3,4-Methylenedioxyamphetamine

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3,4-Methylenedioxyamphetamine
MDA-2D-skeletal.svg
MDA molecule ball.png
Systematic (IUPAC) name
(R) 1-(benzo[1,3]dioxol-5-yl)propan-2-amine
Clinical data
Legal status
Routes Oral, Sublingual, Intranasal
Pharmacokinetic data
Metabolism Hepatic, CYP extensively involved
Excretion Renal
Identifiers
CAS number 4764-17-4 YesY
ATC code None
PubChem CID 1614
DrugBank DB01509
ChemSpider 1555 YesY
ChEMBL CHEMBL6731 YesY
Chemical data
Formula C10H13NO2 
Molecular mass 179.22 g/mol
 YesY (what is this?)  (verify)

3,4-Methylenedioxyamphetamine (MDA), also known as tenamfetamine (INN), or colloquially as "Sally", "Sass", "Sass-a-frass" or "Mellow Drug of America", is a psychoactive drug of the substituted methylenedioxyphenethylamine and substituted amphetamine classes of drugs that is consumed primarily for its entactogenic, psychedelic, and psychostimulant effects. Pharmacologically, MDA acts as a serotonin-norepinephrine-dopamine releasing agent and reuptake inhibitor. Possession of MDA is illegal in most countries. Some limited exceptions exist for scientific and medical research. The recreational use of MDA predates its more widely used analog MDMA (ecstasy).

Use[edit]

Medical[edit]

MDA currently has no accepted medical use.

Recreational[edit]

Although illegal, MDA is bought, sold, and used as a recreational 'love drug', due to its enhancement of empathy.[1] A recreational dose of MDA is commonly between 100 and 160 mg.[2]

Effects[edit]

While MDA is generally similar to MDMA, users report that MDA has more stimulant and psychedelic qualities and less intense entactogenic effects than MDMA. MDA is also considered less predictable than MDMA, with effects varying greatly from person to person. MDA is best known for its enhancement of the experiences of dancing and sex.[medical citation needed]

Overdose[edit]

Symptoms of acute toxicity may include agitation, sweating, increased blood pressure and heart rate, dramatic increase in body temperature, convulsions, and death. Death is usually caused by cardiac effects and subsequent hemorrhaging in the brain (stroke).[3][medical citation needed]

Pharmacology[edit]

Pharmacodynamics[edit]

MDA is a substrate of the serotonin, norepinephrine, and dopamine transporters, as well as a TAAR1 agonist,[4][5] and for that reason, acts as a reuptake inhibitor and releasing agent of serotonin, norepinephrine, and dopamine (or as an SNDRA).[6] It is also an agonist of the 5-HT2A,[7] 5-HT2B,[8] and 5-HT2C receptors,[9] and shows affinity for the α2A-, α2B-, α2C-adrenergic receptors and 5-HT1A and 5-HT7 receptors.[10]

The effect on serotonin may explain the similar euphoric and empathogenic effects of the two compounds MDMA and MDA. However, (S)-MDA has a higher efficacy in stimulating the 5-HT2A receptor than (R)-MDMA; thus MDA tends to cause more psychedelic-like effects, such as visual hallucinations. MDMA can also produce psychedelic-like visual effects, though these are generally less pronounced than those of MDA, or require a heavier dose to become apparent.[citation needed]

Pharmacokinetics[edit]

The "S" optical isomer of MDA is more potent than the "R" optical isomer as a psychostimulant, possessing greater affinity for the three monoamine transporter proteins (SERT, NET and DAT). The duration of the drug has been reported as about 6 to 8 hours.[2]

Physical and chemical properties[edit]

Synthesis[edit]

MDA is typically synthesized from essential oils such as safrole or piperonal.

Synthesis of MDA and related analogs from safrole

History[edit]

MDA was first synthesized by G. Mannish and W. Jacobson in 1910. It was first ingested in July 1930 by Gordon Alles who later licensed the drug to Smith Kline and French.[11] MDA was first used in animal tests in 1939, and human trials began in 1941 in the exploration of possible therapies for Parkinson's disease. From 1949 to 1957, more than 500 human subjects were given MDA in an investigation of its potential use as an antidepressant and/or anorectic by Smith, Kline & French. The United States Army also experimented with the drug, code named EA-1298, while working to develop a truth drug or incapacitating agent. Harold Blauer[12] died in January 1953 after being intravenously injected with 450 mg of the drug. MDA was patented as a cough suppressant by H. D. Brown in 1958, as an ataractic by Smith, Kline & French in 1960, and as an anorectic under the trade name "Amphedoxamine" in 1961. MDA began to appear on the recreational drug scene around 1963 to 1964. It was then inexpensive and readily available as a research chemical from several scientific supply houses. Several researchers, including Claudio Naranjo and Richard Yensen, have explored MDA in the field of psychotherapy.[citation needed]

References[edit]

  1. ^ Monte AP, Marona-Lewicka D, Cozzi NV, Nichols DE. (1993). "Synthesis and pharmacological examination of benzofuran, indan, and tetralin analogues of 3,4-(methylenedioxy)amphetamine". Journal of Medicinal Chemistry 36 (23): 3700–3706. doi:10.1021/jm00075a027. PMID 8246240. Retrieved 20 January 2014. 
  2. ^ a b Baggott MJ, Siegrist JD, Galloway GP, Robertson LC, Coyle JR, Mendelson, JE. Investigating the Mechanisms of Hallucinogen-Induced Visions Using 3,4-Methylenedioxyamphetamine (MDA): A Randomized Controlled Trial in Humans. DOI: 10.1371/journal.pone.0014074
  3. ^ Diaz, Jaime. How Drugs Influence Behavior. Englewood Cliffs: Prentice Hall, 1996.
  4. ^ Lewin AH, Miller GM, Gilmour B (December 2011). "Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class". Bioorg. Med. Chem. 19 (23): 7044–8. doi:10.1016/j.bmc.2011.10.007. PMC 3236098. PMID 22037049. 
  5. ^ Wallach, J.V. (2009). "Endogenous hallucinogens as ligands of the trace amine receptors: A possible role in sensory perception". Medical Hypotheses 72 (1): 91–94. doi:10.1016/j.mehy.2008.07.052. ISSN 0306-9877. 
  6. ^ Rothman R, Baumann M (2006). "Therapeutic potential of monoamine transporter substrates". Curr Top Med Chem 6 (17): 1845–59. PMID 17017961. 
  7. ^ Giuseppe Di Giovanni; Vincenzo Di Matteo; Ennio Esposito (2008). Serotonin-dopamine Interaction: Experimental Evidence and Therapeutic Relevance. Elsevier. pp. 294–. ISBN 978-0-444-53235-0. 
  8. ^ Rothman, Richard B; Baumann, Michael H (2009). "Serotonergic drugs and valvular heart disease". Expert Opinion on Drug Safety 8 (3): 317–329. doi:10.1517/14740330902931524. ISSN 1474-0338. 
  9. ^ Nash J, Roth B, Brodkin J, Nichols D, Gudelsky G (1994). "Effect of the R(-) and S(+) isomers of MDA and MDMA on phosphatidyl inositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors". Neurosci. Lett. 177 (1-2): 111–5. PMID 7824160. 
  10. ^ Manzoni, Olivier Jacques; Ray, Thomas S. (2010). "Psychedelics and the Human Receptorome". PLoS ONE 5 (2): e9019. doi:10.1371/journal.pone.0009019. ISSN 1932-6203. 
  11. ^ The First MDA trip and the measurement of ‘mystical experience’ after MDA, LSD, and Psilocybin http://psychedelicresearch.org/?p=45
  12. ^ The History Channel documented details of his death here http://www.youtube.com/watch?v=ySw-0uY4CUA See minute 2:38 onward.

External links[edit]