MDAI - PsychonautWiki
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 / MDxx
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.

Interactions
Alcohol
MXE
Dissociatives
MDMA
Stimulants
DXM
25x-NBOMe
25x-NBOH
Tramadol
MAOIs
Serotonin releasers
5-HTP
SSRIs
SNRIs


5,6-Methylenedioxy-2-aminoindane (also known as MDAI) is a lesser-known novel entactogen substance of the aminoindane class. It acts as a putatively non-neurotoxic and highly selective serotonin releasing agent (SSRA) with neglible effects on dopamine and norepinephrine.

MDAI was developed by the American medicinal chemist and pharmacologist David E. Nichols during the 1990s at Purdue University.[citation needed] in the 2010s, MDAI was marketed alongside novel entactogens like 5-MAPB, 5-APB, and 6-APB as a legal, grey-market alternative to MDMA in the online research chemical market. It is currently being investigated as a potential alternative to traditional entactogens in the treatment of mental health conditions like anxiety and depression.[citation needed]

Subjective effects include sedation, muscle relaxation, tactile enhancement, anxiety suppression, enhanced empathy and sociability and euphoria. It has been described as producing the non-stimulating effects of prototypical entactogens like MDMA and MDA. It has been suggested that the lack of dopamine and norepinephrine activity limits its ability to produce overtly invigorating, prosocial or euphoric effects but with the benefit of decreased neurotoxicity and side-effects. However, more research is required to validate these claims.

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

 

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.[citation needed]

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

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

Physical effects
 

Visual effects
 

Cognitive effects
 

Auditory effects
 

After effects
 

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

 

This toxicity and harm potential section is a stub.

As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it.
Note: Always conduct independent research and use harm reduction practices if using this substance.

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.

Dependence and abuse 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 entactogens, meaning that after the consumption of MDAI all serotonergic stimulants will have a reduced effect.

Dangerous interactions

Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous or even life-threatening when combined with certain other substances. The following lists some known dangerous interactions (although it is not guaranteed to include all of them).

Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

  • 25x-NBOMe & 25x-NBOH - 25x compounds are highly stimulating and physically straining. Combinations with MDAI should be strictly avoided due to the risk of excessive stimulation and heart strain. This can result in increased blood pressure, vasoconstriction, panic attacks, thought loops, seizures, and heart failure in extreme cases.
  • Alcohol - Combining alcohol with stimulants can be dangerous due to the risk of accidental over-intoxication. Stimulants mask alcohol's depressant effects, which is what most people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects will be left unopposed, which can result in blackouts and severe respiratory depression. If mixing, the user should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - Combinations with DXM should be avoided due to its inhibiting effects on serotonin and norepinephrine reuptake. There is an increased risk of panic attacks and hypertensive crisis, or serotonin syndrome with serotonin releasers (MDMA, methylone, mephedrone, etc.). Monitor blood pressure carefully and avoid strenuous physical activity.
  • MDMA - Any neurotoxic effects of MDMA are likely to be increased when other stimulants are present. There is also a risk of excessive blood pressure and heart strain (cardiotoxicity).
  • MXE - Some reports suggest combinations with MXE may dangerously increase blood pressure and increase the risk of mania and psychosis.
  • Dissociatives - Both classes carry a risk of delusions, mania and psychosis, and these risk may be multiplied when combined.
  • Stimulants - MDAI may be dangerous to combine with other stimulants like cocaine as they can increase one's heart rate and blood pressure to dangerous levels.
  • Tramadol - Tramadol is known to lower the seizure threshold[9] and 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

  • Austria: MDAI is illegal to possess, produce and sell under the NPSG (Neue-Psychoaktive-Substanzen-Gesetz Österreich).[citation needed]
  • Brazil: MDAI is illegal to possess, produce and sell under 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]
  • Germany: MDAI is controlled under the NpSG (New Psychoactive Substances Act)[14] as of November 26, 2016.[15] Production and import with the aim to place it on the market, administration to another person and trading is punishable. Possession is illegal but not penalized.[16]
  • Switzerland: MDAI is a controlled substance specifically named under Verzeichnis E. It is a controlled substance since December 2011.[17]
  • Turkey: MDAI is a classed as drug and is illegal to possess, produce, supply, or import.[18] [19]
  • United Kingdom: MDAI is illegal to produce, supply, or import under the Psychoactive Substance Act, which came into effect on May 26th, 2016.[20]

See also

External links

Discussion

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. doi:10.1007/BF03161089. eISSN 1937-6995. ISSN 1556-9039. OCLC 163567183. 
  10. Gillman, P. K. (2005). "Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity". British Journal of Anaesthesia. 95 (4): 434–441. doi:10.1093/bja/aei210 . eISSN 1471-6771. ISSN 0007-0912. OCLC 01537271. PMID 16051647. 
  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. "Anlage NpSG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 15, 2019. 
  15. "Gesetz zur Bekämpfung der Verbreitung neuer psychoaktiver Stoffe" (PDF) (in German). Bundesanzeiger Verlag. Retrieved December 15, 2019. 
  16. "§ 4 NpSG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 15, 2019. 
  17. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  18. https://resmigazete.gov.tr/eskiler/2014/01/20140125-3.htm
  19. https://resmigazete.gov.tr/eskiler/2014/01/20140125-3-1.pdf
  20. Psychoactive Substances Act 2016 (Legislation.gov.uk) | http://www.legislation.gov.uk/ukpga/2016/2/contents/enacted