3,4-Methylenedioxyamphetamine

{{Short description|Entactogen, stimulant, and psychedelic drug of the amphetamine family}} {{cs1 config|name-list-style=vanc}} {{Use dmy dates|date=July 2020}} {{Infobox drug | Verifiedfields = verified | Watchedfields = verified | verifiedrevid = 646873547 | drug_name = MDA | image = MDA structure.svg | image_class = skin-invert-image | width = 250px | image2 = MDA molecule ball.png | image_class2 = bg-transparent | width2 = 250px

| INN = Tenamfetamine | pregnancy_AU =  | pregnancy_US =  | pregnancy_category = | routes_of_administration = Oral, sublingual, insufflation, intravenous | class = Serotonin–norepinephrine–dopamine releasing agent; Serotonin 5-HT2 receptor agonist; Entactogen; Empathogen; Serotonergic psychedelic; Hallucinogen; Stimulant | ATC_prefix = None | ATC_suffix =

| legal_AU = S9 | legal_BR = F2 | legal_BR_comment = <ref>{{cite web|department=Brazilian Health Regulatory Agency |date=2023-07-24 |title=RDC Nº 804 - Listas de Substâncias Entorpecentes, Psicotrópicas, Precursoras e Outras sob Controle Especial |trans-title=Collegiate Board Resolution No. 804 - Lists of Narcotic, Psychotropic, Precursor, and Other Substances under Special Control|url=https://www.in.gov.br/en/web/dou/-/resolucao-rdc-n-804-de-24-de-julho-de-2023-498447451 |url-status=live |archive-url=https://web.archive.org/web/20230827163149/https://www.in.gov.br/en/web/dou/-/resolucao-rdc-n-804-de-24-de-julho-de-2023-498447451 |archive-date=2023-08-27 |access-date=2023-08-27 |publisher=Diário Oficial da União |language=pt-BR |publication-date=2023-07-25}}</ref> | legal_CA = Schedule I | legal_DE = Anlage I | legal_UK = Class A | legal_US = Schedule I | legal_UN = Psychotropic Schedule I | legal_EU = Fully prohibited | legal_status = SE: Förteckning I

| bioavailability = | protein_bound = | metabolism = Hepatic (CYP extensively involved) | onset = 0.7 hours (range 0.3 to 1.1 hours)<ref name="StraumannVizeliAvedisian2026" /> Peak: 2.0 hours (range 1.0–3.5 hours)<ref name="StraumannVizeliAvedisian2026" /> | elimination_half-life = 8.4–10.9{{nbsp}}hours<ref name="StraumannVizeliAvedisian2026" /><ref name="BaggottGarrisonCoyle2019" /> | duration_of_action = 5–8{{nbsp}}hours (range 1–10 hours)<ref name="Oeri2021" /><ref name="StraumannVizeliAvedisian2026">{{cite journal | vauthors = Straumann I, Vizeli P, Avedisian I, Erne L, Noorshams D, Vukalovic I, Eckert A, Luethi D, Rudin D, Liechti ME | title = Acute effects of MDMA, MDA, lysine-MDMA, and lysine-MDA in a randomized, double-blind, placebo-controlled, crossover trial in healthy participants | journal = Neuropsychopharmacology | volume = 51 | issue = 2 | pages = 476–485 | date = January 2026 | pmid = 40999236 | pmc = 12708835 | doi = 10.1038/s41386-025-02248-3 | url = }}</ref><ref name="BaggottGarrisonCoyle2019" /> | excretion = Renal

| CAS_number_Ref = {{cascite|correct|CAS}} | CAS_number = 4764-17-4 | UNII_Ref = {{fdacite|correct|FDA}} | UNII = XJZ28FJ27W | CAS_supplemental = | PubChem = 1614 | DrugBank_Ref = {{drugbankcite|correct|drugbank}} | DrugBank = DB01509 | ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} | ChemSpiderID = 1555 | ChEMBL_Ref = {{ebicite|correct|EBI}} | ChEMBL = 6731 | ChEBI = 166520 | KEGG_Ref = {{keggcite|correct|kegg}} | KEGG = D12715 | synonyms = MDA; Tenamfetamine; Amphedoxamine; Sally; Sassafras; Sass-a-frass; Sass; Mellow Drug of America; Hug drug; Love; 3,4-Methylenedioxy-α-methylphenethylamine; 5-(2-Aminopropyl)-1,3-benzodioxole; EA-1298; NSC-9978; NSC-27106; SKF-5

| IUPAC_name = 1-(2''H''-1,3-Benzodioxol-5-yl)propan-2-amine | C=10 | H=13 | N=1 | O=2 | SMILES = NC(C)CC1=CC2=C(C=C1)OCO2 | StdInChI_Ref = {{stdinchicite|correct|chemspider}} | StdInChI = 1S/C10H13NO2/c1-7(11)4-8-2-3-9-10(5-8)13-6-12-9/h2-3,5,7H,4,6,11H2,1H3 | StdInChIKey_Ref = {{stdinchicite|correct|chemspider}} | StdInChIKey = NGBBVGZWCFBOGO-UHFFFAOYSA-N }}

'''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">{{cite journal | vauthors = Oeri HE | title = Beyond ecstasy: Alternative entactogens to 3,4-methylenedioxymethamphetamine with potential applications in psychotherapy | journal = J Psychopharmacol | volume = 35 | issue = 5 | pages = 512–536 | date = May 2021 | pmid = 32909493 | pmc = 8155739 | doi = 10.1177/0269881120920420 | url = }}</ref><ref name="HarpreetKarabulutGauld2023" /><ref name="PiHKAL">{{cite book | author1 = Alexander T. Shulgin | author2 = Ann Shulgin | chapter = #100 MDA 3,4-METHYLENEDIOXYAMPHETAMINE | pages = 714–719 | chapter-url = https://www.erowid.org/library/books_online/pihkal/pihkal100.shtml | title = PiHKAL: A Chemical Love Story | date = 1991 | publisher = Transform Press | edition = 1st | location = Berkeley, CA | isbn = 978-0-9630096-0-9 | oclc = 25627628 | url = https://books.google.com/books?id=O8AdHBGybpcC }}</ref> It is usually taken orally.<ref name="Oeri2021" /><ref name="PiHKAL" />

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-HT2A receptor.<ref name="Oeri2021" /> It has a duration of 5 to 8{{nbsp}}hours or around 6{{nbsp}}hours typically.<ref name="Oeri2021" /><ref name="BaggottGarrisonCoyle2019" /><ref name="StraumannVizeliAvedisian2026" />

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">{{cite journal | vauthors = Kaur H, Karabulut S, Gauld JW, Fagot SA, Holloway KN, Shaw HE, Fantegrossi WE | title = Balancing Therapeutic Efficacy and Safety of MDMA and Novel MDXX Analogues as Novel Treatments for Autism Spectrum Disorder | journal = Psychedelic Medicine | volume = 1 | issue = 3 | pages = 166–185 | date = September 2023 | pmid = 40046567 | pmc = 11661495 | doi = 10.1089/psymed.2023.0023 }}</ref> It has been described as the first entactogen.<ref name="BaggottGarrisonCoyle2019" /> MDA has also been described as probably being the most popular analogue of MDMA.<ref name="Sáez-BrionesHernández2013">{{cite journal | vauthors = Sáez-Briones P, Hernández A | title = MDMA (3,4-Methylenedioxymethamphetamine) Analogues as Tools to Characterize MDMA-Like Effects: An Approach to Understand Entactogen Pharmacology | journal = Curr Neuropharmacol | volume = 11 | issue = 5 | pages = 521–534 | date = September 2013 | pmid = 24403876 | pmc = 3763760 | doi = 10.2174/1570159X11311050007 | url = }}</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 the compound's ability to uplift mood and increase empathy.<ref name="MonteMarona-LewickaCozzi1993">{{cite journal | vauthors = Monte AP, Marona-Lewicka D, Cozzi NV, Nichols DE | title = Synthesis and pharmacological examination of benzofuran, indan, and tetralin analogues of 3,4-(methylenedioxy)amphetamine | journal = Journal of Medicinal Chemistry | volume = 36 | issue = 23 | pages = 3700–3706 | date = November 1993 | pmid = 8246240 | doi = 10.1021/jm00075a027 }}</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">{{cite journal | vauthors = Baggott MJ, Siegrist J, Coyle JR, Flower K, Galloway G, Mendelson J | title=Poster Session III (PIII 1-84): PIII-09 Pharmacodynamic Effects of 3,4-Methylenedioxyamphetamine (MDA) | journal=Clinical Pharmacology & Therapeutics | volume=87 | issue=Suppl 1 | date=2010 | issn=0009-9236 | doi=10.1038/clpt.2009.277 | pages=S68–S95 (S70) | quote = In a placebo-controlled, double-blind, within-subjects study, 12 individuals received a single 98 mg/70 kg bw dose of MDA. This is the molar equivalent of 105 mg/ 70 kg bw MDMA, a well-studied dose. [...] MDA increased cortisol by 16.39 ug/dL (95%CI: 13.03-19.74, P < 1e-3) and prolactin by 18.37 ng/mL (95%CI: 7.39-29.35, P < 1e-3). These hormonal changes are comparable to those seen after MDMA. Heart rate increased by 9.05 bpm (95%CI: 6.10-11.99, P < 1e-5) and blood pressure increased by 18.98 / 12.73 mm Hg (Systolic 95%CI: 16.47 - 21.49, P < 1e-7; Diastolic 95%CI: 10.82 - 14.63, P < 1e-4). [...] There were robust self-report VAS changes in both MDMA-like (e.g., “closeness to others”) and hallucinogen-like (e.g., “familiar things seem unfamiliar”, time distortions, closed-eye visuals) effects that were generally similar to those seen after MDMA. [...] MDA is a psychoactive sympathomimetic phenethylamine with effects similar to MDMA. Although differences may exist in the magnitude of physiological effects, the overall profiles appear remarkably similar.}}</ref><ref name="StraumannVizeliAvedisian2026" />

The dose range of MDA given in Alexander Shulgin's book ''PiHKAL'' (''Phenethylamines I Have Known and Loved'') and other sources is 80 to 160{{nbsp}}mg.<ref name="PiHKAL" /><ref name="Oeri2021" /> A wider recreational dose range for MDA of 20 to 200{{nbsp}}mg or more, with a typical dose estimate of 90{{nbsp}}mg, has also been reported.<ref name="LuethiLiechti2018">{{cite journal | vauthors = Luethi D, Liechti ME | title = Monoamine Transporter and Receptor Interaction Profiles in Vitro Predict Reported Human Doses of Novel Psychoactive Stimulants and Psychedelics | journal = Int J Neuropsychopharmacol | volume = 21 | issue = 10 | pages = 926–931 | date = October 2018 | pmid = 29850881 | pmc = 6165951 | doi = 10.1093/ijnp/pyy047 | quote = Supplementary Table S1. Dose estimates and data sources for stimulants. [...]}}</ref> The dose range of MDA is very similar to that of MDMA.<ref name="PiHKAL" /><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="PiHKAL" /> 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">{{cite journal | vauthors = Baggott MJ, Garrison KJ, Coyle JR, Galloway GP, Barnes AJ, Huestis MA, Mendelson JE | title = Effects of the Psychedelic Amphetamine MDA (3,4-Methylenedioxyamphetamine) in Healthy Volunteers | journal = Journal of Psychoactive Drugs | volume = 51 | issue = 2 | pages = 108–117 | date = 2019-03-15 | pmid = 30967099 | doi = 10.1080/02791072.2019.1593560 | s2cid = 106410946 }}</ref> It does not produce profound sensory disruption or overt hallucinations.<ref name="Nichols1986">{{cite journal | vauthors = Nichols DE | title = Differences between the mechanism of action of MDMA, MBDB, and the classic hallucinogens. Identification of a new therapeutic class: entactogens | journal = J Psychoactive Drugs | volume = 18 | issue = 4 | pages = 305–313 | date = 1986 | pmid = 2880944 | doi = 10.1080/02791072.1986.10472362 | url = }}</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" /> Conversely, a clinical study found that it was more stimulating than MDMA.<ref name="StraumannVizeliAvedisian2026" /> 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" /><ref name="StraumannVizeliAvedisian2026" /> 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" /> MDA tends to produce more anxiety and fear than MDMA.<ref name="StraumannVizeliAvedisian2026" />

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">{{cite book | veditors = Iversen LL, Iversen SD, Snyder SH | vauthors = Shulgin AT | title=Stimulants | chapter=Psychotomimetic Drugs: Structure-Activity Relationships | publisher=Springer US | publication-place=Boston, MA | date=1978 | isbn=978-1-4757-0512-6 | doi=10.1007/978-1-4757-0510-2_6 | pages=243–333 | chapter-url=https://bitnest.netfirms.com/external/10.1007/978-1-4757-0510-2_6 | url=https://books.google.com/books?id=h0_uBwAAQBAJ&pg=PA261}}</ref><ref name="PiHKAL" /> High doses of enantiopure (''R'')-MDA, in the range of 120 to 200{{nbsp}}mg, are described as closely resembling the effects of a 200 to 400{{nbsp}}μg dose of LSD-25.<ref name="Shulgin1978" /><ref name="YensenDiLeoRhead1976">{{cite journal | vauthors = Yensen R, Di Leo FB, Rhead JC, Richards WA, Soskin RA, Turek B, Kurland AA | title = MDA-assisted psychotherapy with neurotic outpatients: a pilot study | journal = J Nerv Ment Dis | volume = 163 | issue = 4 | pages = 233–245 | date = October 1976 | pmid = 972325 | doi = 10.1097/00005053-197610000-00002 | url = }}</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="PiHKAL" />

The duration of MDA is about 5 to 8{{nbsp}}hours and is about 2{{nbsp}}hours longer than that of MDMA (3–6{{nbsp}}hours).<ref name="Oeri2021" /><ref name="BaggottGarrisonCoyle2019" /><ref name="StraumannVizeliAvedisian2026" /> Shulgin originally gave a duration of MDA of 8 to 12{{nbsp}}hours in ''PiHKAL'', but he later revised this down to only 3 to 6{{nbsp}}hours.<ref name="PiHKAL" /> Modern clinical studies have given an average duration of 6 to 8{{nbsp}}hours with a range of 0.9 to 10{{nbsp}}hours.<ref name="BaggottGarrisonCoyle2019" /><ref name="StraumannVizeliAvedisian2026" /> The drug's onset is 0.7{{nbsp}}hours (range 0.3 to 1.1{{nbsp}}hours) and its time to peak effects is 2.0{{nbsp}}hours (range 1.0 to 3.5{{nbsp}}hours).<ref name="StraumannVizeliAvedisian2026" />

==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 cardiotoxicity. A 450{{nbsp}}mg intravenous injection of MDA was found to result in death in one case.<ref name="DunlapAndrewsOlson2018" />

==Interactions== {{See also|MDMA#Interactions|Psychedelic drug#Interactions|Trip killer#Serotonergic psychedelic antidotes|Trip killer#Antidotes of other hallucinogens|MDMA/citalopram}}

==Pharmacology== ===Pharmacodynamics=== {{See also|MDMA#Pharmacodynamics|Entactogen#Mechanism of action|Serotonin releasing agent#Effects and comparisons|Monoamine releasing agent#Mechanism of action}}

{| class="wikitable floatright" style="font-size:small;" |+ {{Nowrap|Activities of MDA}} |- ! Target !! Affinity (Ki, nM) |- | {{Abbrlink|SERT|Serotonin transporter}} || 5,600–>10,000 (Ki) 478–4,900 ({{Abbrlink|IC50|half-maximal inhibitory concentration}}) 160–162 ({{Abbrlink|EC50|Half-maximal effective concentration}}) (rat) |- | {{Abbrlink|NET|Norepinephrine transporter}} || 13,000 (Ki) 150–420 ({{Abbr|IC50|half-maximal inhibitory concentration}}) 47–108 ({{Abbr|EC50|Half-maximal effective concentration}}) (rat) |- | {{Abbrlink|DAT|Dopamine transporter}} || >26,000 (Ki) 890–20,500 ({{Abbr|IC50|half-maximal inhibitory concentration}}) 106–190 ({{Abbr|EC50|Half-maximal effective concentration}}) (rat) |- | 5-HT1A || 3,762–>10,000 |- | 5-HT1B || >10,000 |- | 5-HT1D || >10,000 |- | 5-HT1E || >10,000 |- | 5-HT1F || {{Abbr|ND|No data}} |- | 5-HT2A || 3,200–>10,000 (Ki) 630–1,767 ({{Abbr|EC50|half-maximal effective concentration}}) 57–99% ({{Abbrlink|Emax|maximal efficacy}}) |- | 5-HT2B || 91–100 (Ki) 190–850 ({{Abbr|EC50|half-maximal effective concentration}}) 51–80% ({{Abbr|Emax|maximal efficacy}}) |- | 5-HT2C || 3,000–6,418 (Ki) 98–4,800 ({{Abbr|EC50|half-maximal effective concentration}}) 79–118% ({{Abbr|Emax|maximal efficacy}}) |- | 5-HT3 || >10,000 |- | 5-HT4 || {{Abbr|ND|No data}} |- | 5-HT5A || >10,000 |- | 5-HT6 || >10,000 |- | 5-HT7 || 3,548 |- | α1A || 8,700–>10,000 |- | α1B || >10,000 |- | α1D || {{Abbr|ND|No data}} |- | 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 || {{Abbr|ND|No data}} |- | nACh || {{Abbr|ND|No data}} |- | TAAR1 || 220–250 (Ki) (rat) 740 ({{Abbr|EC50|half-maximal effective concentration}}) (rat) 86% ({{Abbr|Emax|maximal efficacy}}) (rat) 160–180 (Ki) (mouse) 580 ({{Abbr|EC50|half-maximal effective concentration}}) (mouse) 102% ({{Abbr|Emax|maximal efficacy}}) (rat) 3,600 ({{Abbr|EC50|half-maximal effective concentration}}) (human) 11% ({{Abbr|Emax|maximal efficacy}}) (human) |- | I1 || >10,000 |- | σ1, σ2 || {{Abbr|ND|No data}} |- class="sortbottom" | colspan="2" style="width: 1px; background-color:var(--background-color-notice-subtle,#eaecf0); color:inherit; text-align: center;" | '''Notes:''' The smaller the value, the more avidly the drug binds to the site. Proteins are human unless otherwise specified. '''Refs:'''<ref name="PDSPKiDatabase">{{cite web | title=PDSP Database | website=UNC | url=https://pdsp.unc.edu/databases/pdsp.php?receptorDD=&receptor=&speciesDD=&species=&sourcesDD=&source=&hotLigandDD=&hotLigand=&testLigandDD=&testFreeRadio=testFreeRadio&testLigand=MDA&referenceDD=&reference=&KiGreater=&KiLess=&kiAllRadio=all&doQuery=Submit+Query | language=zu | access-date=13 December 2024}}</ref><ref name="BindingDB">{{cite web | vauthors = Liu T | title=BindingDB BDBM50005247 (+/-)2-Benzo[1,3]dioxol-5-yl-1-methyl-ethylamine::(-)2-Benzo[1,3]dioxol-5-yl-1-methyl-ethylamine::(R)-(-)-2-Benzo[1,3]dioxol-5-yl-1-methyl-ethylamine::(S)-(+)-2-Benzo[1,3]dioxol-5-yl-1-methyl-ethylamine::2-Benzo[1,3]dioxol-5-yl-1-methyl-ethylamine::2-Benzo[1,3]dioxol-5-yl-1-methyl-ethylamine((R)-(-)-MDA)::3,4-methylenedioxyamphetamine::CHEMBL6731::MDA::MDA, (R,S)::MDA,R(-)::Tenamfetamine::methylenedioxyamphetamine | website=BindingDB | url=https://www.bindingdb.org/rwd/bind/chemsearch/marvin/MolStructure.jsp?monomerid=50005247 | access-date=13 December 2024}}</ref><ref name="Ray2010">{{cite journal | vauthors = Ray TS | title = Psychedelics and the human receptorome | journal = PLOS ONE | volume = 5 | issue = 2 |article-number=e9019 | date = February 2010 | pmid = 20126400 | pmc = 2814854 | doi = 10.1371/journal.pone.0009019 | doi-access = free | bibcode = 2010PLoSO...5.9019R | url = }}</ref><ref name="LuethiKolaczynskaWalter2019">{{cite journal | vauthors = Luethi D, Kolaczynska KE, Walter M, Suzuki M, Rice KC, Blough BE, Hoener MC, Baumann MH, Liechti ME | title = Metabolites of the ring-substituted stimulants MDMA, methylone and MDPV differentially affect human monoaminergic systems | journal = J Psychopharmacol | volume = 33 | issue = 7 | pages = 831–841 | date = July 2019 | pmid = 31038382 | pmc = 8269116 | doi = 10.1177/0269881119844185 | url = }}</ref><ref name="KolaczynskaDucretTrachsel2022" /><ref 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psychoactive aminoalkylbenzofuran derivatives, 5-APB and 6-APB, mimic the effects of 3,4-methylenedioxyamphetamine (MDA) on monoamine transmission in male rats | journal = Psychopharmacology (Berl) | volume = 237 | issue = 12 | pages = 3703–3714 | date = December 2020 | pmid = 32875347 | pmc = 7686291 | doi = 10.1007/s00213-020-05648-z | url = }}</ref><ref name="GainetdinovHoenerBerry2018">{{cite journal | vauthors = Gainetdinov RR, Hoener MC, Berry MD | title = Trace Amines and Their Receptors | journal = Pharmacol Rev | volume = 70 | issue = 3 | pages = 549–620 | date = July 2018 | pmid = 29941461 | doi = 10.1124/pr.117.015305 | url = | doi-access = free }}</ref><ref name="SimmlerBuchyChaboz2016">{{cite journal | vauthors = Simmler LD, Buchy D, Chaboz S, Hoener MC, Liechti ME | title = In Vitro Characterization of Psychoactive Substances at Rat, Mouse, and Human Trace Amine-Associated Receptor 1 | journal = J Pharmacol Exp Ther | volume = 357 | issue = 1 | pages = 134–144 | date = April 2016 | pmid = 26791601 | doi = 10.1124/jpet.115.229765 | url = https://d1wqtxts1xzle7.cloudfront.net/74120533/eae6c6e62565b82d46b4d111bbea0f77b9c2-libre.pdf?1635931703=&response-content-disposition=inline%3B+filename%3DIn_Vitro_Characterization_of_Psychoactiv.pdf&Expires=1746838268&Signature=Sy4fJ90yUhxs68314NxYsW5PAaNrBGePRu35WRR4PIF-3YC7Z~sLdnCn5wfqqbLg9bDEGdt~oW55ugMP3D3jgA0BoRI~~GOb0NQOwrtfUEQK1PQs1uuN9qg5Y1ct8z5NsABm44RgtukkwRMdU6fO7OlfIsQ68hOiFk129Ll7UYqldxD2f1xhE2fTTfsxSpb8cMCJzHn7-ItqLdwnAUPFK7WggDIjmY1kCnaHLwIxMwdJCAq8L6DYzSTg7pZkbR8qlou~GXbTPQt~gYpyZTJp5hgW-7V6K5wLlQ7Z2xE7B0f9wEfuc1W1QNafg125Tr-vvAe4LEGKXV58bnn1bpfWKw__&Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA | archive-url = https://web.archive.org/web/20250509235235/https://d1wqtxts1xzle7.cloudfront.net/74120533/eae6c6e62565b82d46b4d111bbea0f77b9c2-libre.pdf?1635931703=&response-content-disposition=inline%3B+filename%3DIn_Vitro_Characterization_of_Psychoactiv.pdf&Expires=1746838268&Signature=Sy4fJ90yUhxs68314NxYsW5PAaNrBGePRu35WRR4PIF-3YC7Z~sLdnCn5wfqqbLg9bDEGdt~oW55ugMP3D3jgA0BoRI~~GOb0NQOwrtfUEQK1PQs1uuN9qg5Y1ct8z5NsABm44RgtukkwRMdU6fO7OlfIsQ68hOiFk129Ll7UYqldxD2f1xhE2fTTfsxSpb8cMCJzHn7-ItqLdwnAUPFK7WggDIjmY1kCnaHLwIxMwdJCAq8L6DYzSTg7pZkbR8qlou~GXbTPQt~gYpyZTJp5hgW-7V6K5wLlQ7Z2xE7B0f9wEfuc1W1QNafg125Tr-vvAe4LEGKXV58bnn1bpfWKw__&Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA | archive-date = 9 May 2025 }}</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 {{abbrlink|SNDRA|serotonin–norepinephrine–dopamine releasing agent}}).<ref name="Oeri2021" /><ref name="pmid17017961">{{cite journal | vauthors = Rothman RB, Baumann MH | title = Therapeutic potential of monoamine transporter substrates | journal = Current Topics in Medicinal Chemistry | volume = 6 | issue = 17 | pages = 1845–1859 | year = 2006 | pmid = 17017961 | doi = 10.2174/156802606778249766 | url = https://zenodo.org/record/1235860 }}</ref> It is also an agonist of the serotonin 5-HT2A,<ref name="GiovanniMatteo2008">{{cite book| vauthors = Di Giovanni G, Di Matteo V, Esposito E |title=Serotonin–dopamine Interaction: Experimental Evidence and Therapeutic Relevance|url=https://books.google.com/books?id=mPkKtA15KM8C&pg=PA294|year=2008|publisher=Elsevier|isbn=978-0-444-53235-0|pages=294–}}</ref> 5-HT2B,<ref name="RothmanBaumann2009">{{cite journal | vauthors = Rothman RB, Baumann MH | title = Serotonergic drugs and valvular heart disease | journal = Expert Opinion on Drug Safety | volume = 8 | issue = 3 | pages = 317–329 | date = May 2009 | pmid = 19505264 | pmc = 2695569 | doi = 10.1517/14740330902931524 }}</ref> and 5-HT2C receptors<ref name="pmid7824160">{{cite journal | vauthors = Nash JF, Roth BL, Brodkin JD, Nichols DE, Gudelsky GA | title = Effect of the R(−) and S(+) isomers of MDA and MDMA on phosphatidyl inositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors | journal = Neuroscience Letters | volume = 177 | issue = 1–2 | pages = 111–115 | date = August 1994 | pmid = 7824160 | doi = 10.1016/0304-3940(94)90057-4 | author2-link = Bryan Roth | s2cid = 41352480 }}</ref> and shows affinity for the α2A-, α2B-, and α2C-adrenergic receptors and serotonin 5-HT1A and 5-HT7 receptors.<ref name="ManzoniRay2010">{{cite journal | vauthors = Ray TS | title = Psychedelics and the human receptorome | journal = PLOS ONE | volume = 5 | issue = 2 |article-number=e9019 | date = February 2010 | pmid = 20126400 | pmc = 2814854 | doi = 10.1371/journal.pone.0009019 | doi-access = free | bibcode = 2010PLoSO...5.9019R }}</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">{{cite journal | vauthors = Lewin AH, Miller GM, Gilmour B | title = Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class | journal = Bioorganic & Medicinal Chemistry | volume = 19 | issue = 23 | pages = 7044–7048 | date = December 2011 | pmid = 22037049 | pmc = 3236098 | doi = 10.1016/j.bmc.2011.10.007 }}</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">{{cite book | vauthors = Espinoza S, Gainetdinov RR | title=Taste and Smell | chapter=Neuronal Functions and Emerging Pharmacology of TAAR1 | series=Topics in Medicinal Chemistry | publisher=Springer International Publishing | publication-place=Cham | volume=23 | date=2014 | isbn=978-3-319-48925-4 | doi=10.1007/7355_2014_78 | pages=175–194 | quote = Interestingly, the concentrations of amphetamine found to be necessary to activate TAAR1 are in line with what was found in drug abusers [3, 51, 52]. Thus, it is likely that some of the effects produced by amphetamines could be mediated by TAAR1. Indeed, in a study in mice, MDMA effects were found to be mediated in part by TAAR1, in a sense that MDMA auto-inhibits its neurochemical and functional actions [46]. Based on this and other studies (see other section), it has been suggested that TAAR1 could play a role in reward mechanisms and that amphetamine activity on TAAR1 counteracts their known behavioral and neurochemical effects mediated via dopamine neurotransmission. }}</ref><ref name="KuropkaZawadzkiSzpot2023">{{cite journal | vauthors = Kuropka P, Zawadzki M, Szpot P | title = A narrative review of the neuropharmacology of synthetic cathinones-Popular alternatives to classical drugs of abuse | journal = Hum Psychopharmacol | volume = 38 | issue = 3 | article-number = e2866 | date = May 2023 | pmid = 36866677 | doi = 10.1002/hup.2866 | url = | quote = Another feature that distinguishes [synthetic cathinones (SCs)] from amphetamines is their negligible interaction with the trace amine associated receptor 1 (TAAR1). Activation of this receptor reduces the activity of dopaminergic neurones, thereby reducing psychostimulatory effects and addictive potential (Miller, 2011; Simmler et al., 2016). Amphetamines are potent agonists of this receptor, making them likely to self‐inhibit their stimulating effects. In contrast, SCs show negligible activity towards TAAR1 (Kolaczynska et al., 2021; Rickli et al., 2015; Simmler et al., 2014, 2016). [...] It is worth noting, however, that for TAAR1 there is considerable species variability in its interaction with ligands, and it is possible that the in vitro activity of [rodent TAAR1 agonists] may not translate into activity in the human body (Simmler et al., 2016). The lack of self‐regulation by TAAR1 may partly explain the higher addictive potential of SCs compared to amphetamines (Miller, 2011; Simmler et al., 2013). }}</ref><ref name="SimmlerBuserDonzelli2013">{{cite journal | vauthors = Simmler LD, Buser TA, Donzelli M, Schramm Y, Dieu LH, Huwyler J, Chaboz S, Hoener MC, Liechti ME | title = Pharmacological characterization of designer cathinones in vitro | journal = Br J Pharmacol | volume = 168 | issue = 2 | pages = 458–470 | date = January 2013 | pmid = 22897747 | pmc = 3572571 | doi = 10.1111/j.1476-5381.2012.02145.x | url = | quote = β-Keto-analogue cathinones also exhibited approximately 10-fold lower affinity for the TA1 receptor compared with their respective non-β-keto amphetamines. [...] Activation of TA1 receptors negatively modulates dopaminergic neurotransmission. Importantly, methamphetamine decreased DAT surface expression via a TA1 receptor-mediated mechanism and thereby reduced the presence of its own pharmacological target (Xie and Miller, 2009). MDMA and amphetamine have been shown to produce enhanced DA and 5-HT release and locomotor activity in TA1 receptor knockout mice compared with wild-type mice (Lindemann et al., 2008; Di Cara et al., 2011). Because methamphetamine and MDMA auto-inhibit their neurochemical and functional effects via TA1 receptors, low affinity for these receptors may result in stronger effects on monoamine systems by cathinones compared with the classic amphetamines. }}</ref><ref name="DiCaraMaggioAloisi2011">{{cite journal | vauthors = Di Cara B, Maggio R, Aloisi G, Rivet JM, Lundius EG, Yoshitake T, Svenningsson P, Brocco M, Gobert A, De Groote L, Cistarelli L, Veiga S, De Montrion C, Rodriguez M, Galizzi JP, Lockhart BP, Cogé F, Boutin JA, Vayer P, Verdouw PM, Groenink L, Millan MJ | title = Genetic deletion of trace amine 1 receptors reveals their role in auto-inhibiting the actions of ecstasy (MDMA) | journal = J Neurosci | volume = 31 | issue = 47 | pages = 16928–16940 | date = November 2011 | pmid = 22114263 | pmc = 6623861 | doi = 10.1523/JNEUROSCI.2502-11.2011 | url = }}</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">{{cite journal | vauthors = Halberstadt AL, Chatha M, Klein AK, Wallach J, Brandt SD | title = Correlation between the potency of hallucinogens in the mouse head-twitch response assay and their behavioral and subjective effects in other species | journal = Neuropharmacology | volume = 167 | issue = | article-number = 107933 | date = May 2020 | pmid = 31917152 | pmc = 9191653 | doi = 10.1016/j.neuropharm.2019.107933 | url = http://usdbiology.com/cliff/Courses/Advanced%20Seminars%20in%20Neuroendocrinology/Serotonergic%20Psychedelics%2020/Halberstadt%2020%20Neuropharm%20potency%20of%20hallucinogens%20%20head-twitch.pdf}}</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-HT2A 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">{{cite journal | vauthors = Luethi D, Liechti ME | title = Designer drugs: mechanism of action and adverse effects | journal = Arch Toxicol | volume = 94 | issue = 4 | pages = 1085–1133 | date = April 2020 | pmid = 32249347 | pmc = 7225206 | doi = 10.1007/s00204-020-02693-7 | bibcode = 2020ArTox..94.1085L | url = }}</ref><ref name="Baggott2023">{{cite conference | vauthors = Baggott M | title = Beyond Ecstasy: Progress in Developing and Understanding a Novel Class of Therapeutic Medicine | conference = PS2023 [Psychedelic Science 2023, June 19–23, 2023, Denver, Colorado] | date = 23 June 2023 | publisher = Multidisciplinary Association for Psychedelic Studies | location = Denver, CO | url = https://2023.psychedelicscience.org/sessions/beyond-ecstasy-progress-in-developing-and-understanding-a-novel-class-of-therapeutic-medicine/ | access-date = 24 June 2025 | archive-date = 9 January 2025 | archive-url = https://web.archive.org/web/20250109061208/https://2023.psychedelicscience.org/sessions/beyond-ecstasy-progress-in-developing-and-understanding-a-novel-class-of-therapeutic-medicine/ | url-status = dead }}</ref><ref name="Baggott2024">{{cite web | title=Better Than Ecstasy: Progress in Developing a Novel Class of Therapeutic with Matthew Baggott, PhD. | website=YouTube | date=6 March 2024 | url=https://www.youtube.com/watch?v=OnhJvKxwfZI&t=1048 | access-date=20 November 2024}}</ref><ref name="RothmanBaumann2002">{{cite journal | vauthors = Rothman RB, Baumann MH | title = Therapeutic and adverse actions of serotonin transporter substrates | journal = Pharmacol Ther | volume = 95 | issue = 1 | pages = 73–88 | date = July 2002 | pmid = 12163129 | doi = 10.1016/s0163-7258(02)00234-6 | url = }}</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-HT2A receptor agonism than on serotonin release.<ref name="BaggottGarrisonCoyle2019" />

MDA can produce serotonergic neurotoxic effects in rodents.<ref name="Oeri2021" /><ref name="Herndon_2014">{{cite journal | vauthors = Herndon JM, Cholanians AB, Lau SS, Monks TJ | title = Glial cell response to 3,4-(+/-)-methylenedioxymethamphetamine and its metabolites | journal = Toxicological Sciences | volume = 138 | issue = 1 | pages = 130–138 | date = March 2014 | pmid = 24299738 | pmc = 3930364 | doi = 10.1093/toxsci/kft275 }}</ref><ref>{{cite journal | vauthors = Kalant H | title = The pharmacology and toxicology of "ecstasy" (MDMA) and related drugs | journal = CMAJ | volume = 165 | issue = 7 | pages = 917–928 | date = October 2001 | pmid = 11599334 | pmc = 81503 }}</ref> This might in part be due to metabolism of MDA.<ref name="de_la_Torre_2004">{{cite journal | vauthors = de la Torre R, Farré M, Roset PN, Pizarro N, Abanades S, Segura M, Segura J, Camí J | display-authors = 6 | title = Human pharmacology of MDMA: pharmacokinetics, metabolism, and disposition | journal = Therapeutic Drug Monitoring | volume = 26 | issue = 2 | pages = 137–144 | date = April 2004 | pmid = 15228154 | doi = 10.1097/00007691-200404000-00009 }}</ref> In addition, MDA activates a response of the neuroglia, though this subsides after use.<ref name="Herndon_2014" />

<div style="display:inline-grid; margin-right:15px;"> {| class="wikitable" style="font-size:small;" |+ Activities of MDMA, its enantiomers, and related compounds |- ! rowspan="2" | Compound !! colspan="3" | Monoamine release ({{Abbrlink|EC50|half-maximal effective concentration}}, nM) |- ! Serotonin !! Norepinephrine !! Dopamine |- | Amphetamine || {{Abbr|ND|No data}} || {{Abbr|ND|No data}} || {{Abbr|ND|No data}} |- | {{nbsp}}{{nbsp}}(''S'')-Amphetamine (''d'') || 698–1,765 || 6.6–7.2 || 5.8–24.8 |- | {{nbsp}}{{nbsp}}(''R'')-Amphetamine (''l'') || {{Abbr|ND|No data}} || 9.5 || 27.7 |- | Methamphetamine || {{Abbr|ND|No data}} || {{Abbr|ND|No data}} || {{Abbr|ND|No data}} |- | {{nbsp}}{{nbsp}}(''S'')-Methamphetamine (''d'') || 736–1,292 || 12.3–13.8 || 8.5–24.5 |- | {{nbsp}}{{nbsp}}(''R'')-Methamphetamine (''l'') || 4,640 || 28.5 || 416 |- | '''MDA''' || 160 || 108 || 190 |- | {{nbsp}}{{nbsp}}(''S'')-MDA (''d'') || 100 || 50 || 98 |- | {{nbsp}}{{nbsp}}(''R'')-MDA (''l'') || 310 || 290 || 900 |- | MDMA || 49.6–72 || 54.1–110 || 51.2–278 |- | {{nbsp}}{{nbsp}}(''S'')-MDMA (''d'') || 74 || 136 || 142 |- | {{nbsp}}{{nbsp}}(''R'')-MDMA (''l'') || 340 || 560 || 3,700 |- | MDEA || 47 || 2,608 || 622 |- | MBDB || 540 || 3,300 || >100,000 |- | MDAI || 114 || 117 || 1,334 |- |- class="sortbottom" | colspan="4" style="width: 1px; background-color:var(--background-color-notice-subtle,#eaecf0); color:inherit; text-align: center;" | '''Notes:''' The smaller the value, the more strongly the compound produces the effect. '''Refs:'''<ref name="RothmanBaumann2006">{{cite journal | vauthors = Rothman RB, Baumann MH | title = Therapeutic potential of monoamine transporter substrates | journal = Current Topics in Medicinal Chemistry | volume = 6 | issue = 17 | pages = 1845–1859 | date = 2006 | pmid = 17017961 | doi = 10.2174/156802606778249766 }}</ref><ref name="SetolaHufeisenGrande-Allen2003" /><ref name="RothmanBaumannDersch2001">{{cite journal | vauthors = Rothman RB, Baumann MH, Dersch CM, Romero DV, Rice KC, Carroll FI, Partilla JS | title = Amphetamine-type central nervous system stimulants release norepinephrine more potently than they release dopamine and serotonin | journal = Synapse | volume = 39 | issue = 1 | pages = 32–41 | date = January 2001 | pmid = 11071707 | doi = 10.1002/1098-2396(20010101)39:1<32::AID-SYN5>3.0.CO;2-3 | s2cid = 15573624 }}</ref><ref name="RothmanPartillaBaumann2012">{{cite journal | vauthors = Rothman RB, Partilla JS, Baumann MH, Lightfoot-Siordia C, Blough BE | title = Studies of the biogenic amine transporters. 14. Identification of low-efficacy "partial" substrates for the biogenic amine transporters | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 341 | issue = 1 | pages = 251–262 | date = April 2012 | pmid = 22271821 | pmc = 3364510 | doi = 10.1124/jpet.111.188946 }}</ref><ref name="MarusichAntonazzoBlough2016">{{cite journal | vauthors = Marusich JA, Antonazzo KR, Blough BE, Brandt SD, Kavanagh PV, Partilla JS, Baumann MH | title = The new psychoactive substances 5-(2-aminopropyl)indole (5-IT) and 6-(2-aminopropyl)indole (6-IT) interact with monoamine transporters in brain tissue | journal = Neuropharmacology | volume = 101 | pages = 68–75 | date = February 2016 | pmid = 26362361 | pmc = 4681602 | doi = 10.1016/j.neuropharm.2015.09.004 }}</ref><ref name="NagaiNonakaKamimura2007">{{cite journal | vauthors = Nagai F, Nonaka R, Satoh Hisashi Kamimura K | title = The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain | journal = European Journal of Pharmacology | volume = 559 | issue = 2–3 | pages = 132–137 | date = March 2007 | pmid = 17223101 | doi = 10.1016/j.ejphar.2006.11.075 }}</ref><ref name="HalberstadtBrandtWalther2019">{{cite journal | vauthors = Halberstadt AL, Brandt SD, Walther D, Baumann MH | title = 2-Aminoindan and its ring-substituted derivatives interact with plasma membrane monoamine transporters and α2-adrenergic receptors | journal = Psychopharmacology (Berl) | volume = 236 | issue = 3 | pages = 989–999 | date = March 2019 | pmid = 30904940 | pmc = 6848746 | doi = 10.1007/s00213-019-05207-1 | url = }}</ref><ref name="Blough2008">{{cite book | vauthors = Blough B | chapter = Dopamine-releasing agents | veditors = Trudell ML, Izenwasser S | title = Dopamine Transporters: Chemistry, Biology and Pharmacology | pages = 305–320 | date = July 2008 | isbn = 978-0-470-11790-3 | oclc = 181862653 | ol = OL18589888W | publisher = Wiley | location = Hoboken [NJ] | doi = | url = https://books.google.com/books?id=QCagLAAACAAJ | chapter-url = https://bitnest.netfirms.com/external/Books/Dopamine-releasing-agents_c11.pdf }}</ref> |} </div> <div style="display:inline-grid"> {| class="wikitable" style="font-size:small;" |+ {{Nowrap|MDA, MDMA, and enantiomers at serotonin 5-HT2 receptors}} |- ! rowspan="2" | Compound !! colspan="2" | 5-HT2A !! colspan="2" | 5-HT2B !! colspan="2" | 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% || {{Abbr|ND|No data}} || {{Abbr|ND|No data}} |- | {{nbsp}}{{nbsp}}(''S'')-MDA (''d'') || 18,200 || 89% || 100 || 81% || 7,400 || 73% |- | {{nbsp}}{{nbsp}}(''R'')-MDA (''l'') || 5,600 || 95% || 150 || 76% || 7,400 || 76% |- | MDMA || 6,100 || 55% || 2,000–>20,000 || 32% || {{Abbr|ND|No data}} || {{Abbr|ND|No data}} |- | {{nbsp}}{{nbsp}}(''S'')-MDMA (''d'') || 10,300 || 9% || 6,000 || 38% || 2,600 || 53% |- | {{nbsp}}{{nbsp}}(''R'')-MDMA (''l'') || 3,100 || 21% || 900 || 27% || 5,400 || 27% |- class="sortbottom" | colspan="7" style="width: 1px; background-color:var(--background-color-notice-subtle,#eaecf0); color:inherit; text-align: center;" | '''Notes:''' The smaller the Kact or EC50 value, the more strongly the compound produces the effect. '''Refs:'''<ref name="NashRothBrodkin1994">{{cite journal | vauthors = Nash JF, Roth BL, Brodkin JD, Nichols DE, Gudelsky GA | title = Effect of the R(-) and S(+) isomers of MDA and MDMA on phosphatidyl inositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors | journal = Neurosci Lett | volume = 177 | issue = 1–2 | pages = 111–115 | date = August 1994 | pmid = 7824160 | doi = 10.1016/0304-3940(94)90057-4 | url = }}</ref><ref name="SetolaHufeisenGrande-Allen2003" /><ref name="KolaczynskaDucretTrachsel2022">{{cite journal | vauthors = Kolaczynska KE, Ducret P, Trachsel D, Hoener MC, Liechti ME, Luethi D | title = Pharmacological characterization of 3,4-methylenedioxyamphetamine (MDA) analogs and two amphetamine-based compounds: N,α-DEPEA and DPIA | journal = Eur Neuropsychopharmacol | volume = 59 | issue = | pages = 9–22 | date = June 2022 | pmid = 35378384 | doi = 10.1016/j.euroneuro.2022.03.006 | url = https://www.researchgate.net/publication/359686098| doi-access = free }}</ref> |} </div>

===Pharmacokinetics=== The pharmacokinetics of MDA have been studied.<ref name="BaggottGarrisonCoyle2019" /><ref name="BaggottLiGalloway2012">{{cite journal | vauthors=Baggott MJ, Li L, Galloway GP, Scheidweiler KB, Barnes AJ, Huestis MA, Mendelson J | title=Poster Session III (PIII 1-110): PIII-110: Pharmacokinetics of Oral 3,4-Methylenedioxyamphetamine in Humans | journal=Clinical Pharmacology & Therapeutics | volume=91 | issue=Suppl 1 | date=2012 | issn=0009-9236 | doi=10.1038/clpt.2011.363 | pages=S96–S135 | quote = Knowledge of MDA and HMA kinetics in humans is limited to data from MDMA administration studies where minimal formation of these compounds likely leads to inaccurate parameter estimation. We administered a single [98 mg/70 kg body weight] oral dose of MDA to participants in a controlled setting to characterize plasma MDA pharmacokinetics for the first time. [...] Cmax and AUC0-∞ for MDA were 229 ± 39 ng/mL (mean ± SD) and 3636 ± 958 for MDA and 92 ± 61 ng/mL and 1544 ± 741 for the metabolite HMA. Total MDA clearance was 30267 ± 8214 mL/min. There was considerable between-subject variation in metabolite exposure: HMA Cmax and AUC varied over 7-fold and 4-fold, respectively, between the highest and lowest individuals. [...] Pharmacokinetics of MDA resemble those of an iso-molar dose of MDMA, suggesting differences in duration of acute effects between MDA and MDMA are not due to kinetic differences. }}</ref> Its duration of action has been reported to be about 6 to 8{{nbsp}}hours.<ref name="BaggottSiegristGalloway2010">{{cite journal | vauthors = Baggott MJ, Siegrist JD, Galloway GP, Robertson LC, Coyle JR, Mendelson JE | title = Investigating the mechanisms of hallucinogen-induced visions using 3,4-methylenedioxyamphetamine (MDA): a randomized controlled trial in humans | journal = PLOS ONE | volume = 5 | issue = 12 |article-number=e14074 | date = December 2010 | pmid = 21152030 | pmc = 2996283 | doi = 10.1371/journal.pone.0014074 | doi-access = free | bibcode = 2010PLoSO...514074B }}</ref> The duration of MDA is longer than that of MDMA, about 8{{nbsp}}hours for MDA versus 6{{nbsp}}hours for MDMA.<ref name="BaggottGarrisonCoyle2019" /><ref name="BaggottLiGalloway2012" /> The elimination half-life of MDA is 10.9{{nbsp}}hours.<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.<ref name="PiHKAL" /> In relation to other phenethylamines and amphetamines, it is the 3,4-methylenedioxy and α-methyl derivative of phenethylamine, the 3,4-methylenedioxy derivative of amphetamine, and the ''N''-desmethyl derivative of MDMA.<ref name="PiHKAL" /> The compound is a racemic mixture of (''S'')- and (''R'')-enantiomers, (''S'')-MDA and (''R'')-MDA.<ref name="PiHKAL" />

{{Gallery | title = Chemical structures of MDA enantiomers | height = 85 | width = 225 | (S)-MDA.svg | class1=skin-invert-image | (''S'')-MDA | (R)-MDA.svg | class2=skin-invert-image | (''R'')-MDA }}

It is a common contaminant of illicitly produced MDMA.<ref>{{cite web|url=http://www.ecstasydata.org/stats_substance_by_year.php|title=EcstasyData.org: Test Result Statistics: Substances by Year| work = EcstasyData.org |access-date=2017-06-27}}</ref><ref>{{cite web|url=http://idpc.net/profile/Trans-european-drug-information|title=Trans European Drug Information|website=idpc.net|language=en|access-date=2017-06-27|archive-date=4 November 2021|archive-url=https://web.archive.org/web/20211104230649/https://idpc.net/profile/Trans-european-drug-information|url-status=dead}}</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 oil derived chemicals such as safrole or piperonal. Common approaches from these precursors include:

* Bromination of safrole's alkene functional group followed by amine alkylation procedure a:<ref>{{cite journal | vauthors = Muszynski E | title = [Production of some amphetamine derivatives] | journal = Acta Poloniae Pharmaceutica | volume = 18 | pages = 471–478 | date = 1961 | pmid = 14477621 }}</ref><ref name=ShulginIndex>{{cite book| vauthors = Shulgin A, Manning T, Daley P |title=The Shulgin Index, Volume One: Psychedelic Phenethylamines and Related Compounds|date=2011|publisher=Transform Press|location=Berkeley, CA|isbn=978-0-9630096-3-0|page=165|edition=1}}</ref>

class=skin-invert-image|800px|Synthesis of MDA and related analogs from safrole.

* Wacker oxidation of safrole to yield 3,4-methylenedioxyphenylpropan-2-one (MDP2P) followed by reductive amination or ketoxime condensation and reduction to form the final product.<ref name="ShulginIndex" /><ref>{{cite journal | vauthors = Noggle FT, DeRuiter J, Long MJ | title = Spectrophotometric and liquid chromatographic identification of 3,4-methylenedioxyphenylisopropylamine and its N-methyl and N-ethyl homologs | journal = Journal of the Association of Official Analytical Chemists | volume = 69 | issue = 4 | pages = 681–686 | date = 1986 | pmid = 2875058 }}</ref><ref name="MannichJacobsohn1910">{{cite journal | vauthors = Mannich C, Jacobsohn W |title=Über Oxyphenyl-alkylamine und Dioxyphenyl-alkylamine|journal=Berichte der Deutschen Chemischen Gesellschaft|date=1910|volume=41|issue=1|pages=189–197|doi=10.1002/cber.19100430126|url=https://zenodo.org/record/1426387}}</ref> * Henry reaction of piperonal with nitroethane followed by hydrogenation.<ref name="ShulginIndex" /><ref>{{cite journal | vauthors = Ho BT, McIsaac WM, An R, Tansey LW, Walker KE, Englert LF, Noel MB | title = Analogs of alpha-methylphenethylamine (amphetamine). I. Synthesis and pharmacological activity of some methoxy and/or methyl analogs | journal = Journal of Medicinal Chemistry | volume = 13 | issue = 1 | pages = 26–30 | date = January 1970 | pmid = 5412110 | doi = 10.1021/jm00295a007 }}</ref><ref>{{cite journal| vauthors = Butterick JR, Unrau AM |title=Reduction of β-nitrostyrene with sodium bis-(2-methoxyethoxy)-aluminium dihydride. A convenient route to substituted phenylisopropylamines |journal=Journal of the Chemical Society, Chemical Communications|date=1974|volume=8|pages=307–308|doi=10.1039/C39740000307|issue=8}}</ref><ref>{{cite journal | vauthors = Toshitaka O, Hiroaka A |title=Synthesis of Phenethylamine Derivatives as Hallucinogen|journal=Japanese Journal of Toxicology and Environmental Health|date=1992|volume=38|issue=6|pages=571–580|doi=10.1248/jhs1956.38.571|url=https://www.jstage.jst.go.jp/article/jhs1956/38/6/38_6_571/_pdf/-char/en |access-date=20 June 2014|doi-access=free}}</ref><ref name="PiHKAL" /> *Darzens reaction on heliotropin was also done by J. Elks, et al.<ref name="ElksHey1943">{{cite journal| vauthors = Elks J, Hey DH |title=7. β-3 : 4-Methylenedioxyphenylisopropylamine|journal=J. Chem. Soc.|year=1943|pages=15–16|issn=0368-1769|doi=10.1039/JR9430000015}}</ref> This gives MDP2P, which can then be subjected to the conditions mentioned previously. * The "two dogs" or "dopeboy" clandestine method, starting with helional as a precursor. First, helional aldoxime is created using a reaction that involves hydroxylamine hydrochloride. Second, a Beckmann rearrangement is performed on the oxime to form an amide. Third, a Hofmann rearrangement is then done on the amide to form the freebase amine of MDA.<ref>{{Cite web|url=https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3973132|title=Does the 'Two Dogs' Method of Clandestine Synthesis Use Precursors That are not Legally Regulated on the Australian East Coast? by Victor Chiruta, Robert D Renshaw :: SSRN|date=28 November 2021 |ssrn=3973132 |accessdate=11 February 2024 | vauthors = Victor C, D R }}</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>{{cite journal | vauthors = Barnes AJ, De Martinis BS, Gorelick DA, Goodwin RS, Kolbrich EA, Huestis MA | title = Disposition of MDMA and metabolites in human sweat following controlled MDMA administration | journal = Clinical Chemistry | volume = 55 | issue = 3 | pages = 454–462 | date = March 2009 | pmid = 19168553 | pmc = 2669283 | doi = 10.1373/clinchem.2008.117093 }}</ref><ref>R. Baselt, ''Disposition of Toxic Drugs and Chemicals in Man'', 9th edition, Biomedical Publications, Seal Beach, California, 2011, pp. 1078–1080.</ref>

===Analogues and derivatives=== Analogues of MDA include its positional isomer 2,3-methylenedioxyamphetamine (2,3-MDA) and others. MDMA is the ''N''-methyl derivative of MDA. Some other analogues of MDA include 5-APB, 6-APB, 5-APDB, 6-APDB, 5-APBT, 6-APBT, and SDA (3T-MDA), among others.<ref name="PiHKAL" />

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

==History== MDA was first synthesized by Carl Mannich and Willy Jacobsohn in 1910.<ref name="Bernschneider-ReifOxlerFreudenmann2006">{{cite journal | vauthors = Bernschneider-Reif S, Oxler F, Freudenmann RW | title = The origin of MDMA ("ecstasy")--separating the facts from the myth | journal = Pharmazie | volume = 61 | issue = 11 | pages = 966–972 | date = November 2006 | pmid = 17152992 | doi = | url = | quote = According to Merck’s historical personnel files it could be established that Carl Mannich never worked with the company. In a work from 1910, co-authored by Willy Jacobsohn, he described the “valuable pharmacological effects” of “organic phenol-like basic substances”, in particular those of “hordenin”. He tried to synthesize related substances and characterized 3,4- methylendioxyphenyl-isopropylamine as MDA, not MDMA (Mannich and Jacobsohn 1910).}}</ref><ref name="MannichJacobsohn1910" /> It was first taken in July 1930 by Gordon Alles at a total dose of 126{{nbsp}}mg, who experienced hallucinogenic effects, well-being and euphoria, and peripheral effects.<ref name="Alles1959a">{{cite book | author=Gordon A. Alles | chapter = Some Relations Between Chemical Structure and Physiological Action of Mescaline and Related Compounds / Structure and Action of Phenethylamines | veditors = Abramson HA | title = Neuropharmacology: Transactions of the Fourth Conference, September 25, 26, and 27, 1957, Princeton, N. J. | location = New York | publisher = Josiah Macy Foundation | date = 1959 | pages = 181–268 | oclc = 9802642 | url = https://books.google.com/books?id=sDQLAQAAMAAJ&q=%22Some+relations+between+chemical+structure+and+physiological+action+of+mescaline+and+related+compounds%22 | chapter-url = https://bitnest.netfirms.com/external/Books/NeuropharmacologyTrans.4.181#page=5 | archive-url = https://web.archive.org/web/20250321230359/https://bitnest.netfirms.com/external/Books/NeuropharmacologyTrans.4.181#page=5 | archive-date = 21 March 2025 }}</ref><ref name="Alles1959b">{{cite book | author = Gordon A. Alles | chapter = Subjective Reactions to Phenethylamine Hallucinogens | title = A Pharmacologic Approach to the Study of the Mind | date = 1959 | publisher = CC Thomas | location = Springfield | pages = 238–250 (241–246) | isbn = 978-0-398-04254-7 | url = https://books.google.com/books?id=x45rAAAAMAAJ | chapter-url = https://archive.org/details/pharmacologicapp0000univ/page/238/mode/1up}}</ref><ref name="PsychedelicResearch2008" /> However, he did not subsequently describe these effects until 1959.<ref name="BenzenhöferPassie2010">{{cite journal | vauthors = Benzenhöfer U, Passie T | title = Rediscovering MDMA (ecstasy): the role of the American chemist Alexander T. Shulgin | journal = Addiction | volume = 105 | issue = 8 | pages = 1355–61 | date = August 2010 | pmid = 20653618 | doi = 10.1111/j.1360-0443.2010.02948.x | url = }}</ref><ref name="Alles1959a" /><ref name="Alles1959b" /> Alles later licensed the drug to Smith, Kline & French.<ref name="PsychedelicResearch2008">{{cite web | author = Matthew J. Baggott | title = The First MDA trip and the measurement of 'mystical experience' after MDA, LSD, and Psilocybin | url = http://psychedelicresearch.org/?p=45 | date = 18 July 2008 | publisher = Psychedelic Research | archive-url = https://archive.today/20120713055811/http://psychedelicresearch.org/?p=45 | archive-date = 13 July 2012}}</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">{{cite journal | vauthors = Dunlap LE, Andrews AM, Olson DE | title = Dark Classics in Chemical Neuroscience: 3,4-Methylenedioxymethamphetamine | journal = ACS Chem Neurosci | volume = 9 | issue = 10 | pages = 2408–2427 | date = October 2018 | pmid = 30001118 | pmc = 6197894 | doi = 10.1021/acschemneuro.8b00155 | url = https://shaunlacob.com/wp-content/uploads/2020/12/DC-MDMA.pdf}}</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 the emerging field of entactogen-assisted psychotherapy.<ref>{{cite journal | vauthors = Naranjo C, Shulgin AT, Sargent T | title = Evaluation of 3,4-methylenedioxyamphetamine (MDA) as an adjunct to psychotherapy | journal = Medicina et Pharmacologia Experimentalis. International Journal of Experimental Medicine | volume = 17 | issue = 4 | pages = 359–364 | year = 1967 | pmid = 5631047 | doi = 10.1159/000137100 }}</ref><ref>{{cite journal | vauthors = Yensen R, Di Leo FB, Rhead JC, Richards WA, Soskin RA, Turek B, Kurland AA | title = MDA-assisted psychotherapy with neurotic outpatients: a pilot study | journal = The Journal of Nervous and Mental Disease | volume = 163 | issue = 4 | pages = 233–245 | date = October 1976 | pmid = 972325 | doi = 10.1097/00005053-197610000-00002 | s2cid = 41155810 }}</ref>

The International Nonproprietary Name (INN) ''tenamfetamine'' was recommended by the World Health Organization (WHO) in 1986.<ref name="WHO1986">{{cite web | title=INN Recommended List 26 | website= World Health Organization (WHO) | date=9 June 1986 | url=https://www.who.int/publications/m/item/inn-rl-26 | ref={{sfnref| World Health Organization (WHO) |1900}} | access-date=3 November 2024}}</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">{{cite journal | vauthors = Emerson A, Ponté L, Jerome L, Doblin R | title = History and future of the Multidisciplinary Association for Psychedelic Studies (MAPS) | journal = J Psychoactive Drugs | volume = 46 | issue = 1 | pages = 27–36 | date = 2014 | pmid = 24830183 | doi = 10.1080/02791072.2014.877321 | url = https://www.researchgate.net/publication/262381557}}</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== thumb|right|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">{{cite book | vauthors = Elks J | title=The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies | publisher=Springer US | year=2014 | isbn=978-1-4757-2085-3 | url=https://books.google.com/books?id=0vXTBwAAQBAJ&pg=PA1157 | access-date=13 November 2024 | page=1157}}</ref>

===Legal status=== ====Australia==== MDA is schedule 9 prohibited substance under the Poisons Standards.<ref name="Poisons Standard">Poisons Standard (October 2015) [https://www.comlaw.gov.au/Details/F2015L01534/Html/Text#_Toc420496379 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" />

====Canada==== MDA is a Schedule I controlled substance in Canada.<ref name="CDSA">{{cite web | title=Controlled Drugs and Substances Act | website=Department of Justice Canada | url=https://laws-lois.justice.gc.ca/eng/acts/c-38.8/FullText.html | access-date=19 January 2026}}</ref>

====European Union==== MDA is individually classified by countries in the European Union, but generally the countries follow the Convention on Psychotropic Substances.

====United States==== MDA is a Schedule I controlled substance in the United States.<ref name="OrangeBook2026">{{citation | title = Orange Book: List of Controlled Substances and Regulated Chemicals (January 2026) | date = January 2026 | publisher = U.S. Department of Justice: Drug Enforcement Administration (DEA): Diversion Control Division | location = United States | url = https://www.deadiversion.usdoj.gov/schedules/orangebook/orangebook.pdf}}</ref>

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

==References== {{Reflist}}

==External links== * [https://isomerdesign.com/pihkal/explore/100 MDA - Isomer Design] * [https://psychonautwiki.org/wiki/MDA MDA - PsychonautWiki] * [http://www.erowid.org/chemicals/mda/mda.shtml MDA - Erowid] * [http://www.erowid.org/library/books_online/pihkal/pihkal100.shtml MDA - PiHKAL - Erowid] * [http://pihkal.info/read.php?domain=pk&id=100 MDA - PiHKAL - Isomer Design]

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