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MDEA
MDEA is a synthetic entactogen and stimulant of the substituted amphetamine class1, closely related to MDMA and MDA.1 It was introduced for recreational use in the United States in 1985.2 Its effects are generally described as milder and shorter lasting than those of MDMA, with a more sedating quality reported at high doses. MDEA was among the substances found in tablets sold as ecstasy during the mid-1990s.3
Dosage & Duration
Dosage
Doses are population estimates that vary widely between individuals.
Duration
Subjective Effects
Reagent Testing
Expected colorimetric results for common reagent tests. Colors show reaction change over 1–2 minutes.
Pharmacology
Pharmacodynamics
MDEA promotes the release of serotonin, norepinephrine, and dopamine and inhibits their reuptake, increasing their levels in the brain. Its serotonin-releasing activity is relatively greater than its dopamine-releasing activity.1 MDEA also stimulates the release of oxytocin, prolactin, and antidiuretic hormone.
Pharmacokinetics
Dangerous
Highest riskThese combinations are considered extremely harmful and should always be avoided. Reactions to these drugs taken in combination are highly unpredictable and have a potential to cause death.
Tolerance
Tolerance timelines are rules of thumb, not exact schedules, and vary widely between individuals and use patterns.
Dopaminergic stimulants, Serotonergic stimulants, Entactogens
Harm Potential
Addiction & Dependence
Psychological
ModerateWith ongoing use, MDEA may produce moderate addiction risk, substantial abuse potential, and psychological dependence in some users. After dependence has formed, abrupt cessation can be followed by cravings and withdrawal effects.
Physical
LowPhysical dependence is not prominently characterized, though withdrawal effects including cravings may occur with chronic use.
Toxicity
Repeated or high doses of MDEA are likely to carry neurotoxic risk. As a potent serotonin releaser, it is believed to reduce serotonin reuptake transporter availability in the brain, and the timeline for recovery remains uncertain.
Heavy MDEA use over extended periods is likely to harm the cardiovascular system and may contribute to valvulopathy; overdose-level exposure can produce acute tachycardia and hypotension.
MDEA and related compounds are hepatotoxic; regular use may cause liver damage.
Hyperthermia is a significant acute risk, particularly with continuous activity without sufficient rest or rehydration; body temperature may rise to dangerous levels.
Overdose may cause muscle rigidity and rhabdomyolysis.
Psychosis Risk
Regular use may lead to schizophrenia-like symptoms according to available sources.
Seizure Risk
Convulsions are listed among overdose symptoms. Risk may be increased when combined with substances that lower seizure threshold.
History & Culture
Alexander Shulgin researched methylenedioxy compounds during the 1960s.4 In a 1967 laboratory notebook entry, he briefly recorded a colleague's report of having experienced no effect from MDEA. Its synthesis and pharmacological evaluation, alongside related…
Legality
International
MDEA (N-ethyl MDA) is listed in Schedule I of the 1971 Convention on Psychotropic Substances. It is not named in the schedules of the 1961 Single Convention, and it is not one of the precursor chemicals in Tables I or II of the 1988 Convention; those latter instruments therefore do not independently schedule/control exact MDEA.
By Country
References
Source Pages
Citations
Further Reading
Article Status
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