-Psychoaktive-Substanzen-Gesetz Österreich).
  • United Kingdom - Butylone is a Class B drug in the United Kingdom as a result of the cathinone catch-all clause.[15]
  • United States - Butylone is unscheduled in the United States. However it could be considered an analog of methylone or MDMA, thus making it illegal under the scope of the Federal Analog Act.
  • China - As of October 2015 butylone is a controlled substance in China.[16]

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
  15. 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
  16. "关于印发《非药用类麻醉药品和精神药品列管办法》的通知" (in Chinese). China Food and Drug Administration. 27 September 2015. Retrieved 1 October 2015.