MDAI

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Summary sheet: MDAI
MDAI
MDAI.svg
Chemical Nomenclature
Common names MDAI
Substitutive name 5,6-Methylenedioxy-2-aminoindane
Systematic name 6,7-Dihydro-5H-cyclopenta[f][1,3]benzodioxol-6-amine
Class Membership
Psychoactive class Entactogen
Chemical class Aminoindane
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 40 mg
Light 40 - 100 mg
Common 100 - 175 mg
Strong 175 - 300 mg
Heavy 300 mg +
Duration
Total 4 - 6 hours
Onset 20 - 40 minutes
Come up 30 - 60 minutes
Peak 2 - 2.5 hours
Offset 1 - 2 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.

5,6-Methylenedioxy-2-aminoindane (commonly known as MDAI) is an entactogen substance of the aminoindane chemical class that produces entactogenic effects when administered. Notably, this compound primarily produces the non-stimulating effects of prototypical entactogens like MDMA such as sedation, muscle relaxation, and tactile enhancement.

MDAI was developed in the 1990s by a team led by David E. Nichols at Purdue University. It acts as a putatively non-neurotoxic and highly selective serotonin releasing agent (SSRA) with neglible effects on dopamine and norepinephrine. This reportedly limits its potential at producing overtly invigorating, prosocial or euphoric effects.

MDAI has been marketed alongside research chemical entactogens like 5-MAPB, 5-APB, and 6-APB as a legal, grey-market alternative to MDMA.

Very little data exists about the pharmacological properties, metabolism, and toxicity of MDAI, and it has a limited history of human use. It is highly advised to use harm reduction practices if using this substance.

Chemistry

MDAI, or 5,6-methylenedioxy-2-aminoindane, is a synthetic molecule of the aminoindane class with structural similarity to amphetamines. It features the R3 terminal carbon of the propane chain of amphetamine bound to the benzene ring. This creates an indane group, a bicyclic moeity containing a benzene ring fused to a pentane ring. MDAI contains an amino group NH2 bound to R2 of the indane ring. MDAI also contains two oxygen substitutions at R5 and R6 joined by a methylene bridge to form a methylenedioxy group.

MDAI is structurally related to 2-AI, differing by a methylenedioxy ring.

Pharmacology

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This pharmacology section is incomplete.

You can help by adding to it.

MDAI has been shown to inhibit the reuptake of serotonin and has a selective affinity for the serotonin receptor. Studies have shown that the brains of animals treated with MDAI have greater extracellular concentrations of monoamine neural transmitters, most significantly serotonin.

For comparison, MDAI is similar in potency with releasing serotonin to MDA, but significantly less potent than MDMA.[1] 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, be reused and cause entactogenic effects.

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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Auditory 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 here:

Toxicity and harm potential

MDAI and other similar drugs have been widely used in scientific research as they are able to replicate many of the effects of MDMA, but without causing the associated neurotoxicity. No tests have been performed on cardiovascular toxicity.[2][3][4][5][6][7][8]

There is currently no scientific data on the lethal dose of MDAI in humans and the exact toxic dosage is unknown. Due to its action as a serotonin reuptake inhibitor, overdoses of this substance would likely result in serotonin syndrome.

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

Tolerance and addiction potential

Although no formal studies have been conducted, MDAI can be considered somewhat habit-forming with a low potential for abuse and is unlikely to be capable of causing psychological dependence among most users. This is because unlike traditional stimulants, MDAI does not increase concentrations of dopamine. If addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage.

Tolerance to many of the effects of MDAI 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).

MDAI presents cross-tolerance with all entactogenss, meaning that after the consumption of MDAI all serotonergic 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/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 may be increased when combined with other stimulants.
  • Cocaine - This combination may increase strain on the heart to a dangerous degree.

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.

  • Austria: MDAI is illegal to possess, produce and sell under the NPSG. (Neue-Psychoaktive-Substanzen-Gesetz Österreich)[citation needed]
  • Brazil - Possession, production and sale is illegal as it is listed on Portaria SVS/MS nº 344.[11]
  • China - As of October 2015, MDAI is a controlled substance in China.[12]
  • Denmark - MDAI is illegal in Denmark as of September 2015.[13]
  • United Kingdom - It is illegal to produce, supply, or import this drug under the Psychoactive Substance Act, which came into effect on May 26th, 2016.[14]

See also

External links

Community

References

  1. Johnson MP, Conarty PF, Nichols DE. [3H]monoamine releasing and uptake inhibition properties of 3,4-methylenedioxymethamphetamine and p-chloroamphetamine analogs. Eur J Pharmacol. 1991 Jul 23;200(1):9-16. PMID 1685125
  2. Nichols DE, Brewster WK, Johnson MP, Oberlender R, Riggs RM. Nonneurotoxic tetralin and indan analogs of 3,4-(methylenedioxy)amphetamine (MDA). Journal of Medicinal Chemistry. 1990 Feb;33(2):703-10. PMID 1967651
  3. Nichols DE, Johnson MP, Oberlender R. 5-Iodo-2-aminoindan, a non-neurotoxic analog of p-iodoamphetamine. Pharmacology, Biochemistry and Behaviour. 1991 Jan;38(1):135-9. PMID 1826785
  4. Johnson MP, Frescas SP, Oberlender R, Nichols DE. Synthesis and Pharmacological Examination of 1-(3-Methoxy-4-methylphenyl)-2-aminopropane and 5-Methoxy-6-methyl-2-aminoindan: Similarities to 3,4-(Methylenedioxy)methamphetamine (MDMA). Journal of Medicinal Chemistry 1991;34:1662-1668.
  5. Johnson MP, Huang XM, Nichols DE. Serotonin neurotoxicity in rats after combined treatment with a dopaminergic agent followed by a non-neurotoxic 3,4-methylenedioxymethamphetamine (MDMA) analog. Pharmacology, Biochemistry and Behaviour. 1991 Dec;40(4):915-22. PMID 1726189
  6. Nichols DE, Marona-Lewicka D, Huang X, Johnson MP. Novel serotonergic agents. Drug Design and Discovery. 1993;9(3-4):299-312. PMID 8400010
  7. Sprague JE, Johnson MP, Schmidt CJ, Nichols DE. Studies on the mechanism of p-chloroamphetamine neurotoxicity. Biochemical Pharmacology. 1996 Oct 25;52(8):1271-7. PMID 8937435
  8. Cozzi NV, Frescas S, Marona-Lewicka D, Huang X, Nichols DE. Indan analogs of fenfluramine and norfenfluramine have reduced neurotoxic potential. Pharmacology, Biochemistry and Behaviour. 1998 Mar;59(3):709-15. PMID 9512076
  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/10181/3115436/%281%29RDC_130_2016_.pdf/fc7ea407-3ff5-4fc1-bcfe-2f37504d28b7
  12. 关于印发《非药用类麻醉药品和精神药品列管办法》的通知 | http://www.sfda.gov.cn/WS01/CL0056/130753.html
  13. "Lists of euphoriant substances subject to control in Denmark". The Danish Medicines Agency. September 2015. | http://laegemiddelstyrelsen.dk/en/licensing/company-authorisations-and-registrations/euphoriant-substances/lists
  14. Psychoactive Substances Act 2016 (Legislation.gov.uk) | http://www.legislation.gov.uk/ukpga/2016/2/contents/enacted