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For other uses of "Ecstasy", see Ecstasy (disambiguation).
MDMA structure
Ball-and-stick model of an MDMA molecule
Systematic (IUPAC) name
(RS)-1-(Benzo[d] [1,3]dioxol-5-yl)-N-methylpropan-2-amine
Clinical data
Pronunciation /ˈmɛ.θɪ.ln.d.ˈɒ
AHFS/ entry
Legal status
Physical: none
Psychological: moderate[1]
Routes of
Common: oral
Uncommon: sublingual, insufflation, inhalation (vaporization), injection,[3] rectal
Pharmacokinetic data
Metabolism Hepatic, CYP450 extensively involved, including CYP2D6
Metabolites MDA, HMMA, HMA, DHA, MDP2P, MDOH[4]
Onset of action 30–45 minutes (oral)[5]
Biological half-life (R)-MDMA: 5.8 ± 2.2 hours[6]
(S)-MDMA: 3.6 ± 0.9 hours[6]
Duration of action 4–6 hours[5]
Excretion Renal
CAS Number 42542-10-9 YesY[TOXNET]
ATC code None
PubChem CID 1615
DrugBank DB01454 YesY
ChemSpider 1556 YesY
KEGG C07577 YesY
Synonyms 3,4-MDMA, Ecstasy, Molly
PDB ligand ID B41 (PDBe, RCSB PDB)
Chemical data
Formula C11H15NO2
Molar mass 193.25 g·mol−1
Chirality 1 : 1 mixture (racemate)
Physical data
Boiling point 105 °C (221 °F) at 0.4 mmHg (experimental)

MDMA (contracted from 3,4-methylenedioxy-methamphetamine) is a psychoactive drug of the substituted methylenedioxyphenethylamine and substituted amphetamine classes of drugs that is consumed primarily for its euphoric and empathogenic effects. Pharmacologically, MDMA acts as a serotonin-norepinephrine-dopamine releasing agent and reuptake inhibitor.

MDMA has become widely known as ecstasy (shortened to "E", "X", or "XTC"), usually referring to its tablet form, although this term may also include the presence of possible adulterants. The UK term "Mandy" and the US term "Molly" colloquially refer to MDMA in a crystalline powder form that is thought to be free of adulterants.[7][8] In the media "Molly" can sometimes also refer to the related drugs methylone, MDPV, mephedrone or any other of the pharmacological group of compounds commonly known as bath salts.[14]

Possession of MDMA is illegal in most countries. Some limited exceptions exist for scientific and medical research. In 2013 between 9 and 28 million people used ecstasy (0.2% to 0.6% of the global population between the ages of 15 and 65).[15] This was broadly similar to the number for cocaine, substituted amphetamines, and opioids, but far fewer than the number of cannabis users.[15] It is taken in a variety of contexts and is commonly associated with dance parties, raves, and electronic dance music.[16]

MDMA may have health benefits in certain mental disorders, but has potential adverse effects, such as neurotoxicity and cognitive impairment.[17][18] More research is needed in order to determine if its potential usefulness in posttraumatic stress disorder (PTSD) treatment outweighs the risk of persistent neuropsychological harm to a patient.[17][18]



MDMA currently has no accepted medical use.[19]


MDMA is often considered the drug of choice within the rave culture and is also used at clubs, festivals and house parties.[4] In the rave environment, the sensory effects from the music and lighting are often highly synergistic with the drug. The psychedelic amphetamine quality of MDMA offers multiple reasons for its appeals to users in the rave setting. Some users enjoy the feeling of mass communion from the inhibition-reducing effects of the drug, while others use it as party fuel because of the drug's stimulatory effects.[20]

MDMA is sometimes taken in conjunction with other psychoactive drugs, such as LSD, psilocybin mushrooms, and ketamine. Users sometimes use mentholated products while taking MDMA for its cooling sensation.[21]


MDMA has been used as an adjunct to New Age spiritual practices.[22]


Acute effects of MDMA

In general, MDMA users begin reporting subjective effects within 30 to 60 minutes of consumption, hitting a peak at about 75 to 120 minutes which plateaus for about 3.5 hours.[23]

The desired short-term psychoactive effects of MDMA include:

  • Euphoria – a sense of general well-being and happiness[17][24]
  • Increased sociability and feelings of communication being easy or simple[17][24]
  • Entactogenic effects – increased empathy or feelings of closeness with others[17][24]
  • A sense of inner peace[24]
  • Mild hallucination (e.g., colors and sounds are enhanced and mild closed-eye visuals)[24]
  • Enhanced sensation, perception, or sexuality[17][24]

Available forms

The average ecstasy tablet contains 60–70 mg (base equivalent) of MDMA, usually as the hydrochloride salt.[25] Powdered MDMA is typically 30–40% pure, due to bulking agents (e.g., lactose) and binding agents.[25] Tablets sold as ecstasy sometimes only contain 3,4-methylenedioxyamphetamine (MDA) instead of MDMA;[6][25] the proportion of seized ecstasy tablets with MDMA-like impurities has varied annually and by country.[25]

MDMA is also sold in the form of the hydrochloride salt, either as loose crystals or in gelcaps [8] which typically contain ~100 mg of the drug.[citation needed]

Ecstasy tablets
Ecstasy tablets which allegedly contain MDMA, but may contain adulterants
Impure MDMA
A salt of MDMA (typically white) with impurities, resulting in a tan discoloration

Corporate logos on pills

A number of MDMA manufacturers brand their pills with a logo, often being a corporate logo,[26] to help distinguish between suppliers; one of the most notable logos which appeared on pills is the Mitsubishi logo which was very popular during one time.[27][28] There have also been sightings of pills with logos of products or shows popular with children, such as Shaun the Sheep.[29]

Adverse effects

Immediate effects

Bruxism can be a side effect of MDMA prompting some users to suck on pacifiers to avoid teeth grinding.[30]:1082
Mydriasis may be a side effect of MDMA.

The most serious short-term physical health risks of MDMA are hyperthermia and dehydration.[24][31] Cases of life-threatening or fatal hyponatremia (excessively low sodium concentration in the blood) have developed in MDMA users attempting to prevent dehydration by consuming excessive amounts of water without replenishing electrolytes.[24][31][32]

The immediate adverse effects of MDMA use can include:


The effects that last up to a week[17][35] following cessation of moderate MDMA use include:


Long-term effects

MDMA use has been shown to produce brain lesions, a form of brain damage, in the serotonergic neural pathways of animals[2][6], while the question is whether MDMA users may suffer similar neurotoxic brain lesions is still unclear[36]. In addition, long-term exposure to MDMA in humans has been shown to produce marked neurotoxicity in serotonergic axon terminals.[4][24][37] Neurotoxic damage to axon terminals has been shown to persist for more than two years.[37] Brain temperature during MDMA use is positively correlated with MDMA-induced neurotoxicity in animals.[4] Adverse neuroplastic changes to brain microvasculature and white matter also seem to occur in humans using low doses of MDMA.[4] Reduced gray matter density in certain brain structures has also been noted in human MDMA users.[4] In addition, MDMA has immunosuppressive effects in the peripheral nervous system, but pro-inflammatory effects in the central nervous system.[38] Babies of mothers who used MDMA during pregnancy exhibit impaired motor function at 4 months of age, which may reflect either a delay in development or a persistent neurological deficit.[18][39]

MDMA also produces persistent cognitive impairments in human users.[1][17][18] Impairments in multiple aspects of cognition, including memory, visual processing, and sleep have been noted in humans;[17][18] the magnitude of these impairments is correlated with lifetime ecstasy or MDMA usage.[1][17][18] Memory is significantly impacted by ecstasy use, which is associated with marked impairments in all forms of memory (e.g., long-term, short-term, working).[17][18] Some studies indicate repeated recreational users of MDMA have increased rates of depression and anxiety, even after quitting the drug.[40][41][42] Other meta analyses have reported possibility of impairment of executive functioning.[43]

Evidence in animals and humans has shown that, at high doses, MDMA induces a neuroimmune response which, through several mechanisms, increases the permeability of the blood-brain barrier, thereby making the brain more susceptible to environmental toxins and pathogens.[44][45][page needed]

Reinforcement disorders

Approximately 60% of MDMA users experience withdrawal symptoms, including, but not limited to: fatigue, loss of appetite, depression, and trouble concentrating.[6] Tolerance is expected to occur with consistent MDMA use.[6]

MDMA has been shown to induce ΔFosB in the nucleus accumbens.[46] Since MDMA releases dopamine in the mesocorticolimbic projection, the mechanisms by which it induces ΔFosB in the nucleus accumbens are analogous to other psychostimulants.[46][47] Therefore, chronic use of MDMA at high doses can result in altered brain structure and drug addiction, which occur as a consequence of ΔFosB overexpression in the nucleus accumbens.[47]


MDMA overdose symptoms vary widely due to the involvement of multiple organ systems. Some of the more overt overdose symptoms are listed in the table below.

Symptoms of overdose
System Minor or moderate overdose[34] Severe overdose[34]
Central nervous


A number of drug interactions can occur between MDMA and other drugs, including serotonergic drugs.[6][51] MDMA also interacts with drugs which inhibit CYP450 enzymes, like ritonavir (Norvir), particularly CYP2D6 inhibitors.[6] Concurrent use of MDMA with another serotonergic drug can result in a life-threatening condition called serotonin syndrome.[6] Severe overdose resulting in death has also been reported in people who took MDMA in combination with certain monoamine oxidase inhibitors,[6] such as phenelzine (Nardil), tranylcypromine (Parnate), or moclobemide (Aurorix, Manerix).[52]



Serotonin binds to receptors on neurons.
A serotonin transporter moving a serotonin molecule.
MDMA binding to serotonin transporters.
MDMA binds to serotonin transporters preventing serotonin reuptake.

MDMA acts primarily as a presynaptic releasing agent of serotonin, norepinephrine, and dopamine, which arises from its activity at trace amine-associated receptor 1 (TAAR1) and vesicular monoamine transporter 2 (VMAT2).[6][53][54] MDMA is a monoamine transporter substrate (i.e., a substrate for DAT, NET, and SERT), so it enters monoamine neurons via these neuronal membrane transport proteins;[53] by acting as a monoamine transporter substrate, MDMA produces competitive reuptake inhibition at the neuronal membrane transporters (i.e., it competes with endogenous monoamines for reuptake).[53][55] MDMA inhibits both vesicular monoamine transporters (VMATs), the second of which (VMAT2) is highly expressed within monoamine neurons at vesicular membranes.[54] Once inside a monoamine neuron, MDMA acts as a VMAT2 inhibitor and a TAAR1 agonist.[53][54]

Inhibition of VMAT2 by MDMA results in increased concentrations of the associated neurotransmitter (serotonin, norepinephrine, or dopamine) in the cytosol of a monoamine neuron.[54][56] Activation of TAAR1 by MDMA triggers protein kinase A and protein kinase C signaling events which then phosphorylates the associated monoamine transporters – DAT, NET, or SERT – of the neuron.[53] In turn, these phosphorylated monoamine transporters either reverse transport direction – i.e., move neurotransmitters from the cytosol to the synaptic cleft – or withdraw into the neuron, respectively producing neurotransmitter efflux and noncompetitive reuptake inhibition at the neuronal membrane transporters.[53] MDMA has ten times more binding affinity for serotonin transporters than for dopamine and norepinephrine transporters and consequently has mainly serotonergic effects.[30]:1080

In summary, MDMA enters monoamine neurons by acting as a monoamine transporter substrate.[53] MDMA activity at VMAT2 moves neurotransmitters out from synaptic vesicles and into the cytosol;[54] MDMA activity at TAAR1 moves neurotransmitters out of the cytosol and into the synaptic cleft.[53]

MDMA also has weak agonist activity at postsynaptic serotonin receptors 5-HT1 and 5-HT2 receptors, and its more efficacious metabolite MDA likely augments this action.[57][58][59][60] A placebo-controlled study in 15 human volunteers found 100 mg MDMA increased blood levels of oxytocin, and the amount of oxytocin increase was correlated with the subjective prosocial effects of MDMA.[61](S)-MDMA is more effective in eliciting 5-HT, NE, and DA release, while (D)-MDMA is overall less effective, and more selective for 5-HT and NE release (having only a very faint efficacy on DA release).[62]

MDMA is a ligand at both sigma receptor subtypes, though its efficacies at the receptors have not yet been elucidated.[63]


Diagram showing the sequence of MDMA metabolization.

MDMA reaches maximal concentrations in the blood stream between 1.5 and 3 hr after ingestion.[64] It is then slowly metabolized and excreted, with levels of MDMA and its metabolites decreasing to half their peak concentration over the next several hours.[65]

Metabolites of MDMA that have been identified in humans include 3,4-methylenedioxyamphetamine (MDA), 4-hydroxy-3-methoxy-methamphetamine (HMMA), 4-hydroxy-3-methoxyamphetamine (HMA), 3,4-dihydroxyamphetamine (DHA) (also called alpha-methyldopamine (α-Me-DA)), 3,4-methylenedioxyphenylacetone (MDP2P), and 3,4-Methylenedioxy-N-hydroxyamphetamine (MDOH). The contributions of these metabolites to the psychoactive and toxic effects of MDMA are an area of active research. 80% of MDMA is metabolised in the liver, and about 20% is excreted unchanged in the urine.[4]

MDMA is known to be metabolized by two main metabolic pathways: (1) O-demethylenation followed by catechol-O-methyltransferase (COMT)-catalyzed methylation and/or glucuronide/sulfate conjugation; and (2) N-dealkylation, deamination, and oxidation to the corresponding benzoic acid derivatives conjugated with glycine.[34] The metabolism may be primarily by cytochrome P450 (CYP450) enzymes CYP2D6 and CYP3A4 and COMT. Complex, nonlinear pharmacokinetics arise via autoinhibition of CYP2D6 and CYP2D8, resulting in zeroth order kinetics at higher doses. It is thought that this can result in sustained and higher concentrations of MDMA if the user takes consecutive doses of the drug.[66][non-primary source needed]

MDMA and metabolites are primarily excreted as conjugates, such as sulfates and glucuronides.[67] MDMA is a chiral compound and has been almost exclusively administered as a racemate. However, the two enantiomers have been shown to exhibit different kinetics. The disposition of MDMA may also be stereoselective, with the S-enantiomer having a shorter elimination half-life and greater excretion than the R-enantiomer. Evidence suggests[68] that the area under the blood plasma concentration versus time curve (AUC) was two to four times higher for the (R)-enantiomer than the (S)-enantiomer after a 40 mg oral dose in human volunteers. Likewise, the plasma half-life of (R)-MDMA was significantly longer than that of the (S)-enantiomer (5.8 ± 2.2 hours vs 3.6 ± 0.9 hours).[6] However, because MDMA excretion and metabolism have nonlinear kinetics,[69] the half-lives would be higher at more typical doses (100 mg is sometimes considered a typical dose[64]).

Physical and chemical properties

A powdered salt of MDMA
A powdered salt of MDMA
Reactors used in synthesis
Reactors used to synthesize MDMA on an industrial scale in a chemical factory in Cikande, Indonesia

The free base of MDMA is a colorless oil that is insoluble in water.[25] The most common salt of MDMA is the hydrochloride salt;[25] pure MDMA hydrochloride is water-soluble and appears as a white or off-white powder or crystal.[25]


There are numerous methods available in the literature to synthesize MDMA via different intermediates.[70][71][72][73] The original MDMA synthesis described in Merck's patent involves brominating safrole to 1-(3,4-methylenedioxyphenyl)-2-bromopropane and then reacting this adduct with methylamine.[74][75] Most illicit MDMA is synthesized using MDP2P (3,4-methylenedioxyphenyl-2-propanone) as a precursor. MDP2P in turn is generally synthesized from piperonal, safrole or isosafrole.[76] One method is to isomerize safrole to isosafrole in the presence of a strong base, and then oxidize isosafrole to MDP2P. Another method uses the Wacker process to oxidize safrole directly to the MDP2P intermediate with a palladium catalyst. Once the MDP2P intermediate has been prepared, a reductive amination leads to racemic MDMA (an equal parts mixture of (R)-MDMA and (S)-MDMA).[citation needed] Relatively small quantities of essential oil are required to make large amounts of MDMA. The essential oil of Ocotea cymbarum, for example, typically contains between 80 and 94% safrole. This allows 500 ml of the oil to produce between 150 and 340 grams of MDMA.[77]

Synthesis of MDMA from piperonal
Synthesis of MDMA from piperonal
Synthesis of MDMA from piperonal
Synthesis of MDMA and related analogs from safrole
Synthesis of MDMA and related analogs from safrole

Detection in body fluids

MDMA and 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 MDMA or its major metabolites, 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.[78][79][80]


Early research and use

Merck MDMA synthesis patent
Merck patent for synthesizing methylhydrastinine from MDMA
German patents for MDMA synthesis and the subsequent methylhydrastinine synthesis filed by Merck on 24 December 1912 and issued in 1914.

MDMA was first synthesized in 1912 by Merck chemist Anton Köllisch. At the time, Merck was interested in developing substances that stopped abnormal bleeding. Merck wanted to avoid an existing patent held by Bayer for one such compound: hydrastinine. Köllisch developed a preparation of a hydrastinine analogue, methylhydrastinine, at the request of fellow lab members, Walther Beckh and Otto Wolfes. MDMA (called methylsafrylamin, safrylmethylamin or N-Methyl-a-Methylhomopiperonylamin in Merck laboratory reports) was an intermediate compound in the synthesis of methylhydrastinine. Merck was not interested in MDMA itself at the time.[81] On 24 December 1912, Merck filed two patent applications that described the synthesis and some chemical properties of MDMA[82] and its subsequent conversion to methylhydrastinine.[83]

Merck records indicate its researchers returned to the compound sporadically. A 1920 Merck patent describes a chemical modification to MDMA.[84] In 1927, Max Oberlin studied the pharmacology of MDMA while searching for substances with effects similar to adrenaline or ephedrine, the latter being structurally similar to MDMA. Compared to ephedrine, Oberlin observed that it had similar effects on vascular smooth muscle tissue, stronger effects at the uterus, and no "local effect at the eye". MDMA was also found to have effects on blood sugar levels comparable to high doses of ephedrine. Oberlin concluded that the effects of MDMA were not limited to the sympathetic nervous system. Research was stopped "particularly due to a strong price increase of safrylmethylamine", which was still used as an intermediate in methylhydrastinine synthesis. Albert van Schoor performed simple toxicological tests with the drug in 1952, most likely while researching new stimulants or circulatory medications. After pharmacological studies, research on MDMA was not continued. In 1959, Wolfgang Fruhstorfer synthesized MDMA for pharmacological testing while researching stimulants. It is unclear if Fruhstorfer investigated the effects of MDMA in humans.[81]

Outside of Merck, other researchers began to investigate MDMA. In 1953 and 1954, the United States Army commissioned a study of toxicity and behavioral effects in animals injected with mescaline and several analogues, including MDMA. Conducted at the University of Michigan in Ann Arbor, these investigations were declassified in October 1969 and published in 1973.[85][86] A 1960 Polish paper by Biniecki and Krajewski describing the synthesis of MDMA as an intermediate was the first published scientific paper on the substance.[81][86][87]

MDMA may have been in non-medical use in the western United States in 1968.[88] A 1970 report at a meeting of crime laboratory chemists indicates MDMA was being used recreationally in the Chicago area by August of that year.[86][89] MDMA likely emerged as a substitute for its analog methylenedioxyamphetamine (MDA),[90] a drug at the time popular among users of psychedelics[91] which was made a Schedule 1 substance in the United States in 1970.[92][93]

Shulgin's research and therapeutic use

Alexander and Ann Shulgin in December 2011

American chemist and psychopharmacologist Alexander Shulgin reported he synthesized MDMA in 1965 while researching methylenedioxy compounds at Dow Chemical Company, but did not test the psychoactivity of the compound at this time. Around 1970, Shulgin sent instructions for N-methylated MDA (MDMA) synthesis to the founder of a Los Angeles chemical company who had requested them. This individual later provided these instructions to a client in the Midwest.[86]

Shulgin first heard of the psychoactive effects of N-methylated MDA around 1975 from a young student who reported "amphetamine-like content".[86] Around 30 May 1976, Shulgin again heard about the effects of N-methylated MDA,[86] this time from a graduate student in a medicinal chemistry group he advised at San Francisco State University[91][94] who directed him to the University of Michigan study.[95] She and two close friends had consumed 100 mg of MDMA and reported positive emotional experiences.[86] Following the self-trials of a colleague at the University of San Francisco, Shulgin synthesized MDMA and tried it himself in September and October 1976.[86][91] Shulgin first reported on MDMA in a presentation at a conference in Bethesda, Maryland in December 1976.[86] In 1978, he and David E. Nichols published a report on the drug's psychoactive effect in humans. They described MDMA as inducing "an easily controlled altered state of consciousness with emotional and sensual overtones" comparable "to marijuana, to psilocybin devoid of the hallucinatory component, or to low levels of MDA".[96] Believing MDMA allowed users to strip away habits and perceive the world clearly, Shulgin called the drug "window".[95][97]

While not finding his own experiences with MDMA particularly powerful,[95][98] Shulgin was impressed with the drug's disinhibiting effects and believed it could be useful in psychotherapy.[98] Shulgin took to occasionally using MDMA for relaxation, referring to it as "my low-calorie martini", and giving the drug to his friends, researchers, and others whom he thought could benefit from it.[95] One such person was Leo Zeff, a psychotherapist who had been known to use psychedelics in his practice. When he tried the drug in 1977, Zeff was so impressed with the effects of MDMA that he came out of his semi-retirement to promote its use in psychotherapy. Over the following years, Zeff traveled around the U.S. and occasionally to Europe, eventually training an estimated four thousand psychotherapists in the therapeutic use of MDMA.[98][99] Zeff named the drug "Adam", believing it put users in a state of primordial innocence.[91]

Psychotherapists who used MDMA believed the drug eliminated the typical fear response and increased communication. Sessions were usually held in the home of the patient or the therapist. The role therapist was minimized in favor of patient self-discovery accompanied by MDMA induced feelings of empathy. Depression, substance abuse, relationship problems, premenstrual syndrome, and autism were among several psychiatric disorders MDMA assisted therapy was reported to treat.[93] According to psychiatrist George Greer, therapists who used MDMA in their practice were impressed by the results. Anecdotally, MDMA was said to greatly accelerate therapy.[98]

Rising recreational use

In the late seventies and early eighties, "Adam" spread through personal networks of psychotherapists, psychiatrists, users of psychedelics, and yuppies. Hoping MDMA could avoid criminalization like LSD and mescaline, psychotherapists and experimenters attempted to limit the spread of MDMA and information about it while conducting informal research.[93][100] Early MDMA distributors were deterred from large scale operations by the threat of possible legislation.[101] Between the 1970s and the mid-1980s, this network of MDMA users consumed an estimated 500,000 doses.[17][102]

A small recreational market for MDMA developed by the late 1970s,[103] consuming perhaps 10,000 doses in 1976.[92] By the early 1980s MDMA was being used in Boston and New York City nightclubs such as Studio 54 and Paradise Garage.[104][105] Into the early 1980s, as the recreational market slowly expanded, production of MDMA was dominated by a small group of therapeutically minded Boston chemists. Having commenced production in 1976, this "Boston Group" did not keep up with growing demand and shortages frequently occurred.[101]

Perceiving a business opportunity, Michael Clegg, the Southwest distributor for the Boston Group, started his own "Texas Group" backed financially by Texas friends.[101][106] In 1981,[101] Clegg had coined "Ecstasy" as a slang term for MDMA to increase its marketability.[97][100] Starting in 1983,[101] the Texas Group mass-produced MDMA in a Texas lab[100] or imported it from California[97] and marketed tablets using pyramid sales structures and toll-free numbers.[102] MDMA could be purchased via credit card and taxes were paid on sales.[101] Under the brand name "Sassyfras", MDMA tablets were sold in brown bottles.[100] The Texas Group advertised "Ecstasy parties" at bars and discos, describing MDMA as a "fun drug" and "good to dance to".[101] MDMA was openly distributed in Austin and Dallas area bars and nightclubs, becoming popular with yuppies, college students, and gays.[101][90][102]

Recreational use also increased after several cocaine dealers switched to distributing MDMA following experiences with the drug.[102] A California laboratory that analyzed confidentially submitted drug samples first detected MDMA in 1975. Over the following years the number of MDMA samples increased, eventually exceeding the number of MDA samples in the early 1980s.[107][108] By the mid-1980s, MDMA use had spread to colleges around the United States.[101]:33

Media attention and scheduling

United Kingdom

In the United Kingdom, MDMA was made illegal in 1977 by a modification order to the existing Misuse of Drugs Act 1971. Although MDMA was not named explicitly in this legislation, the order extended the definition of Class A drugs to include various ring-substituted phenethylamines.[109][110]

United States

July 27, 1984 Federal Register notice of the proposed MDMA scheduling

In an early media report on MDMA published in 1982, a Drug Enforcement Administration (DEA) spokesman stated the agency would ban the drug if enough evidence for abuse could be found.[101] By mid-1984, MDMA use was becoming more noticed. Bill Mandel reported on "Adam" in a June 10 San Francisco Chronicle article, but misidentified the drug as methyloxymethylenedioxyamphetamine (MMDA). In the next month, the World Health Organization identified MDMA as the only substance out of twenty phenethylamines to be seized a significant number of times.[100]

After a year of planning and data collection, MDMA was proposed for scheduling by the DEA on 27 July 1984 with a request for comments and objections.[100][111] The DEA was surprised when a number of psychiatrists, psychotherapists, and researchers objected to the proposed scheduling and requested a hearing.[93] In a Newsweek article published the next year, a DEA pharmacologist stated that the agency had been unaware of its use among psychiatrists.[112] An initial hearing was held on 1 February 1985 at the DEA offices in Washington, D.C. with administrative law judge Francis L. Young presiding.[100] It was decided there to hold three more hearings that year: Los Angeles on June 10, Kansas City, Missouri on July 10–11, and Washington, D.C. on October 8–11.[93][100]

Sensational media attention was given to the proposed criminalization and the reaction of MDMA proponents, effectively advertising the drug.[93] In response to the proposed scheduling, the Texas Group increased production from 1985 estimates of 30,000 tablets a month to as many as 8,000 per day, potentially making two million ecstasy tablets in the months before MDMA was made illegal.[113] By some estimates the Texas Group distributed 500,000 tablets per month in Dallas alone.[97] According to one knowledgeable individual, the Texas Group produced more MDMA in eighteen months than all other distribution networks combined across their entire histories.[101] By May 1985, MDMA use was widespread in California, Texas, southern Florida, and the northeastern United States.[88][114] According to the DEA there was evidence of use in twenty-eight states[115] and Canada.[88] Urged by Senator Lloyd Bentsen, the DEA announced an emergency Schedule I classification of MDMA on 31 May 1985. The agency cited increased distribution in Texas, escalating street use, and new evidence of MDA (an analog of MDMA) neurotoxicity as reasons for the emergency measure.[114][116][117] The ban took effect one month later on 1 July 1985[113] in the midst of Nancy Reagan's "Just Say No" campaign.[118][119]

As a result of several expert witnesses testifying that MDMA had an accepted medical usage, the administrative law judge presiding over the hearings recommended that MDMA be classified as a Schedule III substance. Despite this, DEA administrator John C. Lawn overruled and classified the drug as Schedule I.[93] Later Harvard psychiatrist Lester Grinspoon sued the DEA, claiming that the DEA had ignored the medical uses of MDMA, and the federal court sided with Grinspoon, calling Lawn's argument "strained" and "unpersuasive", and vacated MDMA's Schedule I status. Despite this, less than a month later Lawn reviewed the evidence and reclassified MDMA as Schedule I again, claiming that the expert testimony of several psychiatrists claiming over 200 cases where MDMA had been used in a therapeutic context with positive results could be dismissed because they weren't published in medical journals.[93][citation needed] No double blind studies had yet been conducted as to the efficacy of MDMA for psychotherapy.[citation needed]

United Nations

While engaged in scheduling debates in the United States, the DEA also pushed for international scheduling.[113] In 1985 the World Health Organization's Expert Committee on Drug Dependence recommended that MDMA be placed in Schedule I of the 1971 United Nations Convention on Psychotropic Substances. The committee made this recommendation on the basis of the pharmacological similarity of MDMA to previously scheduled drugs, reports of illicit trafficking in Canada, drug seizures in the United States, and lack of well-defined therapeutic use. While intrigued by reports of psychotherapeutic uses for the drug, the committee viewed the studies as lacking appropriate methodological design and encouraged further research. Committee chairman Paul Grof dissented, believing international control was not warranted at the time and a recommendation should await further therapeutic data.[120] The Commission on Narcotic Drugs added MDMA to Schedule I of the convention on 11 February 1986.[121]


A 1995 Vibe Tribe rave in Erskineville, New South Wales, Australia being broken up by police. MDMA use spread globally along with rave culture.
A 2000 United States Air Force video dramatizing the dangers of MDMA abuse.

The use of MDMA in Texas clubs declined rapidly after criminalization, although by 1991 the drug remained popular among young middle-class whites and in nightclubs.[101]:46 In 1985, MDMA use became associated with Acid House on the Spanish island of Ibiza.[101]:50[122] Thereafter in the late 1980s, the drug spread alongside rave culture to the UK and then to other European and American cities.[101]:50 Illicit MDMA use became increasingly widespread among young adults in universities and later, in high schools. Since the mid-1990s, MDMA has become the most widely used amphetamine-type drug by college students and teenagers.[30]:1080 MDMA became one of the four most widely used illicit drugs in the U.S., along with cocaine, heroin, and cannabis.[97] According to some estimates as of 2004, only marijuana attracts more first time users in the U.S.[97]

After MDMA was criminalized, most medical use stopped, although some therapists continued to prescribe the drug illegally. Later,[when?] Charles Grob initiated an ascending-dose safety study in healthy volunteers. Subsequent legally-approved MDMA studies in humans have taken place in the U.S. in Detroit (Wayne State University), Chicago (University of Chicago), San Francisco (UCSF and California Pacific Medical Center), Baltimore (NIDANIH Intramural Program), and South Carolina, as well as in Switzerland (University Hospital of Psychiatry, Zürich), the Netherlands (Maastricht University), and Spain (Universitat Autònoma de Barcelona).[123]

"Molly", short for 'molecule', was recognized as a slang term for crystalline or powder MDMA in the 2000s.[124][125]

In 2010, the BBC reported that use of MDMA had decreased in the UK in previous years. This may be due to increased seizures during use and decreased production of the precursor chemicals used to manufacture MDMA. Unwitting substitution with other drugs, such as mephedrone and methamphetamine,[126] as well as legal alternatives to MDMA, such as BZP, MDPV, and methylone, are also thought to have contributed to its decrease in popularity.[127]

Society and culture

Global estimates of illegal drug users in 2013
(in millions of users)[128]
Substance Best
type stimulants
33.90 13.87 53.81
Cannabis 181.79 128.48 232.07
Cocaine 17.04 13.80 20.73
Ecstasy 18.79 9.34 28.39
Opiates 16.53 12.92 20.46
Opioids 32.42 27.99 37.56

Legal status

MDMA is legally controlled in most of the world under the UN Convention on Psychotropic Substances and other international agreements, although exceptions exist for research and limited medical use. In general, the unlicensed use, sale or manufacture of MDMA are all criminal offences.


In Australia, MDMA was declared an illegal substance in 1986 because of its harmful effects and potential for abuse. It is classed as a Schedule 9 Prohibited Substance in the country, meaning it is available for scientific research purposes only. Any other type of sale, use or manufacture is strictly prohibited by law. Permits for research uses on humans must be approved by a recognized ethics committee on human research. In Western Australia under the Misuse of Drugs Act 1981 4.0g of MDMA is the amount required determining a court of trial, 2.0g is considered a presumption with intent to sell or supply and 28.0g is considered trafficking under Australian law.[129]

United Kingdom

In the United Kingdom, MDMA is illegal under a 1977 modification to the Misuse of Drugs Act 1971[110] thereby making it illegal to sell, buy, or possess the drug without a licence. Penalties include a maximum of seven years and/or unlimited fine for possession; life and/or unlimited fine for production or trafficking.

United States

In the United States, MDMA is currently placed in Schedule I of the Controlled Substances Act.[130] In a 2011 federal court hearing the American Civil Liberties Union successfully argued that the sentencing guideline for MDMA/ecstasy is based on outdated science, leading to excessive prison sentences.[131] Other courts have upheld the sentencing guidelines. The United States District Court for the Eastern District of Tennessee explained its ruling by noting that "an individual federal district court judge simply cannot marshal resources akin to those available to the Commission for tackling the manifold issues involved with determining a proper drug equivalency."[132]


In the Netherlands, the Expert Committee on the List (Expertcommissie Lijstensystematiek Opiumwet) issued a report in June 2011 which discussed the evidence for harm and the legal status of MDMA, arguing in favor of maintaining it on List I.[132][133][134]


In Canada, MDMA is listed as a Schedule 1[135] as it is an analogue of amphetamine.[136] The CDSA was updated as a result of the Safe Streets Act changing amphetamines from Schedule III to Schedule I in March 2012.


UNODC map showing the use of ecstasy by country in 2013 for the global population aged 15-64.


In 2008 the European Monitoring Centre for Drugs and Drug Addiction noted that although there were some reports of tablets being sold for as little as 1, most countries in Europe then reported typical retail prices in the range of €3 to €9 per tablet, typically containing 25–65 mg of MDMA.[137] By 2014 the EMCDDA reported that the range was more usually between €5 and €10 per tablet, typically containing 57–102 mg of MDMA, although MDMA in powder form was becoming more common.[138]

North America

The United Nations Office on Drugs and Crime stated in its 2014 World Drug Report that U.S. ecstasy retail prices range from US$1 to $70 per pill, or from $15,000 to $32,000 per kilogram.[139] A new research area named Drug Intelligence aims to automatically monitor distribution networks based on image processing and machine learning techniques, in which an Ecstasy pill picture is analyzed to detect correlations among different production batches.[140] These novel techniques allow police scientists to facilitate the monitoring of illicit distribution networks. Among adolescent users in the United States between 1999 and 2008, girls were more likely to use MDMA than boys.[141]


MDMA is particularly expensive in Australia, costing A$15–A$30 per tablet. In terms of purity data for Australian MDMA, the average is around 34%, ranging from less than 1% to about 85%. The majority of tablets contain 70–85 mg of MDMA. Most MDMA enters Australia from the Netherlands, the UK, Asia, and the U.S.[142]

Harm assessment

In a 2011 survey of 292 clinical experts in Scotland, MDMA ranked 13th in personal harm and 16th in social harm out of 19 common recreational drugs.[143]

Researchers such as David Nutt disagree with the categorization of MDMA with other more harmful drugs,[144] especially when compared to alcohol which ranked as the most harmful drug using a multicriteria approach.[145][146] A 2010 UK study which took into account impairment of cognitive functioning placed MDMA at number 17 out of 20 recreational drugs.[147] In a 2011 survey of 292 clinical experts in Scotland, MDMA ranked 16th in both personal harm and social harm out of 19 common recreational drugs.[143]


MAPS is currently funding pilot studies investigating the use of MDMA in PTSD therapy[148] and social anxiety therapy for autistic adults.[149] MDMA has also been proposed as an adjunct to substance abuse treatment.[150]

A review of the safety and efficacy of MDMA as a treatment for various disorders, particularly PTSD, indicated that MDMA has therapeutic efficacy in some patients;[18] however, it emphasized that MDMA is not a safe medical treatment due to lasting neurotoxic and cognition impairing effects in humans.[18] The author noted that oxytocin and D-cycloserine are potentially safer co-drugs in PTSD treatment, albeit with limited evidence of efficacy.[18] This review and a second corroborating review by a different author both concluded that, because of MDMA's demonstrated potential to cause lasting harm in humans (e.g., serotonergic neurotoxicity and persistent memory impairment), "considerably more research must be performed" on its efficacy in PTSD treatment to determine if the potential treatment benefits outweigh its potential to cause long-term harm to a patient.[17][18]


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