6-APB

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Summary sheet: 6-APB
6-APB
6-APB.svg
Chemical Nomenclature
Common names 6-APB, "Benzofury"
Substitutive name 6-(2-Aminopropyl)benzofuran
Systematic name 1-(1-Benzofuran-6-yl)propan-2-amine
Class Membership
Psychoactive class Entactogen
Chemical class Benzofuran
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
15 - 30 - 60 - 90 - 120 mg
Light Strong
Threshold 15 - 30 mg
Light 30 - 60 mg
Common 60 - 90 mg
Strong 90 - 120 mg
Heavy 120 mg +
Duration
Total 7 - 10 hours
Onset 30 - 60 minutes
Come up 60 - 120 minutes
Peak 3 - 4 hours
Offset 2 - 3 hours
After effects 6 - 48 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.

6-(2-Aminopropyl)benzofuran (also known as 6-APB and "Benzofury") is a novel entactogen substance of the benzofuran class. Its characteristic effects include anxiety suppression, disinhibition, muscle relaxation, and euphoria. It is structurally related to entactogens like MDA, MDMA, 5-APB, and 5-MAPB.

6-APB was first synthesized in 1993 by David E. Nichols as a potential non-neurotoxic alternative to MDMA.[1] However, it did not come into popular recreational use until over a decade later, where it briefly entered the rave scene and global research chemicals market. It was sold along with other novel benzofuran entactogens under the name "Benzofury" before its sale and import were subsequently banned.[citation needed]

Very little data exists about the pharmacological properties, metabolism, and toxicity of 6-APB, and it has only a brief history of human usage. It has been marketed alongside research chemical entactogens like 5-MAPB and 5-APB as a legal, grey-market alternative to MDMA, and is typically commercially distributed by online research chemical vendors. It is highly advised to use harm reduction practices if using this substance.

History and culture

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The synthesis of 6-APB was first reported by a team led by the medicinal chemist and psychedelic researcher David E. Nichols at Purdue University. They were examining the role of the MDA dioxle ring structure in interacting with serotonergic neurons. It was also partly an effort to find an alternative to MDMA, which was gaining recognition as a potentially useful adjunct in psychotherapy, but was also being linked to neurotoxic effects.[1]

Human usage was not documented until 2010, when it emerged for sale on the research chemical market. It was particularly prominent in the UK "legal highs" market, where it was sold under the name "Benzofury".[citation needed]

On June 10, 2013 6-APB and a number of analogues were classified as Temporary Class Drugs in the UK following an ACMD recommendation.[2] On November 28, 2013 the ACMD recommended that 6-APB and related benzofurans should become Class B, Schedule 1 substances. On March 5, 2014 the UK Home Office announced that 6-APB would be made a class B drug on 10 June 2014 alongside every other benzofuran entactogen and many structurally related drugs.[3]

Chemistry

6-APB, also known as 6-(2-aminopropyl)benzofuran, is a synthetic molecule of the benzofuran class. The benzofuran class of substances are members of the amphetamine and phenylethylamine classes. Molecules of this class contain a phenethylamine core bound to an amino (NH2) group through an ethyl chain with an additional methyl substitution at Rα. 6-APB does not contain a methyl substitution on RN. It is composed of an an oxygen-substituted benzofuran ring fused at R3 and R4 of the phenyl ring.

Notably, 6-APB shares this benzofuran ring with related compounds such as 5-APB, 5-MAPB, and 6-MAPB.

Three distinct batches have been in circulation since its initial release to markets. Originally, only hydrochloride was available, and its dosage range shared characteristics most similar to that of MDA in terms of dose-response. However, succinate and fumarate batches both entered the market, and have very different effects by weight, and vastly different loose bulk densities.[citation needed]

Pharmacology

6-APB is a serotoninnorepinephrinedopamine reuptake inhibitor (SNDRI) with Ki values of 117, 150, and 2698 nM for the norepinephrine transporter (NET), dopamine transporter (DAT), and serotonin transporter (SERT), respectively.[4] 6-APB also possesses additional activity as a releasing agent of these monoamine neurotransmitters.[5]

6-APB is a potent full agonist of the serotonin 5-HT2B receptor (Ki = 3.7 nM)[4], with higher affinity for this target than any other site.[6] Moreover, unlike MDMA, 6-APB shows 100-fold selectivity for the 5-HT2B receptor over the 5-HT2A and 5-HT2C receptors.[6][7]

Aside from the 5-HT2B receptor, 6-APB has also been found to bind with high affinity to the α2C-adrenergic receptor subtype (Ki = 45 nM), although the clinical significance of this action is unknown.[4]

The potent agonism of the 5-HT2B receptor makes it likely that 6-APB would be cardiotoxic with chronic or long-term use, as seen with other 5-HT2B receptor agonists such as the withdrawn serotonergic anorectic fenfluramine.[4][8]

The monoamine neurotransmitters known as serotonin, dopamine and noradrenaline are the global neurotransmitters that modulate the brain's ability to feel pleasure, motivation, reward, planning, attention, and focus. When their reuptake is inhibited or their release is promoted, these neurotransmitters accumulate in the synaptic cleft (gaps between neurons) to non-ordinary levels, which makes them able to be reused. The result is neuronal activation at a multitude of brain regions which has the net result of producing a combination of stimulating, relaxing, disinhibiting and euphoric effects.[9]

Subjective effects

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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Transpersonal 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

Due to only having a short history of human use, the toxicity and harm potential is not exactly known. Due to its similarity to MDMA, it is likely that the administration of repeated or high dosages of 6-APB may be both neurotoxic and cardiotoxic[10][11] in some form.

The exact toxic dosage is unknown. It is strongly recommended that one use harm reduction practices when using this substance.

Short-term health concerns

Short-term physical health risks of 6-APB consumption include dehydration, insomnia, and hyperthermia (overheating).[12] Continuous activity without sufficient rest or rehydration may cause body temperature to rise to dangerous levels, and loss of fluid via excessive sweating puts the body at further risk as the stimulating and euphoric properties of the substance may render the user oblivious to their energy expenditure for quite some time. Diuretics such as alcohol may exacerbate these risks further.

Although it has not been formally studied, small changes in ambient temperature may cause large changes in 6-APB-induced serotonergic neurotoxicity as is the case with MDMA.[13][14]

Long-term health concerns

The neurotoxicity of 6-APB is subject to ongoing debate. It was specifically designed to be less neurotoxic than MDA or MDMA by circumventing the production of certain metabolic byproducts thought to underlie their toxicity (specifically alpha-methyl-dopamine).[citation needed] Although it is likely to be physically safe to try in a responsible context, it is completely possible that the administration of repeated or high dosages of 6-APB could result in neurotoxicity in some form, presenting as deficits in cognitive, affective and psychomotor function.

As with MDMA, the long-term, heavy usage of 6-APB (i.e. regular daily or weekly usage) is likely cardiotoxic and may lead to valvulopathy (heart valve issues) via its significant affinity for the 5-HT2B receptor.[15][16]

Tolerance and addiction potential

As with other stimulants, the chronic use of 6-APB 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.

As a potent releaser of serotonin, tolerance builds quickly with prolonged and repeated use to the point that the substance eventually loses any positive effects and instead leaves the user in an uncomfortable state of anxious, dysphoric stimulation. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3-4 weeks for the tolerance to be reduced to half and 6-8 weeks to be back at baseline (in the absence of further consumption). 6-APB presents cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of 6-APB 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.
  • 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.[17]
  • Stimulants - The potential neurotoxic effects of 6-APB may be significantly increased when combined with other stimulants.[citation needed]
  • Cocaine - This combination may cause severe strain on the heart, potentially resulting in a heart attack or stroke.

Serotonin syndrome risk

Combinations with the following substances may increase the level of neurotransmitters such as serotonin and dopamine to dangerous or even fatal levels.

There is an increased risk of serotonin syndrome when 6-APB is taken with many antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs).[citation needed] Additionally, if 6-APB is taken with SSRIs and SNRIs, it is likely to be significantly less effective if it produces any discernible effects at all.

Legal status

  • Australia and New Zealand: Certain countries contain a "substantially similar" catch-all clause in their drug law, such as New Zealand and Australia. This includes 6-APB as it is similar in chemical structure to the class A drug MDA, meaning 6-APB may be viewed as a controlled substance analogue in these jurisdictions.[citation needed]
  • Canada: 6-APB is Schedule III in Canada as it is an analogue of MDA. The CDSA was updated as a result of the Safe Streets Act changing amphetamines from Schedule 3 to Schedule 1.[citation needed]
  • Germany: 6-APB is illegal in Germany.[19]
  • Italy: 6-APB is illegal in Italy.[20]
  • Sweden: 6-APB is prohibited in Sweden as a "health hazard" as of 2009.[citation needed]
  • United Kingdom: On June 10, 2013, 6-APB and some analogues were classified as Temporary Class Drugs in the U.K. following an ACMD recommendation. On March 5, 2014, the U.K. Home Office announced that 6-APB would be made a class B drug on 10 June 2014 alongside every other benzofuran entactogen and many structurally related drugs.[21]
  • United States: 6-APB is unscheduled in the United States, but not currently approved by the Food and Drug Administration for human consumption.[citation needed]

See also

External links

Literature

References

  1. 1.0 1.1 Monte, A. P., Marona-Lewicka, D., Cozzi, N. V., & Nichols, D. E. (1993). Synthesis and pharmacological examination of benzofuran, indan, and tetralin analogs of 3, 4-(methylenedioxy) amphetamine. Journal of Medicinal Chemistry, 36(23), 3700-3706. https://doi.org/10.1021/jm00075a027
  2. Advisory Council on the Misuse of Drugs, Jeremy Browne (4 June 2013). "Temporary class drug order on benzofury and NBOMe compounds - letter from ACMD". GOV.UK.
  3. UK Home Office (28 April 2014). "The Misuse of Drugs Act 1971 (Ketamine etc.) (Amendment) Order 2014". The National Archives.
  4. 4.0 4.1 4.2 4.3 Iversen L, Gibbons S, Treble R, Setola V, Huang XP, Roth BL (2013). "Neurochemical profiles of some novel psychoactive substances". Eur. J. Pharmacol. 700 (1-3): 147–51. PMID 23261499. https://doi.org10.1016/j.ejphar.2012.12.006
  5. Rickli A, Kopf S, Hoener MC, Liechti ME (2015). "Pharmacological profile of novel psychoactive benzofurans". Br. J. Pharmacol. 172 (13): 3412–25. PMID 25765500. https://doi.org/10.1111/bph.13128
  6. 6.0 6.1 Canal CE, Murnane KS (2017). "The serotonin 5-HT2C receptor and the non-addictive nature of classic hallucinogens". J. Psychopharmacol. (Oxford). 31 (1): 127–143. PMID 27903793. https://doi.org/10.1177/0269881116677104
  7. US patent 7045545, Karin Briner, Joseph Paul Burkhart, Timothy Paul Burkholder, Matthew Joseph Fisher, William Harlan Gritton, Daniel Timothy Kohlman, Sidney Xi Liang, Shawn Christopher Miller, Jeffrey Thomas Mullaney, Yao-Chang Xu, Yanping Xu, "Aminoalkylbenzofurans as serotonin (5-HT(2c)) agonists", published 19 January 2000, issued 16 May 2006
  8. Advisory Council on the Misuse of Drugs, Jeremy Browne (4 June 2013). "Temporary class drug order on benzofury and NBOMe compounds - letter from ACMD". GOV.UK.
  9. New Insights into the Mechanism of Action of Amphetamines | http://www.annualreviews.org/doi/abs/10.1146/annurev.pharmtox.47.120505.105140
  10. Drug-induced Valvulopathy: An Update | tpx.sagepub.com/content/38/6/837.full
  11. Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/17950805
  12. Drug-induced hyperthermia | http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2044.1993.tb07423.x/abstract;jsessionid=FC30A9B157A2BAFC81048D8595714565.f02t03
  13. (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/9634574
  14. Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population | http://jop.sagepub.com/content/20/3/400
  15. Drug-induced Valvulopathy: An Update | tpx.sagepub.com/content/38/6/837.full
  16. Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/17950805
  17. 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
  18. 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
  19. "Anlage II BtMG - Einzelnorm)". Retrieved 2018-01-12. 
  20. http://www.salute.gov.it/imgs/C_17_pagineAree_3729_listaFile_itemName_0_file.pdf
  21. http://www.legislation.gov.uk/uksi/2014/1106/contents/made