MDMA Stats & Data
[Cl-].CNC(C)Cc1ccc2OCOc2c1.[H+]LUWHVONVCYWRMZ-UHFFFAOYSA-NInteraction Warnings
The neurotoxic effects of MDMA may be increased when combined with other stimulants.
This combination may increase strain on the heart.
Pharmacology
DrugBankDescription
An N-substituted amphetamine analog. It is a widely abused drug classified as a hallucinogen and causes marked, long-lasting changes in brain serotonergic systems. It is commonly referred to as MDMA or ecstasy. It is a widely abused drug classified as a hallucinogen and causes marked, long-lasting changes in brain serotonergic systems.
Mechanism of Action
It enters neurons via carriage by the monoamine transporters. Once inside, MDMA inhibits the vesicular monoamine transporter, which results in increased concentrations of serotonin, norepinephrine, and dopamine into the cytoplasm, and induces their release by reversing their respective transporters through a process known as phosphorylation. It also acts as a weak 5-HT1 and 5-HT2 receptor agonist. MDMA's unusual entactogenic effects have been hypothesized to be, at least partly, the result of indirect oxytocin secretion via activation of the serotonin system. Oxytocin is a hormone released following events like hugging, orgasm, and childbirth, and is thought to facilitate bonding and the establishment of trust. Based on studies in rats, MDMA is believed to cause the release of oxytocin, at least in part, by both directly and indirectly agonizing the serotonin 5-HT1A receptor.
Pharmacodynamics
MDMA acts as a releasing agent of serotonin, norepinephrine, and dopamine.
Metabolism
Midomafetamine, or MDMA, is reported to undergo extensive CYP-mediated hepatic metabolism, with CYP2D6 playing a major role in humans. Other CYP enzymes contributing to MDMA metabolism are CYP3A4 and COMT. MDMA is metabolized via two primary metabolic pathways. It may undergo O-demethylenation followed by catechol-O-methyltransferase (COMT)-catalyzed methylation and/or glucuronide/sulfate conjugation. In contrast, it may also undergo N-dealkylation, deamination, and oxidation to the corresponding benzoic acid derivatives conjugated with glycine. Due to autoinhibition of CYP2D6 and CYP2D8, MDMA displays a complex, nonlinear pharmacokinetics profile, with the zeroth order kinetics occurring 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.
Indication
Clinical trials are now testing the therapeutic potential of MDMA for post-traumatic stress disorder (PTSD) and anxiety associated with terminal cancer. MDMA is one of the four most widely used illicit drugs in the U.S.
Half-life
6–10 (though duration of effects is typically actually 3–5 hours)
Elimination
renal
Receptor Profile
Receptor Actions
Receptor Binding
History & Culture
1912–1959
MDMA was first synthesized in 1912 by German chemist Anton Köllisch while working at the pharmaceutical company Merck. Contrary to persistent myths about the compound being developed as an appetite suppressant or psychotherapy aid, it was actually created as an intermediate in the synthesis of methylhydrastinine, a potential hemostatic agent intended to control abnormal bleeding. Merck's interest in this project stemmed from a desire to circumvent an existing patent held by competitor Bayer for a similar compound called hydrastinine. The synthesis was described in German patent 274350, filed on December 24, 1912, though Merck showed no interest in MDMA as an active agent itself. The compound remained largely forgotten until 1927, when Merck chemist Max Oberlin conducted the first pharmacological tests while searching for substances with effects similar to adrenaline or ephedrine. Oberlin noted structural similarities to ephedrine and found that MDMA had comparable effects on blood glucose levels, similar actions on vascular smooth muscle, and stronger effects on uterine tissue. However, research was discontinued due to rising costs of the starting materials needed for synthesis. In 1952, Albert van Schoor performed simple toxicological tests at Merck, likely while investigating potential stimulants or circulatory medications. In 1959, Wolfgang Fruhstorfer synthesized MDMA for further pharmacological testing, though it remains unclear whether human effects were investigated. Outside of Merck, the United States Army commissioned toxicological studies between 1953 and 1954 at the University of Michigan, examining behavioral effects in animals injected with mescaline and several analogues including MDMA. This research remained classified until 1969 and was not published until 1973, and may have been conducted with the possibility of developing MDMA as a chemical incapacitant or interrogation aid.
1965–1978
Although MDMA may have been in non-medical use in the western United States as early as 1968, its psychoactive properties did not receive sustained attention until the work of American chemist Alexander Shulgin. According to Shulgin, he synthesized MDMA in 1965 while researching methylenedioxy compounds at Dow Chemical Company, though he did not investigate its psychoactive potential at that time. Around 1970, Shulgin provided synthesis instructions to a Los Angeles chemical company founder, who subsequently passed them to a contact in the Midwest. By August 1970, reports at meetings of crime laboratory chemists indicated MDMA was being used recreationally in the Chicago area. The drug likely emerged as a substitute for MDA, a structurally related compound that had become popular among psychedelic users and was subsequently placed in Schedule I in 1970. Shulgin first learned of MDMA's psychoactive effects around 1975 from a student who described its "amphetamine-like content." The following year, a graduate student he advised at San Francisco State University described positive emotional experiences after she and two friends had consumed 100 mg of the compound. Following self-experimentation by a colleague, Shulgin synthesized MDMA and tried it himself in September and October 1976. He first reported on the drug at a conference in Bethesda, Maryland in December 1976. In 1978, Shulgin and pharmacologist David E. Nichols published the first scientific report describing MDMA's psychoactive effects in humans, characterizing it 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."
1977–1985
While Shulgin did not find his own experiences with MDMA particularly powerful, he was impressed by its capacity to reduce inhibitions and believed it could have therapeutic utility. He conceptualized the drug as allowing users to strip away habitual patterns and perceive the world more clearly, leading him to call it "window." Shulgin occasionally used MDMA for personal relaxation, referring to it as "my low-calorie martini," and introduced the compound to friends, researchers, and others he thought might benefit from it. In 1977, Shulgin introduced MDMA to Leo Zeff, a semi-retired psychotherapist who had previously used psychedelic substances in his practice. Zeff was profoundly impressed and came out of retirement to promote its therapeutic applications. Over the following years, he traveled throughout the United States and occasionally to Europe, eventually training an estimated four thousand psychotherapists in its use. Zeff named the drug "Adam," believing it allowed users to access a state of primordial innocence. Psychotherapists who employed MDMA reported that it eliminated typical fear responses and enhanced communication. Sessions were typically conducted in the patient's or therapist's home, with the therapist's role minimized in favor of patient self-discovery facilitated by MDMA-induced feelings of empathy and openness. The drug was reportedly used to treat depression, substance use disorders, relationship difficulties, premenstrual syndrome, and autism. Practitioners claimed it dramatically accelerated the therapeutic process. In the western United States, it was used in couples counseling and became known as "empathy" in some therapeutic circles. Therapists and experimenters attempted to limit the spread of information about the drug while conducting informal research, hoping to avoid the criminalization that had befallen LSD and mescaline.
1976–1985
While therapeutic interest developed among psychotherapists and experimenters, a parallel recreational market began to emerge. A small scene had developed by the late 1970s, consuming perhaps 10,000 doses in 1976. MDMA spread through personal networks of therapists, psychiatrists, psychedelic users, and affluent young professionals. Early distributors were deterred from large-scale operations by concern over possible legal restrictions. Between the 1970s and mid-1980s, this relatively contained network consumed an estimated 500,000 doses. Into the early 1980s, production was dominated by a small group of therapeutically-minded chemists based in Boston who had begun manufacturing in 1976. This "Boston Group" struggled to keep pace with growing demand, and shortages frequently occurred. MDMA began appearing in nightlife contexts, spreading to nightclubs in Boston and New York City such as Studio 54 and Paradise Garage. Perceiving a commercial opportunity, Michael Clegg, who served as the Southwest distributor for the Boston Group, established his own "Texas Group" with financial backing from Texas associates. In 1981, Clegg coined the term "Ecstasy" as a marketing-friendly street name. Beginning in 1983, the Texas Group mass-produced MDMA in a Texas laboratory or imported it from California, distributing tablets through pyramid sales structures and toll-free telephone numbers. The operation accepted credit card payments and paid taxes on sales. Marketed under the brand name "Sassyfras," MDMA tablets were sold in brown bottles. The Texas Group advertised "Ecstasy parties" at bars and discotheques, positioning MDMA as a "fun drug" that was "good to dance to." It was openly distributed throughout Austin and the Dallas-Fort Worth area, gaining popularity among young professionals, college students, and gay communities.
1984–1988
After a year of planning and data collection, the Drug Enforcement Administration proposed scheduling MDMA on July 27, 1984. The agency was surprised when numerous psychiatrists, psychotherapists, and researchers filed objections and requested hearings. A DEA pharmacologist later acknowledged the agency had been unaware of MDMA's use in psychiatric practice. Administrative hearings were convened in February, June, July, and October of 1985 in Washington D.C., Los Angeles, and Kansas City. The sensationalist media coverage surrounding the proposed criminalization effectively advertised the drug to a broader public. In response to impending prohibition, the Texas Group dramatically escalated production from an estimated 30,000 tablets monthly to as many as 8,000 per day, potentially manufacturing two million tablets before the ban took effect. By some accounts, the organization was distributing 500,000 tablets per month in Dallas alone. By May 1985, MDMA use had become widespread in California, Texas, southern Florida, and the northeastern United States, with evidence of distribution in twenty-eight states and Canada. Urged by Senator Lloyd Bentsen, the DEA announced an emergency Schedule I classification on May 31, 1985, citing increased distribution, escalating street use, and new evidence of neurotoxicity from the structurally related compound MDA. The ban took effect one month later on July 1, 1985, coinciding with Nancy Reagan's "Just Say No" campaign. Based on expert testimony that MDMA possessed accepted medical applications, the presiding administrative law judge recommended classification as Schedule III, which would have permitted continued medical use. However, DEA Administrator John C. Lawn overruled this recommendation. Harvard psychiatrist Lester Grinspoon subsequently sued the DEA, arguing the agency had improperly disregarded evidence of medical utility. A federal court agreed, characterizing Lawn's reasoning as "strained" and "unpersuasive," and vacated the Schedule I classification. Less than a month later, however, Lawn reimposed Schedule I status, dismissing testimony from psychiatrists describing over 200 beneficial therapeutic cases on the grounds that these had not been published in peer-reviewed journals. The classification effectively terminated clinical research and therapeutic use in the United States.
1986–present
Following prohibition, MDMA continued to spread through underground rave and dance music cultures, eventually becoming one of the most popular recreational drugs worldwide. By 2014, it was estimated to be among the most widely used recreational substances globally, alongside cocaine and cannabis. Efforts to restore medical access began almost immediately after scheduling. In 1986, Rick Doblin founded the Multidisciplinary Association for Psychedelic Studies (MAPS) to work within regulatory frameworks toward making MDMA and other psychedelic substances available for therapeutic applications. Building on earlier anecdotal reports from therapists, MAPS pursued rigorous clinical research on MDMA-assisted psychotherapy for post-traumatic stress disorder. In 2017, the U.S. Food and Drug Administration granted breakthrough therapy designation, recognizing the treatment's potential. The terminology surrounding MDMA continued to evolve after prohibition. While "Ecstasy" (often shortened to "E," "X," or "XTC") became the dominant street term for pressed pills and tablets, the term "Molly" (short for "molecule") emerged in the 2000s as slang for crystalline or powder MDMA purported to be of high purity. The British equivalent "Mandy" serves a similar function. However, both terms have evolved into generic terminology for various euphoric stimulants sold in powder or crystal form, regardless of actual MDMA content.
Subjective Effect Notes
physical: The physical effects of MDMA can be broken down into five components all of which progressively intensify proportional to dosage.
cognitive: The general head space of MDMA is described by many as one of extreme mental stimulation, feelings of love or empathy and powerful euphoria. It contains a large number of typical psychedelic, entactogenic and stimulant cognitive effects.
Effect Profile
Curated + 2,846 ReportsMild auditory effects, headspace, and body load with low visuals
User Experiences
Strong empathy, euphoria, and sensory enhancement with moderate stimulation
User Experiences
Moderate euphoria and stimulation with mild anxiety/jitters, low focus
User Experiences
Duration Timeline
BluelightEmpirical Duration
Erowid ReportsCommunity Effects
TripSitTolerance & Pharmacokinetics
drugs.wikiTolerance Decay
Acute tachyphylaxis develops within a single session (subsequent doses feel weaker while adverse effects rise). Community and clinical literature suggest substantial tolerance persists for at least 1–2 weeks, with more complete recovery typically requiring 4–6+ weeks; frequent spacing shorter than this increases after‑effects and blunting. Data are mostly observational/anecdotal with limited controlled human repeat‑dose studies.
Cross-Tolerances
Demographics
Gender Distribution
Age Distribution
Reports Over Time
Effect Analysis
Erowid + BluelightEffects aggregated from 2,262 experience reports (2,212 Erowid + 634 Bluelight)
Effect Sentiment Distribution
Confidence Distribution
Positive Effects 57
Adverse Effects 31
Dose-Response Correlation
How effect frequency changes across dose levels
View data table
| Effect | Light (n=34) | Common (n=87) | Strong (n=51) | Heavy (n=96) |
|---|---|---|---|---|
| Empathy | 61.8% | 70.1% | 72.5% | 58.3% |
| Euphoria | 58.8% | 63.2% | 60.8% | 66.7% |
| Music Enhancement | 55.9% | 66.7% | 54.9% | 55.2% |
| Anxiety | 58.8% | 57.5% | 56.9% | 54.2% |
| Tactile Enhancement | 58.8% | 37.9% | 37.3% | 33.3% |
| Color Enhancement | 55.9% | 36.8% | 31.4% | 35.4% |
| Stimulation | 55.9% | 54.0% | 51.0% | 44.8% |
| Visual Distortions | 38.2% | 51.7% | 41.2% | 53.1% |
| Sedation | 38.2% | 34.5% | 39.2% | 30.2% |
| Confusion | 29.4% | 25.3% | 39.2% | 33.3% |
| Nausea | 35.3% | 29.9% | 19.6% | 22.9% |
| Introspection | 35.3% | 23.0% | 15.7% | 20.8% |
| Focus Enhancement | 29.4% | 34.5% | 31.4% | 21.9% |
| Closed-Eye Visuals | 29.4% | 18.4% | 17.6% | 18.8% |
| Auditory Effects | 8.8% | 28.7% | 17.6% | 26.0% |
Subjective Effect Ontology
Experience ReportsStructured effect tags extracted from 2,846 Erowid & Bluelight experience reports using a controlled vocabulary of 220+ canonical effects across 15 domains.
Auditory
Cognitive
Emotional
Gastrointestinal
Motor
Selfhood
Somatic
Tactile
Temporal
Visual
Dose–Effect Mapping
Experience ReportsHow reported effects shift across dose tiers, based on 2212 experience reports.
| Effect | Light (n=34) | Common (n=87) | Strong (n=51) | Heavy (n=96) | |
|---|---|---|---|---|---|
| empathy | → | ||||
| euphoria | → | ||||
| music enhancement | → | ||||
| anxiety | → | ||||
| tactile enhancement | ↓ | ||||
| color enhancement | ↓ | ||||
| stimulation | ↓ | ||||
| visual distortions | ↑ | ||||
| sedation | ↓ | ||||
| confusion | → | ||||
| nausea | ↓ | ||||
| introspection | ↓ | ||||
| focus enhancement | ↓ | ||||
| closed-eye visuals | ↓ | ||||
| auditory effects | ↑ | ||||
| pupil dilation | ↓ | ||||
| body high | ↓ | ||||
| jaw clenching | → | ||||
| dissociation | ↓ | ||||
| sweating | ↓ |
Showing top 20 of 35 effects
Risk Escalation
Sentiment AnalysisAverage frequency of positive vs adverse effects across dose tiers
View effect breakdown
Adverse Effects
| Effect | Light (n=34) | Common (n=87) | Strong (n=51) | Heavy (n=96) | Change |
|---|---|---|---|---|---|
| Anxiety | -7% | ||||
| Confusion | +13% | ||||
| Nausea | -35% | ||||
| Pupil Dilation | -24% | ||||
| Jaw Clenching | -2% | ||||
| Sweating | -44% | ||||
| Muscle Tension | -14% | ||||
| Increased Heart Rate | -58% | ||||
| Motor Impairment | -29% | ||||
| Headache | -11% | ||||
| Thought Loops | — | -52% | |||
| Memory Suppression | — | +28% | |||
| Psychosis | — | — | +34% | ||
| Seizure | — | — | -28% | ||
| Appetite Suppression | — | -64% |
Positive Effects
| Effect | Light (n=34) | Common (n=87) | Strong (n=51) | Heavy (n=96) | Change |
|---|---|---|---|---|---|
| Empathy | -5% | ||||
| Euphoria | +13% | ||||
| Music Enhancement | -1% | ||||
| Tactile Enhancement | -43% | ||||
| Color Enhancement | -36% | ||||
| Stimulation | -19% | ||||
| Introspection | -41% | ||||
| Focus Enhancement | -25% | ||||
| Body High | -42% | ||||
| Creativity Enhancement | -47% | ||||
| Pain Relief | — | +23% |
Dosage Distribution
Dose distribution from experience reports
Oral
Insufflated
Real-World Dose Distribution
62K DosesFrom 3095 individual dose entries
Oral (n=653)
Insufflated (n=97)
Smoked (n=10)
Intravenous (n=10)
Rectal (n=11)
Common Combinations
Most co-occurring substances in experience reports
Form / Preparation
Most common forms and preparations reported
Body-Weight Dosing
Dose relative to body weight from reports with weight data
Oral
Insufflated
Unknown
Rectal
Redose Patterns
Redosing behavior across 1490 reports
Legal Status
| Country | Status | Notes |
|---|---|---|
| Australia | Schedule 8 (Controlled Drug) | Reclassified to Schedule 8 as of July 1, 2023, allowing for limited authorized medical use. Personal quantities under 1.5 grams or 5 single doses have been decriminalized in the Australian Capital Territory since October 28, 2023. |
| Austria | Illegal | Prohibited under the Suchtmittelgesetz (SMG). Possession, production, and sale are criminal offenses. |
| Belgium | Illegal | Possession, production, and sale are prohibited under national drug legislation. |
| Brazil | Controlled substance | Listed under Portaria SVS/MS nº 344. Production, distribution, and possession are illegal. |
| Canada | Schedule I (CDSA) | Controlled under the Controlled Drugs and Substances Act. Prior to the March 2012 Safe Streets and Communities Act, MDMA and amphetamines were classified under the less restrictive Schedule III. |
| Czech Republic | Schedule I | Classified as a Schedule I controlled substance under national legislation. |
| Denmark | Illegal | Possession, production, and sale are prohibited under Danish drug control legislation. |
| Egypt | Schedule 3 | Requires a prescription or license for legal possession. Unauthorized possession, production, and distribution are prohibited. |
| Finland | Controlled substance (hard drug) | Listed in Finland's controlled substances registry in the hard-drug category. Possession, production, and sale without authorization are illegal. |
| France | Stupéfiant | Classified as a narcotic substance under French law. Possession, purchase, sale, and manufacture are prohibited. |
| Germany | Anlage I BtMG | Controlled under Anlage I of the Betäubungsmittelgesetz (Narcotics Act) since August 1, 1986. Manufacturing, possessing, importing, exporting, buying, selling, procuring, or dispensing without a license is illegal. |
| Italy | Tabella I | Listed in Tabella I of the controlled substances tables (Tabelle delle sostanze stupefacenti e psicotrope). Possession, purchase, and sale are prohibited. |
| Latvia | Schedule I | Classified as a Schedule I controlled substance. Possession, production, and distribution are illegal. |
| Luxembourg | Prohibited | Classified as a prohibited substance under national drug legislation. |
| Netherlands | List I (Opiumwet) | Classified as a hard drug under the Opium Act. Sale, manufacture, and possession of large amounts are illegal. While possession of small quantities for personal use is technically still illegal, it is generally not prosecuted. |
| New Zealand | Class B1 | Reclassified from the less restrictive Class B2 to Class B1 on August 2, 2005. Possession, manufacture, and supply carry significant criminal penalties. |
| Norway | Schedule I | Classified under the most restrictive category in Norwegian drug legislation. Buying or possessing without a license is illegal. |
| Peru | Decriminalized (personal use) | Under Article 2999 of the Peruvian penal code, personal possession of up to 250 milligrams of MDMA is not considered a criminal offense. Production and sale remain illegal. |
| Portugal | Decriminalized (personal use) | Since July 2001 under Law 30/2000, personal possession of less than 1 gram is not a criminal offense. The substance may be confiscated and the individual referred to a dissuasion commission. Production, sale, and trafficking remain criminal offenses. |
| Russia | Schedule I (prohibited) | Classified as a Schedule I prohibited substance. Possession, production, and distribution are criminal offenses. |
| Sweden | Illegal | Possession, production, and sale are prohibited under Swedish drug control legislation. |
| Switzerland | Controlled (Verzeichnis D) | Specifically listed as a controlled substance under Verzeichnis D of Swiss narcotics legislation. |
| United Kingdom | Class A | Controlled under the Misuse of Drugs Act 1971, which was amended in 1977 to include ring-substituted amphetamines and further amended in 1985 to specifically reference MDMA. Class A carries the most severe penalties for possession, supply, and production. |
| United States | Schedule I | Classified as Schedule I under the Controlled Substances Act since July 1, 1985, initially on an emergency basis. Manufacturing, buying, possessing, or distributing without a DEA license is illegal. Despite an administrative law judge recommending Schedule III placement to allow medical use, the DEA director overruled and maintained Schedule I status. |
Harm Reduction
drugs.wikiAlways verify identity and purity: use a multi‑step reagent sequence (e.g., Marquis→Mecke→Simon’s) and, where available, take advantage of FT‑IR/GC‑MS drug‑checking services; cathinones and PMA/PMMA have been repeatedly found in the market and can be lethal at typical MDMA doses. Start with a single, conservative dose and avoid redosing; MDMA displays non‑linear pharmacokinetics (CYP2D6 auto‑inhibition), so redoses can produce disproportionate plasma increases and toxicity. Maintain a moderate ambient temperature and take regular cool‑down breaks, especially when dancing; MDMA impairs thermoregulation and increases heat production, raising hyperthermia risk in hot, crowded venues. Hydration: sip isotonic fluids rather than plain water; typical harm‑reduction guidance is ≤500 mL/h when active and ~250 mL/h when resting to reduce hyponatremia risk. Hyponatremia risk is increased by excessive hypotonic fluid intake, MDMA‑induced vasopressin release, and is reported more often in females and in those on SSRIs/SNRIs. Avoid combining with serotonergic agents (MAOIs, SSRIs/SNRIs, tramadol, DXM, linezolid) due to serotonin toxicity risk; seek urgent care for agitation, clonus, hyperthermia, heavy sweating, or confusion. Certain medicines (fluoxetine/paroxetine/quinidine; ritonavir/cobicistat) can markedly elevate MDMA blood levels via CYP inhibition—use is strongly discouraged. People with cardiovascular disease, hypertension, epilepsy, or bipolar disorder are at higher risk of adverse events; sleep deprivation and dehydration further increase risk. Do not take 5‑HTP or other serotonergic supplements within 24 h before/after MDMA due to possible serotonin excess; magnesium may reduce bruxism in some users but evidence is limited. Post‑use mood dips and sleep disruption are common for 1–3 days; plan for rest, nutrition, and gentle rehydration; frequent use (e.g., <4–6 weeks between sessions) is associated with more pronounced after‑effects. Pill/tablet strengths vary widely (including 200–300 mg units); weigh powders and do not assume pill logos indicate content.
References
Data Sources
Cited References
- Bluelight: MDMA Threshold Dose Discussion (2019)
- EMCDDA: MDMA Drug Profile
- Erowid: MDMA Basics
- Erowid: MDMA Dosage
- Erowid: MDMA FAQ
- Erowid: MDMA Neurotoxicity Article (Baggott)
- Kalant 2001 - Pharmacology & Toxicology of Ecstasy
- MAPS MDMA-Assisted Therapy Phase 3 Trial (2021)
- MDMA and Bipolar Disorder Interaction
- MDMA Clinically Relevant Drug Interactions with MAOIs
- Non-linear Pharmacokinetics of MDMA (de la Torre 2000)
- Parrott 2013 - MDMA Neurotoxicity Review
- RollSafe MDMA Wiki
- Serotonin Syndrome Case Series (FAERS 2022)
- Serotonin Syndrome Overview
- TripSit: Drug Combinations Chart
- Reddit: r/researchchemicals MDMA Dosing Discussions
Drugs.wiki References
- Erowid MDMA Dosage
- Kalant H. Pharmacology and toxicology of MDMA (Ecstasy). 2001.
- de la Torre R. Non-linear pharmacokinetics of MDMA in humans. 2000.
- DrugBank: MDMA (DB01454)
- Parrott AC. Human psychobiology of MDMA/ecstasy: a review. 2013.
- Erowid MDMA Neurotoxicity (Baggott)
- TripSit: Combinations Chart and MDMA facts
- Clinically relevant drug interactions with MAOIs (review) 2022.
- PubChem Compound Summary: MDMA (CID 1615)
- Drug checking: international results database (aggregates of FT‑IR/GC‑MS)
- Saferparty (Zurich) harm-reduction facts and pill warnings