DOI

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Summary sheet: DOI


DOI
DOI.svg
Chemical Nomenclature
Common names DOI
Substitutive name 2,5-Dimethoxy-4-iodoamphetamine
Systematic name 1-(4-Iodo-2,5-dimethoxyphenyl)-2-propanamine
Class Membership
Psychoactive class Psychedelic
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.



Oral
Dosage
Threshold 0.5 mg
Light 0.5 - 1 mg
Common 1 - 2 mg
Strong 2 - 3 mg
Heavy 3 mg +
Duration
Total 16 - 24 hours
Onset 1 - 2 hours
Come up 1.5 - 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.

2,5-Dimethoxy-4-iodoamphetamine (also known as DOI) is a lesser-known psychedelic substance of the phenethylamine chemical class. It is a member of the DOx family of psychedelic amphetamines.

The synthesis of DOI was first reported in 1972[1] and its usage in humans was first documented by Alexander Shulgin in the 1991 book PiHKAL ("Phenethylamines I Have Known and Loved").[citation needed] DOI is very well-researched compared to most psychedelics. It is regularly used in research as a radioligand to map serotonin-2A receptors in the brain.[citation needed]

The effects of DOI are often compared to those of LSD, although notable differences can be distinguished. Besides the significantly longer duration, the experience is commonly reported to be more stimulating than LSD, with a more pronounced body load and a less complex head space. The after effects include long-lasting residual stimulation and difficulty sleeping, which, depending on the dose and time taken during the day, may persist for days afterwards.[2]

DOI is sometimes sold as a substitute for LSD, or even sold falsely as LSD. This can be dangerous because DOI does not have the same established safety profile as LSD.[3]

Along with its sensitive dose-response and unusually long duration, many reports also suggest that this substance may be overly difficult to use safely for those who are not already experienced with psychedelics. Therefore it is highly advised to approach this highly dose-sensitive, and long-lasting psychedelic substance with the proper amount of precaution and harm reduction practices if using it.

History and culture

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DOI was first synthesized by a team at the University of Alberta in 1972.[4]

Chemistry

DOI, or 2,5-Dimethoxy-4-iodoamphetamine, is a molecule of the amphetamine class. Amphetamines are substituted phenethylamines containing a phenyl ring bound to an amino (NH2) group through an ethyl chain and a methyl group bound to the alpha carbon Rα. DOI contains methoxy functional groups OCH3 attached to carbons R2 and R5 as well as an iodine atom attached to carbon R4 of the phenyl ring. DOI is the amphetamine, or alpha-methylated analogue, of the phenethylamine 2C-I.[5]

Pharmacology

Further information: Serotonergic psychedelic

DOI's psychedelic effects are believed to come from its efficacy as an agonist at the 5-HT2A, 5-HT2B and 5-HT2C receptors.[6] However, the role of these interactions and how they result in the psychedelic experience continues to remain the subject of ongoing scientific inquiry.

DOI and its isomers binding profiles to specific 5HT receptor sets can be seen in the chart below:

Binding Profile of DOI and its isomers
Receptor Ki (racemic DOI)[7] Ki (R-DOI)[7] Ki (S-DOI)[7] Intrinsic activity[6]
5-HT1A 2355 nM 3843 nM ND ND
5-HT1B 1261 nM ND ND ND
5-HT1D 1241.3 nM ND ND ND
5-HT1E 2970 nM ND ND ND
5-HT1F 2125.44 nM ND ND ND
5-HT2A 0.68 nM 0.65 nM 0.65 nM Partial agonist.
5-HT2B 20.03 nM 53.70318 nM 28.183829 nM Partial agonist/full agonist
5-HT2C 2.38 nM 5.370318 nM 8.317638 nM Partial agonist/full agonist
5-HT5A 1000 nM ND ND ND
5-HT5A 1000 nM ND ND ND
5-HT6 >10000 nM ND ND ND

Besides its action as a psychedelic, DOI has been shown to be an extremely potent inhibitor of tumour necrosis factor-alpha inflammation at picomolar concentrations in cell studies. TNF-alpha is an important target for research into degenerative conditions such as rheumatoid arthritis and Alzheimer's disease where the disease process involves tissue damage through chronic inflammation. This could make DOI and other 5-HT2A agonists an entirely new area for development of novel treatments for these conditions.[8]

DOI has also been shown to induce rapid growth and reorganization of dendritic spines and synaptic connections with other neurons, processes known to underlie neuroplasticity.[9]

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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Visual effects
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Cognitive effects
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Multi-sensory 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

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This toxicity and harm potential section is a stub.

As such, it may contain incomplete or even dangerously wrong information. You can help by expanding or correcting it.
We also recommend that you conduct independent research and use harm reduction practices when using this substance.

The toxicity and long-term health effects of recreational DOI do not seem to have been studied in any scientific context and the exact toxic dose is unknown. This is because DOI is a research chemical with very little history of human usage.

Anecdotal reports from users suggests that there are no negative health effects attributed to simply trying it by itself at low to moderate doses and using it very sparingly (but nothing can be completely guaranteed). Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

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

Overdose

The risk of DOI overdose is present starting in the heavy dose range, although sensitive users may overdose at doses lower than these. Non-oral routes also seem to exhibit a higher chance of overdosing, perhaps owing to differences in bioavailability, potency and unpredictability of dosage and effects. Overdose effects typically include bizzare, delusional and sometimes violent behavior, amnesia, numbness, confusion and anxiety. The user may not be able to communicate and can be severely agitated. At appropriately high doses, more serious side effects include panic attacks, seizures, dangerously elevated heart rate, blood pressure and vasoconstriction.[citation needed] Severe vasoconstriction typically develops to its peak several hours into the intoxication and may need medical assistance if blood flow is significantly cut off for extended periods of time.

In the event of an overdose, benzodiazepines can be administered to mitigate the hyperagitative effects.[citation needed] A powerful vasodilator may also need to be administered to prevent a hypertensive emergency, or in more serious cases, necrosis, organ failure and death from the resulting hypoxia.[citation needed] As a result, emergency medical services should always be sought in the event of a DOI overdose.

Tolerance and addiction potential

DOI is not habit-forming and the desire to use it can actually decrease with use. It is most often self-regulating.

Tolerance to the effects of DOI are built almost immediately after ingestion. After that, it takes about 5-7 days for the tolerance to be reduced to half and 10-14 days to be back at baseline (in the absence of further consumption). DOI presents cross-tolerance with all psychedelics, meaning that after the consumption of DOI all psychedelics will have a reduced effect.

Dangerous interactions

Although many psychoactive substances are safe to use on their own, they can quickly become dangerous or even life-threatening when combined with other substances. The following lists some known dangerous combinations, but may not include all of them. A combination that appears to be safe in low doses can still increase the risk of injury or death. Independent research should always be conducted to ensure that a combination of two or more substances is safe to consume.

Legal status

  • Austria: DOI is illegal to possess, produce and sell under the NPSG (Neue-Psychoaktive-Substanzen-Gesetz Österreich).[citation needed]
  • Australia: DOI is not listed as a prohibited substance in The Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP).[11]
  • Brazil: DOI is illegal to possess, produce and sell as it is listed on Portaria SVS/MS nº 344.[12]
  • Canada: DOI is listed as a Schedule 1[13] drug as it is an analogue of amphetamine.[14] The CDSA was updated as a result of the Safe Streets Act changing amphetamines from Schedule 3 to Schedule 1.
  • Denmark: DOI became illegal on April 8, 2007.[citation needed]
  • Latvia: DOI is a Schedule I controlled substance.[15]
  • Sweden: DOI is a Schedule I substance as of August 30, 2007; this was published by the Medical Products Agency in their regulation LVFS 2007:10.[16]
  • United Kingdom: DOI is illegal to produce, supply, or import under the Psychoactive Substance Act, which came into effect on May 26th, 2016.[17]
  • United States: DOI is not scheduled in the United States, but it is likely that it would be considered an analog (of DOB) in which case sales or possession could be prosecuted under the Federal Analogue Act. DOI is regularly used in animal and in vitro research.[citation needed]
    • Florida: DOI is a Schedule I controlled substance in the state of Florida.[18]

See also

External links

Discussion

References

  1. Coutts, R. T., & Malicky, J. L. (1973). The synthesis of some analogs of the hallucinogen 1-(2, 5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM). Canadian Journal of Chemistry, 51(9), 1402-1409. https://doi.org/10.1139/v73-210
  2. Cite error: Invalid <ref> tag; no text was provided for refs named DOI TiHKAL
  3. LSD BLOTTER ACID MIMICS (ACTUALLY CONTAINING 4-IODO-2,5-DIMETHOXYAMPHETAMINE (DOI) AND 4-CHLORO-2,5-DIMETHOXYAMPHETAMINE (DOC)) IN LANTANA, FLORIDA | http://web.archive.org/web/20090204025435/http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg0608/mg0608.html
  4. Coutts, R. T., & Malicky, J. L. (1973). The synthesis of some analogs of the hallucinogen 1-(2, 5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM). Canadian Journal of Chemistry, 51(9), 1402-1409. https://doi.org/10.1139/v73-210
  5. http://isomerdesign.com/PiHKAL/read.php?domain=pk&id=67
  6. 6.0 6.1 Head-twitch response in rodents induced by the hallucinogen 2,5-dimethoxy-4-iodoamphetamine: a comprehensive history, a re-evaluation of mechanisms, and its utility as a model (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/22517680
  7. 7.0 7.1 7.2 Roth, BL; Driscol, J (12 January 2011). "PDSP Ki Database". Psychoactive Drug Screening Program (PDSP). University of North Carolina at Chapel Hill and the United States National Institute of Mental Health. Retrieved 4 March 2014.
  8. Serotonin 5-Hydroxytryptamine2A Receptor Activation Suppresses Tumor Necrosis Factor-α-Induced Inflammation with Extraordinary Potency | Journal of Pharmacology and Experimental Therapeutics (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/18708586
  9. Jones, K. A., Srivastava, D. P., Allen, J. A., Strachan, R. T., Roth, B. L., & Penzes, P. (2009). Rapid modulation of spine morphology by the 5-HT2A serotonin receptor through kalirin-7 signaling. Proceedings of the National Academy of Sciences, 106(46), 19575-19580. PMID: 19889983. https://doi.org/10.1073/pnas.0905884106
  10. 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. doi:10.1007/BF03161089
  11. Therapeutic Goods Administration. Australian Government Department of Health and Ageing | http://www.comlaw.gov.au/Details/F2013L01607/229bdf2e-7014-4379-b751-0b584f55d699
  12. http://portal.anvisa.gov.br/documents/10181/3115436/%281%29RDC_130_2016_.pdf/fc7ea407-3ff5-4fc1-bcfe-2f37504d28b7
  13. Canadian Legal Information Institute (CanLII). Controlled Drugs and Substances Act, S.C. 1996, c. 19, as amended | http://isomerdesign.com/Cdsa/schedule.php?schedule=1&section=18.5&structure=C
  14. Canadian Legal Information Institute (CanLII). Controlled Drugs and Substances Act, S.C. 1996, c. 19, as amended | http://isomerdesign.com/Cdsa/definitions.php?structure=C
  15. Noteikumi par Latvijā kontrolējamajām narkotiskajām vielām, psihotropajām vielām un prekursoriem (2,5-Dimetoksifeniletānamīni) | http://likumi.lv/doc.php?id=121086
  16. Läkemedelsverkets författningssamling | http://www.lakemedelsverket.se/upload/lvfs/LVFS_2007-10.pdf
  17. Psychoactive Substances Act 2016 (Legislation.gov.uk) | http://www.legislation.gov.uk/ukpga/2016/2/contents/enacted
  18. The 2015 Florida Statutes Title XLVI CRIMES Chapter 893 DRUG ABUSE PREVENTION AND CONTROL | http://leg.state.fl.us/statutes/index.cfm?App_mode=Display_Statute&URL=0800-0899/0893/0893.html