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Summary sheet: MMDA


MMDA (3-Methoxy-4,5-methylenedioxyamphetamine; also known as 5-Methoxy-MDA) is an obscure psychoactive substituted amphetamine with entactogenic and [[Psychoactive class::psychedelic] properties. It is a closely related structural analog of mescaline and MDA.[1]

In a 1967 lab notebook entry, Alexander Shulgin briefly mentioned a colleague's report of no effect from the substance with a 100mg dose.[2] Shulgin later tested the compound at a range of higher doses and characterized the substance in his book "PiHKAL" ("Phenethylamines I Have Known and Loved").[3]

In the United States, MDEA was introduced recreationally in 1985 as a legal substitute to the newly banned MDMA before it was made a Schedule I substance two years later on August 13, 1987 under the Federal Analog Act.[4] Since then, MDEA has rarely been sold on its own and has largely been used as an occasional additive or substitute ingredient in pills of "Ecstasy" (for instance, studies conducted in the 1990s found MDEA present in approximately four percent of ecstasy tablets).[5]

While MDEA shares many of the core entactogenic properties of MDMA, it is slightly less potent and considered to be more "stoning", lacking the pro-socializing and energizing "magic" most party-goers seek in their MDMA experiences. As a result, it is largely considered by most people to be a less desirable variant of MDMA and is thus rarely produced and sold in the illicit drug market, typically showing up only in small batches synthesized and distributed by hobbyist clandestine chemists.


General formula of a phenethylamine molecule

MDEA, also known as 3,4-methylenedioxy-N-ethylamphetamine, is a synthetic molecule of the substituted amphetamine family. Molecules of the amphetamine class contain a phenethylamine core featuring a phenyl ring bound to an amino (NH2) group through an ethyl chain with an additional methyl substitution at Rα. Additionally, MDEA contains an ethyl substitution on RN, which is a single carbon extension of the methyl group present in MDMA. MDEA also contains substitutions at R3 and R4 of the phenyl ring with oxygen groups that are incorporated into a methylenedioxy ring through a methylene bridge. MDEA shares this methylenedioxy ring with other drugs like MDMA, MDA and MDAI.


MDEA has been shown to act as a releasing agent and reuptake inhibitor of the key monoamine neurotransmitters serotonin, dopamine and noradrenaline[6] which are the neurotransmitters in charge of pleasure, reward, motivation and focus. This is done by inhibiting the reuptake and reabsorption of monoamine neurotransmitters after they have performed their function of transmitting a neural impulse, essentially allowing them to accumulate and be reused in a manner which causes physically stimulating and euphoric effects.[7] The previously mentioned "stoning" effects have been theorized to arise from the higher relative activity MDEA has on releasing serotonin over dopamine compared to MDMA.

It has also been noted that MDEA, even at lower doses, stimulates the release of oxytocin and prolactin, two hormones that have a role in the feeling of trust and love. [8]

Subjective effects

This subjective effects section is a stub.

As such, it is still in progress and may contain incomplete or wrong information.

You can help by expanding or correcting it.

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), a research literature based on anecdotal reports and the personal experiences of PsychonautWiki contributors. As a result, they should be regarded with a healthy degree of skepticism. It is worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become much more likely with higher doses and may include addiction, serious injury, or death.

Physical effects

  • Spontaneous tactile sensations - The "body high" of MDEA can be characterized as a moderate to extreme euphoric relaxing sensation that encompasses the entire body. It is capable of becoming overwhelmingly pleasurable at higher doses to the point of "flooring" or immobilizing the user. This sensation maintains a consistent presence that steadily rises with the onset and hits its limit once the peak has been reached.
  • Stimulation - In terms of its effects on the user's physical energy levels, MDEA is commonly regarded as significantly less stimulating and energizing than MDMA, while still retaining its core entactogenic effects. Unlike MDMA, which encourages activities such as running, climbing and dancing in a way that makes it a popular choice for musical events such as festivals and raves. The distinct style of stimulation which MDEA presents can be described as mildly to moderately forced, trending more towards sedation and relaxation. This means that at higher doses, it becomes difficult or impossible to keep still as jaw clenching, involuntarily body shakes and vibrations become present, resulting in an extreme unsteadiness of the hands and a general lack of motor control, though to a far lesser degree than with MDMA.
  • Vibrating vision - At high doses, a person's eyeballs may begin to spontaneously wiggle back and forth in a rapid motion, causing the vision to become blurry and temporarily out of focus. This is a condition known as nystagmus.
  • Dehydration - Like related entactogenic stimulants, feelings of dry mouth and dehydration are a universal experience with MDEA; this effect is a product of an increased heart rate and metabolism. While it is important to avoid becoming dehydrated (especially when out dancing in a hot environment) there have been a number of users who have suffered from water intoxication through over-drinking, so it is advised that users simply sip at the water and never over-drink.
  • Difficulty urinating - Higher doses of MDEA result in an overall difficulty when it comes to urination. This is an effect that is completely temporary and harmless. It is caused by MDEA’s promotion of the release of anti-diuretic hormone (ADH); ADH is responsible for regulating urination. This effect can be lessened by simply relaxing, but can be significantly relieved by placing a hot flannel over the genitals to warm them up and encourage blood flow.
  • Appetite suppression
  • Bodily control enhancement
  • Brain zaps
  • Increased blood pressure
  • Increased bodily temperature - As MDEA is a serotonin releasing agent, rise in core body temperature tends to be high and consistent throughout the experience. Caution must be taken as too high of a dose results in serotonin syndrome which can be fatal if left untreated.
  • Increased heart rate
  • Increased perspiration
  • Perception of decreased weight
  • Physical euphoria
  • Pupil dilation
  • Stamina enhancement
  • Tactile enhancement
  • Teeth grinding - This component is usually only present in the higher dose range, and to a lesser extent than the teeth grinding associated with MDMA.
  • Temporary erectile dysfunction

Cognitive effects

The cognitive effects of MDEA can be broken down into several components which progressively intensify proportional to dosage. The broad head space of MDEA is described by many as one of moderate mental stimulation, feelings of love, warmth or empathy and powerful relaxing euphoria. It contains a large number of typical psychedelic, entactogenic and stimulant cognitive effects.

The most prominent of these cognitive effects generally include:

Visual effects


MDEA presents an array of visual enhancements which are mild in comparison to traditional psychedelics, but still distinctively present. These generally include:



Hallucinatory states

MDEA is capable of producing a unique range of low and high level hallucinatory states in a fashion that is significantly less consistent and reproducible than that of many other commonly used psychedelics. These effects are far more common during the offset of the experience and commonly include:

Auditory effects

After effects

The effects which occur during the offset of a stimulant experience generally feel negative and uncomfortable in comparison to the effects which occurred during its peak. This is often referred to as a "comedown" and occurs because of neurotransmitter depletion. Its effects commonly include:

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

Short-term health concerns

Short-term physical health risks of MDEA consumption include dehydration, insomnia, hyperthermia,[9][10] and hyponatremia.[11] Continuous activity without sufficient rest or rehydration may cause body temperature to rise to dangerous levels, and loss of fluid via excessive perspiration puts the body at further risk as the stimulatory and euphoric qualities of the drug may render the user oblivious to their energy expenditure for quite some time. Diuretics such as alcohol may exacerbate these risks further.

The exact toxic dosage is unknown, but considered to be far greater than its active dose.

Long-term health concerns

As with MDMA, the neurotoxicity of MDEA use has long been the subject of debate. Scientific study has resulted in the general agreement that, although it is physically safe to try in a responsible context, the administration of repeated or high dosages of MDEA is most certainly neurotoxic in some form.

Like other powerful serotonin releasing agents, MDEA is thought to cause down-regulation of serotonin reuptake transporters in the brain. The rate at which the brain recovers from serotonergic changes is unclear. One study demonstrated lasting serotonergic changes in some animals exposed to MDMA, which likely applies to MDEA as well.[12] Other studies have suggested that the brain may recover from serotonergic damage.[13][14][15]

Like with MDMA, the long-term heavy use of MDEA is likely similarly cardiotoxic, leading to valvulopathy through its actions on the 5-HT2B receptor.[16] In one study, 28% of long-term users (2-3 doses per week for a mean of 6 years, mean of age 24.3 years) had developed clinically evident valvular heart disease.[17]

It is strongly recommended that one use harm reduction practices when using this drug.

Tolerance and addiction potential

As with other stimulants, the chronic use of MDEA can be considered moderately addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage.

Tolerance to many of the effects of MDEA develops with prolonged and repeated use. This results in users having to administer increasingly larger doses to achieve the same effects. After that, it takes about 1 months for the tolerance to be reduced to half and 2-3 months to be back at baseline (in the absence of further consumption). MDEA presents cross-tolerance with [[Cross-tolerance::all dopaminergic and serotonergic stimulants and entactogens]], meaning that after the consumption of MDEA all of these will have a reduced effect.

Dangerous interactions

Although many psychoactive substances are reasonably safe to use on their own, they can suddenly become dangerous or even life-threatening when combined with other substances. The following list includes some known dangerous combinations (although it is not guaranteed to include all of them). Independent research (e.g. Google, DuckDuckGo) should always be conducted to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

  • ]] & ]] - Members of the 25x family are highly stimulating and physically straining. Combinations with stimulants should be avoided due to the risk of excessive stimulation. This can result in panic attacks, thought loops, seizures, increased blood pressure, vasoconstriction, and heart failure in extreme cases.
  • ]] - Alcohol can be dangerous to combine with stimulants due to the risk of accidental over-intoxication. Stimulants mask the sedative effects of alcohol, which is the main factor people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects of alcohol are left unopposed, which can result in blackouts and respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • ]] - Combinations with DXM should be handled with extreme care due to DXM's effects on serotonin and norepinephrine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome with stimulants that increase levels of serotonin (MDMA, methylone, mephedrone, etc.). Monitor blood pressure carefully and avoid strenuous physical activity.
  • ]] - The neurotoxic effects of MDMA may be increased when combined with other stimulants. There is also a risk of excessive heart strain.
  • ]] - Combinations with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • ]] - MMDA can be potentially dangerous in combination with other stimulants like cocaine as they can increase one's heart rate and blood pressure to dangerous levels.
  • ]] - Tramadol lowers the seizure threshold.[18] Combinations with stimulants may further increase this risk.
  • ]] - This combination may increase the amount of neurotransmitters such as dopamine to dangerous or even fatal levels. Examples include syrian rue, banisteriopsis caapi, and some antidepressants.[19]
  • Stimulants - The neurotoxic effects of MDEA may be increased when combined with other stimulants.
  • Cocaine - This combination may increase strain on the heart.

Serotonin syndrome risk

Combinations with the following substances can cause dangerously high serotonin levels. Serotonin syndrome requires immediate medical attention and can be fatal if left untreated.

There is an increased risk of serotonin syndrome when MDEA is taken with many antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs). Additionally, if MDEA is taken with SSRIs and SNRIs, the MDEA will be significantly less powerful or may have no distinguishable effects at all.

Legal issues


This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

  • UK: MDEA is a Class A drug.
  • USA: MDEA is a Schedule I drug.

See also

External links


  1. PiHKAL |
  2. Rediscovering MDMA (ecstasy): the role of the American chemist Alexander T. Shulgin|doi=10.1111/j.1360-0443.2010.02948.x}}
  3. PiHKAL|
  4. PiHKAL|
  5. The Neuropsychopharmacology and Toxicology of 3,4-methylenedioxy-N-ethyl-amphetamine (MDEA) |
  6. The Neuropsychopharmacology and Toxicology of 3,4-methylenedioxy-N-ethyl-amphetamine (MDEA) |
  7. New Insights into the Mechanism of Action of Amphetamines |
  8. Passie, Torsten, MD. Healing with Entactogens. Santa Cruz: Multidisciplinary Association for Psychedelic Studies, n.d. Print.
  9. Drug-induced hyperthermia |;jsessionid=FC30A9B157A2BAFC81048D8595714565.f02t03
  10. Small changes in ambient temperature cause large changes in 3,4-methylenedioxymethamphetamine (MDMA)-induced serotonin neurotoxicity and core body temperature in the rat ( / NCBI) |
  11. Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population |
  12. Reorganization of ascending 5-HT axon projections in animals previously exposed to the recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDEA, "ecstasy") ( / NCBI) |
  13. In vivo detection of short- and long-term MDEA neurotoxicity--a positron emission tomography study in the living baboon brain ( / NCBI) |
  14. Reneman L, Lavalaye J, Schmand B, de Wolff FA, van den Brink W, den Heeten GJ, Booij J (2001). "Cortical serotonin transporter density and verbal memory in individuals who stopped using 3,4-methylenedioxymethamphetamine (MDEA or "ecstasy"): preliminary findings". Arch. Gen. Psychiatry 58 (10): 901–6.
  15. Selvaraj, S. et al (2009) "Brain Serotonin transporter binding in former users of MDEA ("ecstasy")." British Journal of Psychiatry. 194: 355-359. |
  16. Drug-induced Valvulopathy: An Update |
  17. Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease. ( / NCBI) |
  18. Talaie, H.; Panahandeh, R.; Fayaznouri, M. R.; Asadi, Z.; Abdollahi, M. (2009). "Dose-independent occurrence of seizure with tramadol". Journal of Medical Toxicology. 5 (2): 63–67. doi:10.1007/BF03161089. eISSN 1937-6995. ISSN 1556-9039. OCLC 163567183. 
  19. Gillman, P. K. (2005). "Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity". British Journal of Anaesthesia. 95 (4): 434–441. doi:10.1093/bja/aei210Freely accessible. eISSN 1471-6771. ISSN 0007-0912. OCLC 01537271. PMID 16051647. 
  20. Gillman, P. K. (2005). "Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity". British Journal of Anaesthesia. 95 (4): 434–441. doi:10.1093/bja/aei210Freely accessible. eISSN 1471-6771. ISSN 0007-0912. OCLC 01537271. PMID 16051647.