3,4-Methylenedioxyamphetamine

3,4-Methylenedioxyamphetamine (MDA) is an entactogen, stimulant, and psychedelic drug of the amphetamine and MDxx families that is encountered mainly as a recreational drug.<ref name="Oeri2021">Template:Cite journal</ref><ref name="HarpreetKarabulutGauld2023" /><ref name="PiHKAL1991">Template:Cite book</ref> It is usually taken orally.<ref name="Oeri2021" /><ref name="PiHKAL1991" />

In terms of its pharmacology, MDA is a serotonin–norepinephrine–dopamine releasing agent (SNDRA) and a serotonin 5-HT₂ receptor agonist, including of the serotonin 5-HT_2A receptor.<ref name="Oeri2021" /> It has a duration of 5 to 8Template:Nbsphours.<ref name="Oeri2021" /><ref name="BaggottGarrisonCoyle2019" />

MDA has a long history of psychotherapeutic and recreational use that predates that of MDMA, dating back to at least the mid-1960s.<ref name="Oeri2021" /><ref name="Sáez-BrionesHernández2013" /><ref name="HarpreetKarabulutGauld2023">Template:Cite journal</ref> It has been described as the first entactogen.<ref name="BaggottGarrisonCoyle2019" /> MDA has also been described as probably the most popular analogue of MDMA.<ref name="Sáez-BrionesHernández2013">Template:Cite journal</ref> In most countries, the drug is a controlled substance and its possession and sale are illegal.

Use and effects

MDA is bought, sold, and used as a recreational drug due to its enhancement of mood and empathy.<ref name="MonteMarona-LewickaCozzi1993">Template:Cite journal</ref> It produces MDMA-like effects, including entactogenic and stimulant effects, as well as mild psychedelic effects.<ref name="BaggottGarrisonCoyle2019" /><ref name="BaggottSiegristGalloway2010" /><ref name="BaggottSiegristCoyle2010">Template:Cite journal</ref>

The dose range of MDA given in Alexander Shulgin's book PiHKAL (Phenethylamines I Have Known and Loved) and other sources is 80 to 160Template:Nbspmg.<ref name="PiHKAL1991" /><ref name="Oeri2021" /> A wider recreational dose range for MDA of 20 to 200Template:Nbspmg or more, with a typical dose estimate of 90Template:Nbspmg, has also been reported.<ref name="LuethiLiechti2018">Template:Cite journal</ref> The dose range of MDA is very similar to that of MDMA.<ref name="PiHKAL1991" /><ref name="Oeri2021" /><ref name="LuethiLiechti2018" /><ref name="BaggottGarrisonCoyle2019" />

The effects of MDA include euphoria, empathy, emotional amplification, relaxation, feeling at peace with the world, increased introspection, self-awareness, and acceptance, authenticity, clarity of thought, a desire to communicate with others and relate personal issues, and emotional bonding with others.<ref name="Oeri2021" /><ref name="Nichols1986" /><ref name="Shulgin1978" /> These effects led to MDA being called the "love drug" or "hug drug".<ref name="Nichols1986" /><ref name="PiHKAL1991" /> MDA also produces mild psychedelic effects, including brightened colors, closed-eye visuals or complex mental imagery, synaesthesia, and rarely mild hallucinations.<ref name="Oeri2021" /><ref name="BaggottGarrisonCoyle2019">Template:Cite journal</ref> It does not produce profound sensory disruption or overt hallucinations.<ref name="Nichols1986">Template:Cite journal</ref><ref name="Shulgin1978" /> In any case, the drug has still been found to produce mystical or spiritual experiences.<ref name="BaggottSiegristGalloway2010" /><ref name="BaggottGarrisonCoyle2019" />

MDA shares most of MDMA's qualitative and emotional effects, including entactogenic and stimulant effects.<ref name="Oeri2021" /><ref name="Shulgin1978" /><ref name="BaggottGarrisonCoyle2019" /> However, it has been said to be slightly less stimulating than MDMA.<ref name="Oeri2021" /><ref name="BaggottGarrisonCoyle2019" /> In addition, MDA's hallucinogenic effects are much greater than those of MDMA, although still less than those of classical psychedelics like psilocybin.<ref name="Oeri2021" /><ref name="Nichols1986" /><ref name="BaggottGarrisonCoyle2019" /> Another difference between the two drugs is that MDA appears to produce a more introverted and emotionally intense prosocial state, while MDMA encourages a more extroverted and gregarious prosocial state.<ref name="BaggottGarrisonCoyle2019" />

Besides its psychoactive effects, MDA produces sympathomimetic effects such as increased heart rate and blood pressure, among other physiological effects.<ref name="Sáez-BrionesHernández2013" /><ref name="Shulgin1978" /><ref name="BaggottGarrisonCoyle2019" />

In terms of the individual enantiomers of MDA, (R)-MDA produces psychedelic effects and some entactogenic effects, while (S)-MDA is non-hallucinogenic, produces similar entactogenic effects as the racemate, and has considerable stimulant effects.<ref name="Nichols1986" /><ref name="Shulgin1978">Template:Cite book</ref><ref name="PiHKAL1991" /> High doses of enantiopure (R)-MDA, in the range of 120 to 200Template:Nbspmg, are described as closely resembling the effects of LSD, for instance doses of 200 to 400Template:Nbspμg.<ref name="Shulgin1978" /><ref name="YensenDiLeoRhead1976">Template:Cite journal</ref> Enantiopure (R)-MDA at high doses produces more robust psychedelic effects than typical doses of racemic MDA.<ref name="Shulgin1978" /><ref name="YensenDiLeoRhead1976" /><ref name="PiHKAL1991" />

The duration of MDA is about 5 to 8Template:Nbsphours and is about 2Template:Nbsphours longer than that of MDMA (3–6Template:Nbsphours).<ref name="Oeri2021" /><ref name="BaggottGarrisonCoyle2019" /> Shulgin originally gave a duration of MDA of 8 to 12Template:Nbsphours in PiHKAL, but he later revised this down to only 3 to 6Template:Nbsphours.<ref name="PiHKAL1991" /> A modern clinical study gave a duration of 6 to 8Template:Nbsphours.<ref name="BaggottGarrisonCoyle2019" />

Side effects

Side effects of MDA include sympathomimetic effects like increased heart rate and blood pressure as well as increased cortisol and prolactin levels.<ref name="BaggottGarrisonCoyle2019" /><ref name="BaggottSiegristCoyle2010" />

Overdose

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).<ref name="Diaz">Template:Cite book</ref>Template:Medical citation needed

Pharmacology

Pharmacodynamics

Template:Nowrap

Target	Affinity (Ki, nM)
Template:Abbrlink	5,600–>10,000 (Ki) 478–4,900 (Template:Abbrlink) 160–162 (Template:Abbrlink) (rat)
Template:Abbrlink	13,000 (Ki) 150–420 (Template:Abbr) 47–108 (Template:Abbr) (rat)
Template:Abbrlink	>26,000 (Ki) 890–20,500 (Template:Abbr) 106–190 (Template:Abbr) (rat)
5-HT1A	3,762–>10,000
5-HT1B	>10,000
5-HT1D	>10,000
5-HT1E	>10,000
5-HT1F	Template:Abbr
5-HT2A	3,200–>10,000 (Ki) 630–1,767 (Template:Abbr) 57–99% (Template:Abbrlink)
5-HT2B	91–100 (Ki) 190–850 (Template:Abbr) 51–80% (Template:Abbr)
5-HT2C	3,000–6,418 (Ki) 98–4,800 (Template:Abbr) 79–118% (Template:Abbr)
5-HT3	>10,000
5-HT4	Template:Abbr
5-HT5A	>10,000
5-HT6	>10,000
5-HT7	3,548
α1A	8,700–>10,000
α1B	>10,000
α1D	Template:Abbr
α2A	1,100–2,600
α2B	690
α2C	229
β1, β2	>10,000
D1–D5	>10,000–>20,000
H1–H4	>10,000–>13,000
M1–M5	Template:Abbr
nACh	Template:Abbr
TAAR1	220–250 (Ki) (rat) 740 (Template:Abbr) (rat) 86% (Template:Abbr) (rat) 160–180 (Ki) (mouse) 580 (Template:Abbr) (mouse) 102% (Template:Abbr) (rat) 3,600 (Template:Abbr) (human) 11% (Template:Abbr) (human)
I1	>10,000
σ1, σ2	Template:Abbr
Notes: The smaller the value, the more avidly the drug binds to the site. Proteins are human unless otherwise specified. Refs:<ref name="PDSPKiDatabase">Template:Cite web</ref><ref name="BindingDB">Template:Cite web</ref><ref name="Ray2010">Template:Cite journal</ref><ref name="LuethiKolaczynskaWalter2019">Template:Cite journal</ref><ref name="KolaczynskaDucretTrachsel2022" /><ref name="RickliKopfHoener2015">Template:Cite journal</ref><ref name="SetolaHufeisenGrande-Allen2003">Template:Cite journal</ref> <ref name="Blough2008" /><ref name="BrandtWaltersPartilla2020">Template:Cite journal</ref><ref name="GainetdinovHoenerBerry2018">Template:Cite journal</ref><ref name="SimmlerBuchyChaboz2016">Template:Cite journal</ref>

MDA is a substrate of the serotonin, norepinephrine, dopamine, and vesicular monoamine transporters, and in relation to this, acts as a reuptake inhibitor and releasing agent of serotonin, norepinephrine, and dopamine (that is, it is an Template:Abbrlink).<ref name="Oeri2021" /><ref name="pmid17017961">Template:Cite journal</ref> It is also an agonist of the serotonin 5-HT_2A,<ref name="GiovanniMatteo2008">Template:Cite book</ref> 5-HT_2B,<ref name="RothmanBaumann2009">Template:Cite journal</ref> and 5-HT_2C receptors<ref name="pmid7824160">Template:Cite journal</ref> and shows affinity for the α_2A-, α_2B-, and α_2C-adrenergic receptors and serotonin 5-HT_1A and 5-HT₇ receptors.<ref name="ManzoniRay2010">Template:Cite journal</ref>

In addition to its actions as a monoamine releasing agent, MDA is a potent high-efficacy partial agonist or full agonist of the rodent TAAR1.<ref name="GainetdinovHoenerBerry2018" /><ref name="SimmlerBuchyChaboz2016" /> Conversely, MDA is much weaker in terms of potency as an agonist of the human TAAR1.<ref name="GainetdinovHoenerBerry2018" /><ref name="SimmlerBuchyChaboz2016" /><ref name="LewinMillerGilmour2011">Template:Cite journal</ref> Moreover, MDA acts as a very weak partial agonist or antagonist of the human TAAR1 rather than as an efficacious agonist.<ref name="GainetdinovHoenerBerry2018" /><ref name="SimmlerBuchyChaboz2016" /> TAAR1 activation is thought to auto-inhibit and constrain the effects of amphetamines that act as TAAR1 agonists, for instance MDMA in rodents.<ref name="EspinozaGainetdinov2014">Template:Cite book</ref><ref name="KuropkaZawadzkiSzpot2023">Template:Cite journal</ref><ref name="SimmlerBuserDonzelli2013">Template:Cite journal</ref><ref name="DiCaraMaggioAloisi2011">Template:Cite journal</ref>

MDA fully substitutes for MDMA in rodent drug discrimination tests.<ref name="Oeri2021" /> However, its prosocial effects in rodents are said to not fully resemble those of MDMA.<ref name="Sáez-BrionesHernández2013" /><ref name="Sáez-BrionesCastroMaass2011">Sáez-Briones P, Castro V, Maass M, Mundaca E, Villagra M, Díaz-Véliz G. Modelo animal de interacción social: administración aguda de MDMA (3-4-metilendioximetanfetamina “Extasis”) y algunos de sus análogos en ratas Sprague-Dawley. Rev. Farmacol. Chile. 2011;4: 72.</ref> MDA also substitutes for stimulants like dextroamphetamine and cocaine in drug discrimination tests.<ref name="Oeri2021" /><ref name="Sáez-BrionesHernández2013" /><ref name="Nichols1986" /> The (S)-optical isomer of MDA is more potent than the (R)-optical isomer as a psychostimulant, possessing greater activity at the monoamine transporters.<ref name="Oeri2021" /><ref name="Nichols1986" /> MDA and (R)-MDA but not (S)-MDA fully substitute for serotonergic psychedelics including DOM, LSD, and mescaline.<ref name="Oeri2021" /><ref name="HalberstadtChathaKlein2020" /><ref name="Sáez-BrionesHernández2013" /> Similarly, MDA and (R)-MDA produce the head-twitch response, a behavioral proxy of psychedelic effects, in rodents.<ref name="HalberstadtChathaKlein2020">Template:Cite journal</ref> However, the head-twitch response they produce is very weak in magnitude compared to other related psychedelics such as the DOx drugs.<ref name="HalberstadtChathaKlein2020" /> On the other hand, the response is more similar in magnitude to that of Ariadne.<ref name="HalberstadtChathaKlein2020" />

In terms of the subjective and behavioral effects of MDA, it is thought that serotonin release is required for its entactogenic effects, dopamine release is required for its euphoriant (rewarding and addictive) effects, dopamine and norepinephrine release are required for its psychostimulant effects, and direct agonism of the serotonin 5-HT_2A receptor is required for its mild psychedelic effects.<ref name="Oeri2021" /> The entactogenic effects of drugs like MDA are thought to dependent on a precise balance of serotonin and dopamine release as well as serotonin receptor agonism.<ref name="LuethiLiechti2020">Template:Cite journal</ref><ref name="Baggott2023">Template:Cite conference</ref><ref name="Baggott2024">Template:Cite web</ref><ref name="RothmanBaumann2002">Template:Cite journal</ref><ref name="BaggottGarrisonCoyle2019" /> The longer duration of MDA compared to MDMA appears to be related to pharmacodynamics as opposed to pharmacokinetics, for instance the effects of MDA depending relatively more on serotonin 5-HT_2A receptor agonism than on serotonin release.<ref name="BaggottGarrisonCoyle2019" />

MDA can produce serotonergic neurotoxic effects in rodents.<ref name="Oeri2021" /><ref name="Herndon_2014">Template:Cite journal</ref><ref>Template:Cite journal</ref> This might in part be due to metabolism of MDA.<ref name="de_la_Torre_2004">Template:Cite journal</ref> In addition, MDA activates a response of the neuroglia, though this subsides after use.<ref name="Herndon_2014" />

Activities of MDMA, its enantiomers, and related compounds

Compound	Monoamine release (Template:Abbrlink, nM)
	Serotonin	Norepinephrine	Dopamine
Amphetamine	Template:Abbr	Template:Abbr	Template:Abbr
Template:NbspTemplate:Nbsp(S)-Amphetamine (d)	698–1,765	6.6–7.2	5.8–24.8
Template:NbspTemplate:Nbsp(R)-Amphetamine (l)	Template:Abbr	9.5	27.7
Methamphetamine	Template:Abbr	Template:Abbr	Template:Abbr
Template:NbspTemplate:Nbsp(S)-Methamphetamine (d)	736–1,292	12.3–13.8	8.5–24.5
Template:NbspTemplate:Nbsp(R)-Methamphetamine (l)	4,640	28.5	416
MDA	160	108	190
Template:NbspTemplate:Nbsp(S)-MDA (d)	100	50	98
Template:NbspTemplate:Nbsp(R)-MDA (l)	310	290	900
MDMA	49.6–72	54.1–110	51.2–278
Template:NbspTemplate:Nbsp(S)-MDMA (d)	74	136	142
Template:NbspTemplate:Nbsp(R)-MDMA (l)	340	560	3,700
MDEA	47	2,608	622
MBDB	540	3,300	>100,000
MDAI	114	117	1,334
Notes: The smaller the value, the more strongly the compound produces the effect. Refs:<ref name="RothmanBaumann2006">Template:Cite journal</ref><ref name="SetolaHufeisenGrande-Allen2003" /><ref name="RothmanBaumannDersch2001">Template:Cite journal</ref><ref name="RothmanPartillaBaumann2012">Template:Cite journal</ref><ref name="MarusichAntonazzoBlough2016">Template:Cite journal</ref><ref name="NagaiNonakaKamimura2007">Template:Cite journal</ref><ref name="HalberstadtBrandtWalther2019">Template:Cite journal</ref><ref name="Blough2008">Template:Cite book</ref>

Template:Nowrap

Compound	5-HT2A		5-HT2B		5-HT2C
	EC50 (nM)	Emax	EC50 (nM)	Emax	EC50 (nM)	Emax
Serotonin	53	92%	1.0	100%	22	91%
MDA	1,700	57%	190	80%	Template:Abbr	Template:Abbr
Template:NbspTemplate:Nbsp(S)-MDA (d)	18,200	89%	100	81%	7,400	73%
Template:NbspTemplate:Nbsp(R)-MDA (l)	5,600	95%	150	76%	7,400	76%
MDMA	6,100	55%	2,000–>20,000	32%	Template:Abbr	Template:Abbr
Template:NbspTemplate:Nbsp(S)-MDMA (d)	10,300	9%	6,000	38%	2,600	53%
Template:NbspTemplate:Nbsp(R)-MDMA (l)	3,100	21%	900	27%	5,400	27%
Notes: The smaller the Kact or EC50 value, the more strongly the compound produces the effect. Refs:<ref name="NashRothBrodkin1994">Template:Cite journal</ref><ref name="SetolaHufeisenGrande-Allen2003" /><ref name="KolaczynskaDucretTrachsel2022">Template:Cite journal</ref>

Pharmacokinetics

The pharmacokinetics of MDA have been studied.<ref name="BaggottGarrisonCoyle2019" /><ref name="BaggottLiGalloway2012">Template:Cite journal</ref> Its duration of action has been reported to be about 6 to 8Template:Nbsphours.<ref name="BaggottSiegristGalloway2010">Template:Cite journal</ref> The duration of MDA is longer than that of MDMA, about 8Template:Nbsphours for MDA versus 6Template:Nbsphours for MDMA.<ref name="BaggottGarrisonCoyle2019" /><ref name="BaggottLiGalloway2012" /> The elimination half-life of MDA is 10.9Template:Nbsphours.<ref name="BaggottGarrisonCoyle2019" /> Differences in the duration of MDA versus MDMA may be due pharmacodynamics rather than pharmacokinetics.<ref name="BaggottGarrisonCoyle2019" /><ref name="BaggottLiGalloway2012" />

Chemistry

MDA is a substituted methylenedioxylated phenethylamine and amphetamine derivative. In relation to other phenethylamines and amphetamines, it is the 3,4-methylenedioxy, α-methyl derivative of β-phenylethylamine, the 3,4-methylenedioxy derivative of amphetamine, and the N-desmethyl derivative of MDMA.

It is a common adulterant of illicitly produced MDMA.<ref>Template:Cite web</ref><ref>Template:Cite web</ref>

Synonyms

In addition to 3,4-methylenedioxyamphetamine, MDA is also known by other chemical synonyms such as the following:

• α-Methyl-3,4-methylenedioxy-β-phenylethylamine
• 1-(3,4-Methylenedioxyphenyl)-2-propanamine
• 1-(1,3-Benzodioxol-5-yl)-2-propanamine

Synthesis

MDA is typically synthesized from essential oils such as safrole or piperonal. Common approaches from these precursors include:

• Reaction of safrole's alkene functional group with a halogen containing mineral acid followed by amine alkylation.<ref>Template:Cite journal</ref><ref name=ShulginIndex>Template:Cite book</ref>

Synthesis of MDA and related analogs from safrole

• Wacker oxidation of safrole to yield 3,4-methylenedioxyphenylpropan-2-one (MDP2P) followed by reductive amination<ref name="ShulginIndex" /><ref>Template:Cite journal</ref> or via reduction of its oxime.<ref name="Mannich">Template:Cite journal</ref>
• Henry reaction of piperonal with nitroethane followed by nitro compound reduction.<ref name="ShulginIndex" /><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref name="PiHKAL1991" />
• Darzens reaction on heliotropin was also done by J. Elks, et al.<ref name="ElksHey1943">Template:Cite journal</ref> This gives MDP2P, which was then subjected to a Leuckart reaction.
• The "two dogs" or "dopeboy" clandestine method, starting with helional as a precursor. First, an oxime is created using hydroxylamine. Then, a Beckmann rearrangement is performed with nickel acetate to form the amide. Then a Hofmann rearrangement is done to form the freebase amine of MDA. Then it is purified with an acid base extraction.<ref>Template:Cite web</ref>

Detection in body fluids

MDA may be quantitated in blood, plasma or urine to monitor for use, confirm a diagnosis of poisoning or assist in the forensic investigation of a traffic or other criminal violation or a sudden death. Some drug abuse screening programs rely on hair, saliva, or sweat as specimens. Most commercial amphetamine immunoassay screening tests cross-react significantly with MDA and major metabolites of MDMA, but chromatographic techniques can easily distinguish and separately measure each of these substances. The concentrations of MDA in the blood or urine of a person who has taken only MDMA are, in general, less than 10% those of the parent drug.<ref>Kolbrich EA, Goodwin RS, Gorelick DA, Hayes RJ, Stein EA, Huestis MA. Plasma pharmacokinetics of 3,4-methylenedioxymethamphetamine after controlled oral administration to young adults. Ther. Drug Monit. 30: 320–332, 2008.</ref><ref>Template:Cite journal</ref><ref>R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 9th edition, Biomedical Publications, Seal Beach, California, 2011, pp. 1078–1080.</ref>

Derivatives and analogues

Analogues of MDA include its positional isomer 2,3-methylenedioxyamphetamine (2,3-MDA) and others.

MDA constitutes part of the core structure of the β-adrenergic receptor agonist protokylol.

History

MDA was first synthesized by Carl Mannich and W. Jacobsohn in 1910.<ref name=Mannich /> It was first taken in July 1930 by Gordon Alles at a total dose of 126Template:Nbspmg, who experienced hallucinogenic effects, well-being and euphoria, and peripheral effects.<ref name="Alles1959a">Template:Cite book</ref><ref name="Alles1959b">Template:Cite book</ref><ref name="PsychedelicResearch2008" /> However, he did not subsequently describe these effects until 1959.<ref name="BenzenhöferPassie2010">Template:Cite journal</ref><ref name="Alles1959a" /><ref name="Alles1959b" /> Alles later licensed the drug to Smith, Kline & French.<ref name="PsychedelicResearch2008">Template:Cite web</ref> 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.<ref name="Shulgin1978" /> However, it was found to be detrimental in people with Parkinson's disease.<ref name="Shulgin1978" /> The drug was described as having analeptic effects in humans in 1953.<ref name="Shulgin1978" /> From 1949 to 1957, more than five hundred human subjects were given MDA in an investigation of its potential use as an antidepressant or appetite suppressant by Smith, Kline & French.<ref name="Shulgin1978" />

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 died in January 1953 after being intravenously injected, without his knowledge or consent, with 450 mg of the drug as part of Project MKUltra.<ref name="DunlapAndrewsOlson2018">Template:Cite journal</ref> MDA was patented 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.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref>

The International Nonproprietary Name (INN) tenamfetamine was recommended by the World Health Organization (WHO) in 1986.<ref name="WHO1986">Template:Cite web</ref> It was recommended in the same published list in which the INN of 2,5-dimethoxy-4-bromoamphetamine (DOB), brolamfetamine, was recommended.<ref name="WHO1986" /> These events suggest that MDA and DOB were under development as potential pharmaceutical drugs at the time.<ref name="WHO1986" /> The Multidisciplinary Association for Psychedelic Studies (MAPS) was also founded in 1986.<ref name="EmersonPontéJerome2014">Template:Cite journal</ref>

Matthew J. Baggott and colleagues conducted some of the first modern clinical studies of MDA in humans and published their findings in the 2010s.<ref name="BaggottGarrisonCoyle2019" /><ref name="BaggottSiegristGalloway2010" /><ref name="BaggottSiegristCoyle2010" />

Society and culture

MDA as prepared for recreational use.

Names

When MDA was under development as a potential pharmaceutical drug, it was given the International Nonproprietary Name (INN) of tenamfetamine.<ref name="Elks2014">Template:Cite book</ref>

Legal status

Australia

MDA is schedule 9 prohibited substance under the Poisons Standards.<ref name="Poisons Standard">Poisons Standard (October 2015) comlaw.gov.au</ref> A schedule 9 substance is listed as a "Substances which may be abused or misused, the manufacture, possession, sale or use of which should be prohibited by law except when required for medical or scientific research, or for analytical, teaching or training purposes with approval of Commonwealth and/or State or Territory Health Authorities."<ref name="Poisons Standard" />

United States

MDA is a Schedule I controlled substance in the US.

Research

MDA has been studied in entactogen-assisted psychotherapy.<ref name="Oeri2021" /><ref name="Sáez-BrionesHernández2013" />

See also

• Substituted methylenedioxyphenethylamine

External links

• MDA - Isomer Design
• MDA - PsychonautWiki
• MDA - Erowid
• MDA - PiHKAL - Erowid
• MDA - PiHKAL - Isomer Design