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Revision as of 00:05, 13 February 2015 editZouloum (talk | contribs)19 edits Changed CA legal status to Schedule I. It is an amphetamine analog which is Schedule I since 2012.← Previous edit		Latest revision as of 00:25, 15 January 2025 edit undoOAbot (talk | contribs)Bots442,978 editsm Open access bot: doi updated in citation with #oabot.
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			{{Short description|Empathogen-entactogen, psychostimulant, and psychedelic drug of the amphetamine family}}
	{{medref|date=January 2015}}
			{{cs1 config|name-list-style=vanc}}
			{{Use dmy dates|date=July 2020}}
	{{Drugbox
			{{Infobox drug
	| Verifiedfields = changed
			| Verifiedfields = verified
	| Watchedfields = changed
			| Watchedfields = verified
	| verifiedrevid = 477217624
			| verifiedrevid = 646873547
	| IUPAC_name = (R) 1-(benzodioxol-5-yl)propan-2-amine
	| image = MDA-2D-skeletal.svg		| image = MDA-2D-skeletal.svg
			| image_class = skin-invert-image
			| width =
	| image2 = MDA molecule ball.png		| image2 = MDA molecule ball.png
			| width2 =
	<!--Clinical data-->		<!--Clinical data-->
	| tradename =		| drug_name =
			| INN = Tenamfetamine
			| class = ]; ]; ]; ]; ] ] ]
	| pregnancy_AU = <!-- A / B1 / B2 / B3 / C / D / X -->		| pregnancy_AU = <!-- A / B1 / B2 / B3 / C / D / X -->
	| pregnancy_US = <!-- A / B / C / D / X -->		| pregnancy_US = <!-- A / B / C / D / X -->
	| pregnancy_category =		| pregnancy_category =
	| legal_AU = S9		| 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=] |language=pt-BR |publication-date=2023-07-25}}</ref>
	| legal_CA = Schedule I		| legal_CA = Schedule I
			| legal_DE = Anlage I
	| legal_UK = ]
			| legal_UK = Class A
	| legal_US = Schedule I		| legal_US = Schedule I
	| legal_UN = ]		| legal_UN = Psychotropic Schedule I
	| routes_of_administration = Oral, Sublingual, Intranasal		| routes_of_administration = ], ], ], ]
	<!--Pharmacokinetic data-->		<!--Pharmacokinetic data-->
	| bioavailability =		| bioavailability =
	| protein_bound =		| protein_bound =
	| metabolism = ], ] extensively involved		| metabolism = ] (] extensively involved)
	| elimination_half-life = unknown		| elimination_half-life = 10.9{{nbsp}}hours<ref name="BaggottGarrisonCoyle2019" />
			| duration_of_action = 6–8{{nbsp}}hours<ref name="BaggottGarrisonCoyle2019" />
	| excretion = ]		| excretion = ]
	<!--Identifiers-->		<!--Identifiers-->
	| CAS_number_Ref = {{cascite|changed|??}}		| CAS_number_Ref = {{cascite|correct|CAS}}
	| CAS_number = 4764-17-4		| CAS_number = 4764-17-4
			| UNII_Ref = {{fdacite|correct|FDA}}
	| CAS_supplemental =
			| UNII = XJZ28FJ27W
			| CAS_supplemental =
	| ATC_prefix = None		| ATC_prefix = None
	| ATC_suffix =		| ATC_suffix =
	| PubChem = 1614		| PubChem = 1614
	| DrugBank_Ref = {{drugbankcite|correct|drugbank}}		| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
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	| ChEMBL_Ref = {{ebicite|correct|EBI}}		| ChEMBL_Ref = {{ebicite|correct|EBI}}
	| ChEMBL = 6731		| 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
	<!--Chemical data-->		<!--Chemical data-->
			| IUPAC_name = 1-(2''H''-1,3-Benzodioxol-5-yl)propan-2-amine
	| C=10 | H=13 | N=1 | O=2
			| C = 10 | H = 13 | N = 1 | O = 2
	| molecular_weight = 179.22 g/mol
	| smiles = NC(C)CC1=CC2=C(C=C1)OCO2		| SMILES = NC(C)CC1=CC2=C(C=C1)OCO2
			<!--
	| InChI = 1/C10H13NO2/c1-7(11)4-8-2-3-9-10(5-8)13-6-12-9/h2-3,5,7H,4,6,11H2,1H3		| InChI = 1/C10H13NO2/c1-7(11)4-8-2-3-9-10(5-8)13-6-12-9/h2-3,5,7H,4,6,11H2,1H3
	| InChIKey = NGBBVGZWCFBOGO-UHFFFAOYAO		| InChIKey = NGBBVGZWCFBOGO-UHFFFAOYAO-->
	| StdInChI_Ref = {{stdinchicite|correct|chemspider}}		| 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		| 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
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	}}		}}
			'''3,4-Methylenedioxyamphetamine''' ('''MDA'''), sometimes referred to as ''sass'', is an ], ], and ] of the ] family that is encountered mainly as a ]. In its ], MDA is a ] (SNDRA). In most countries, the drug is a ] and its possession and sale are illegal.
	'''3,4-Methylenedioxyamphetamine''' ('''MDA'''), also known as '''tenamfetamine''' (]), or colloquially as "'''Sally'''", "'''Sass'''", "'''Sass-a-frass'''" or "'''Mellow Drug of America'''", is a psychoactive drug of the ] and ] ] that is consumed primarily for its ]ic, ], and ] effects. Pharmacologically, MDA acts as a serotonin-norepinephrine-dopamine ] and ]. ] of MDA is illegal in most countries. Some limited exceptions exist for scientific and medical research. The recreational use of MDA predates its more widely used analog ] (ecstasy).
			MDA is rarely sought as a recreational drug compared to other ]; however, it remains widely used due to it being a primary metabolite,<ref>{{cite journal | vauthors = Crean RD, Davis SA, Von Huben SN, Lay CC, Katner SN, Taffe MA | title = Effects of (+/-)3,4-methylenedioxymethamphetamine, (+/-)3,4-methylenedioxyamphetamine and methamphetamine on temperature and activity in rhesus macaques | journal = Neuroscience | volume = 142 | issue = 2 | pages = 515–525 | date = October 2006 | pmid = 16876329 | pmc = 1853374 | doi = 10.1016/j.neuroscience.2006.06.033 }}</ref> the product of hepatic N-dealkylation,<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> of ]. It is also a common ] 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>
	==Use==
			{{TOC limit|3}}
			==Uses==
	===Medical===		===Medical===
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	===Recreational===		===Recreational===
			MDA is bought, sold, and used as a ] due to its enhancement of ] and ].<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> A recreational dose of MDA is sometimes cited as being between 100 and 160&nbsp;mg.<ref name="BaggottSiegristGalloway2010"/> It produces ]-like effects, including ] and ] 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>
	Although illegal, MDA is bought, sold, and used as a recreational 'love drug', due to its enhancement of empathy.<ref>{{cite journal|last=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|year=1993|volume=36|issue=23|pages=3700–3706|pmid=8246240|url=http://www.ncbi.nlm.nih.gov/pubmed/8246240#|accessdate=20 January 2014|doi=10.1021/jm00075a027}}</ref> A recreational dose of MDA is commonly between 100 and 160&nbsp;mg.<ref name="Baggott"/>
	==Effects==		==Side effects==
			]s of MDA include ] effects like increased ] and ] as well as increased ] and ] levels.<ref name="BaggottGarrisonCoyle2019" /><ref name="BaggottSiegristCoyle2010" />
	{{expand section|date=January 2015}}
	While MDA is generally similar to MDMA, users report that MDA has more stimulant and ] qualities and less intense ]ic effects than MDMA. MDA is also considered less predictable than MDMA, with effects varying greatly from person to person. MDA is best known for its enhancement of the experiences of dancing and sex.{{medical citation needed|date=November 2014}}
	==Overdose==		==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 cardiac effects and subsequent hemorrhaging in the brain (stroke).<ref name="Diaz">Diaz, Jaime. How Drugs Influence Behavior. Englewood Cliffs: Prentice Hall, 1996.</ref> The ] (LD<sub>50</sub>) in mice has been reported as 92&nbsp;mg/kg by ].{{mcn|date=January 2015}}		Symptoms of acute toxicity may include ], sweating, ] and ], ], ]s, and death. Death is usually caused by ] and subsequent ] (]).<ref name="Diaz">{{cite book | vauthors = Diaz J| title = How Drugs Influence Behavior | location = Englewood Cliffs | publisher = Prentice Hall | date = 1996 }}</ref>{{medical citation needed|date=January 2015}}
	==Pharmacology==		==Pharmacology==
	===Pharmacodynamics===		===Pharmacodynamics===
			{{See also|MDMA#Pharmacodynamics|Empathogen#Mechanism of action|Serotonin releasing agent#Effects and comparisons|Monoamine releasing agent#Mechanism of action}}
	MDA is a ] of the ], ], and ]s, as well as a ] ],<ref name="pmid22037049">{{cite journal | author = Lewin AH, Miller GM, Gilmour B | title = Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class | journal = Bioorg. Med. Chem. | volume = 19 | issue = 23 | pages = 7044–8 |date=December 2011 | pmid = 22037049 | pmc = 3236098 | doi = 10.1016/j.bmc.2011.10.007 | url = }}</ref><ref name="Wallach2009">{{cite journal|last1=Wallach|first1=J.V.|title=Endogenous hallucinogens as ligands of the trace amine receptors: A possible role in sensory perception|journal=Medical Hypotheses|volume=72|issue=1|year=2009|pages=91–94|issn=03069877|doi=10.1016/j.mehy.2008.07.052}}</ref> and for that reason, acts as a ] and ] of ], ], and ] (or as an ]).<ref name="pmid17017961">{{vcite2 journal | vauthors = Rothman RB, Baumann MH | title = Therapeutic potential of monoamine transporter substrates | journal = Curr Top Med Chem | volume = 6 | issue = 17 | pages = 1845–59 | year = 2006 | pmid = 17017961 | doi = | url = http://www.eurekaselect.com/77046/article}}</ref> It is also an ] of the ],<ref name="GiovanniMatteo2008">{{cite book|author1=Giuseppe Di Giovanni|author2=Vincenzo Di Matteo|author3=Ennio Esposito|title=Serotonin-dopamine Interaction: Experimental Evidence and Therapeutic Relevance|url=http://books.google.com/books?id=mPkKtA15KM8C&pg=PA294|year=2008|publisher=Elsevier|isbn=978-0-444-53235-0|pages=294–}}</ref> ],<ref name="RothmanBaumann2009">{{cite journal|last1=Rothman|first1=Richard B|last2=Baumann|first2=Michael H|title=Serotonergic drugs and valvular heart disease|journal=Expert Opinion on Drug Safety|volume=8|issue=3|year=2009|pages=317–329|issn=1474-0338|doi=10.1517/14740330902931524}}</ref> and ]s,<ref name="pmid7824160">{{vcite2 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 = 111–5 | year = 1994 | pmid = 7824160 | doi = | url = }}</ref> and shows ] for the ], ], ]s and ] and ]s.<ref name="ManzoniRay2010">{{cite journal|last1=Manzoni|first1=Olivier Jacques|last2=Ray|first2=Thomas S.|title=Psychedelics and the Human Receptorome|journal=PLoS ONE|volume=5|issue=2|year=2010|pages=e9019|issn=1932-6203|doi=10.1371/journal.pone.0009019}}</ref>
			{| class="wikitable floatleft" style="font-size:small;"
	The effect on serotonin may explain the similar ] and empathogenic effects of the two compounds MDMA and MDA. However, (S)-MDA has a higher efficacy in stimulating the ] than (R)-MDMA; thus MDA tends to cause more psychedelic-like effects, such as visual ]s. MDMA can also produce psychedelic-like visual effects, though these are generally less pronounced than those of MDA, or require a heavier dose to become apparent.{{cn|date=January 2015}}
			|+ {{Nowrap|Activities of MDA}}
			|-
			! ] !! ] (K<sub>i</sub>, nM)
			|-
			| {{Abbrlink|SERT|Serotonin transporter}} || 5,600–>10,000 (K<sub>i</sub>)<br />478–4,900 ({{Abbrlink|IC<sub>50</sub>|half-maximal inhibitory concentration}})<br />160–162 ({{Abbrlink|EC<sub>50</sub>|Half-maximal effective concentration}}) (rat)
			|-
			| {{Abbrlink|NET|Norepinephrine transporter}} || 13,000 (K<sub>i</sub>)<br />150–420 ({{Abbr|IC<sub>50</sub>|half-maximal inhibitory concentration}})<br />47–108 ({{Abbr|EC<sub>50</sub>|Half-maximal effective concentration}}) (rat)
			|-
			| {{Abbrlink|DAT|Dopamine transporter}} || >26,000 (K<sub>i</sub>)<br />890–20,500 ({{Abbr|IC<sub>50</sub>|half-maximal inhibitory concentration}})<br />106–190 ({{Abbr|EC<sub>50</sub>|Half-maximal effective concentration}}) (rat)
			|-
			| ] || 3,762–>10,000
			|-
			| ] || >10,000
			|-
			| ] || >10,000
			|-
			| ] || >10,000
			|-
			| ] || {{Abbr|ND|No data}}
			|-
			| ] || 3,200–>10,000 (K<sub>i</sub>)<br />630–1,767 ({{Abbr|EC<sub>50</sub>|half-maximal effective concentration}})<br />57–99% ({{Abbrlink|E<sub>max</sub>|maximal efficacy}})
			|-
			| ] || 91–100 (K<sub>i</sub>)<br />190–850 ({{Abbr|EC<sub>50</sub>|half-maximal effective concentration}})<br />51–80% ({{Abbr|E<sub>max</sub>|maximal efficacy}})
			|-
			| ] || 3,000–6,418 (K<sub>i</sub>)<br />98–4,800 ({{Abbr|EC<sub>50</sub>|half-maximal effective concentration}})<br />79–118% ({{Abbr|E<sub>max</sub>|maximal efficacy}})
			|-
			| ] || >10,000
			|-
			| ] || {{Abbr|ND|No data}}
			|-
			| ] || >10,000
			|-
			| ] || >10,000
			|-
			| ] || 3,548
			|-
			| ] || 8,700–>10,000
			|-
			| ] || >10,000
			|-
			| ] || {{Abbr|ND|No data}}
			|-
			| ] || 1,100–2,600
			|-
			| ] || 690
			|-
			| ] || 229
			|-
			| ], ] || >10,000
			|-
			| ]–] || >10,000–>20,000<!-- D1: >12,000; D2: >20,000; D3: >17,000; D4: >10,000; D5: >10,000 -->
			|-
			| ]–] || >10,000–>13,000 <!-- H1: >13,000; H2, H3, H4: >10,000 -->
			|-
			| ]–] || {{Abbr|ND|No data}}
			|-
			| ] || {{Abbr|ND|No data}}
			|-
			| ] || 220–250 (K<sub>i</sub>) (rat)<br />740 ({{Abbr|EC<sub>50</sub>|half-maximal effective concentration}}) (rat)<br />86% ({{Abbr|E<sub>max</sub>|maximal efficacy}}) (rat)<br />160–180 (K<sub>i</sub>) (mouse)<br />580 ({{Abbr|EC<sub>50</sub>|half-maximal effective concentration}}) (mouse)<br />102% ({{Abbr|E<sub>max</sub>|maximal efficacy}}) (rat)<br />3,600 ({{Abbr|EC<sub>50</sub>|half-maximal effective concentration}}) (human)<br />11% ({{Abbr|E<sub>max</sub>|maximal efficacy}}) (human)
			|-
			| ] || >10,000
			|-
			| ], ] || {{Abbr|ND|No data}}
			|- class="sortbottom"
			| colspan="2" style="width: 1px; background-color:#eaecf0; 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-Benzodioxol-5-yl-1-methyl-ethylamine::(-)2-Benzodioxol-5-yl-1-methyl-ethylamine::(R)-(-)-2-Benzodioxol-5-yl-1-methyl-ethylamine::(S)-(+)-2-Benzodioxol-5-yl-1-methyl-ethylamine::2-Benzodioxol-5-yl-1-methyl-ethylamine::2-Benzodioxol-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 | pages = 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">{{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 = | doi-access = free }}</ref><ref name="RickliKopfHoener2015">{{cite journal | vauthors = Rickli A, Kopf S, Hoener MC, Liechti ME | title = Pharmacological profile of novel psychoactive benzofurans | journal = Br J Pharmacol | volume = 172 | issue = 13 | pages = 3412–3425 | date = July 2015 | pmid = 25765500 | pmc = 4500375 | doi = 10.1111/bph.13128 | url = }}</ref><ref name="SetolaHufeisenGrande-Allen2003">{{cite journal | vauthors = Setola V, Hufeisen SJ, Grande-Allen KJ, Vesely I, Glennon RA, Blough B, Rothman RB, Roth BL | title = 3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") induces fenfluramine-like proliferative actions on human cardiac valvular interstitial cells in vitro | journal = Mol Pharmacol | volume = 63 | issue = 6 | pages = 1223–1229 | date = June 2003 | pmid = 12761331 | doi = 10.1124/mol.63.6.1223 | url = }}</ref><ref name="Blough2008" /><ref name="BrandtWaltersPartilla2020">{{cite journal | vauthors = Brandt SD, Walters HM, Partilla JS, Blough BE, Kavanagh PV, Baumann MH | title = The 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 }}</ref>
			|}
			MDA is a ] of the ], ], ], and ]s, and in relation to this, acts as a ] and ] of ], ], and ] (that is, it is an {{abbrlink|SNDRA|serotonin–norepinephrine–dopamine releasing agent}}).<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 ] of the serotonin ],<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> ],<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 ]<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 ] for the ], ], and ] and serotonin ] and ].<ref name="ManzoniRay2010">{{cite journal | vauthors = Ray TS | title = Psychedelics and the human receptorome | journal = PLOS ONE | volume = 5 | issue = 2 | pages = e9019 | date = February 2010 | pmid = 20126400 | pmc = 2814854 | doi = 10.1371/journal.pone.0009019 | doi-access = free | bibcode = 2010PLoSO...5.9019R }}</ref>
			The (''S'')-] of MDA is more potent than the (''R'')-] as a psychostimulant, possessing greater affinity for the three ]s.
			In terms of the subjective and behavioral effects of MDA, it is thought that ] release is required for its empathogenic effects, dopamine release is required for its ] (] and ]) effects, ] and ] release is required for its ] effects, and direct agonism of the serotonin 5-HT<sub>2A</sub> receptor is required for its mild psychedelic effects.{{Medical citation needed|date=March 2017}}
			In addition to its actions as a monoamine releasing agent, MDA is a potent high-] ] or ] of the rodent TAAR1.<ref name="GainetdinovHoenerBerry2018" /><ref name="SimmlerBuchyChaboz2016" /> Conversely, MDA is much weaker in terms of ] 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 ] 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 | publisher=Springer International Publishing | publication-place=Cham | volume=23 | date=2014 | isbn=978-3-319-48925-4 | doi=10.1007/7355_2014_78 | page=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 . 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 . 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 | pages = e2866 | date = May 2023 | pmid = 36866677 | doi = 10.1002/hup.2866 | url = | quote = Another feature that distinguishes 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 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>
			{| class="wikitable" style="font-size:small;"
			|+ Activities of MDMA, its enantiomers, and related compounds
			|-
			! rowspan="2" | Compound !! colspan="3" | ] ({{Abbrlink|EC<sub>50</sub>|half-maximal effective concentration}}, nM)
			|-
			! ] !! ] !! ]
			|-
			| ] || {{Abbr|ND|No data}} || {{Abbr|ND|No data}} || {{Abbr|ND|No data}}
			|-
			| {{nbsp}}{{nbsp}}] (''d'') || 698–1,765 || 6.6–7.2 || 5.8–24.8
			|-
			| {{nbsp}}{{nbsp}}] (''l'') || {{Abbr|ND|No data}} || 9.5 || 27.7
			|-
			| ] || {{Abbr|ND|No data}} || {{Abbr|ND|No data}} || {{Abbr|ND|No data}}
			|-
			| {{nbsp}}{{nbsp}}] (''d'') || 736–1,292 || 12.3–13.8 || 8.5–24.5
			|-
			| {{nbsp}}{{nbsp}}] (''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
			|-
			| ] || 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
			|-
			| ] || 47 || 2,608 || 622
			|-
			| ] || 540 || 3,300 || >100,000
			|-
			| ] || 114 || 117 || 1,334
			|-
			|- class="sortbottom"
			| colspan="4" style="width: 1px; background-color:#eaecf0; 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 | doi = | url = https://books.google.com/books?id=QCagLAAACAAJ | chapter-url = https://bitnest.netfirms.com/external/Books/Dopamine-releasing-agents_c11.pdf }}</ref>
			|}
	===Pharmacokinetics===		===Pharmacokinetics===
			The ] 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 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 ] 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 | pages = 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 ] of MDA is 10.9{{nbsp}}hours.<ref name="BaggottGarrisonCoyle2019" /> Differences in the duration of MDA versus MDMA may be due ] rather than pharmacokinetics.<ref name="BaggottGarrisonCoyle2019" /><ref name="BaggottLiGalloway2012" />
			==Chemistry==
	The "S" ] of MDA is more potent than the "R" ] as a psychostimulant, possessing greater affinity for the three ] proteins (], ] and ]). The duration of the drug has been reported as about 6 to 8 hours.<ref name="Baggott">
			MDA is a ] ] ] and ] ]. In relation to other phenethylamines and amphetamines, it is the 3,4-methylenedioxy, α-methyl derivative of ], the 3,4-methylenedioxy derivative of ], and the ''N''-] derivative of MDMA.
	Baggott MJ, Siegrist JD, Galloway GP, Robertson LC, Coyle JR, Mendelson, JE. Investigating the Mechanisms of Hallucinogen-Induced Visions Using 3,4-Methylenedioxyamphetamine (MDA): A Randomized Controlled Trial in Humans. DOI: 10.1371/journal.pone.0014074</ref>
			===Synonyms===
	==Physical and chemical properties==
			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===		===Synthesis===
	MDA is typically synthesized from essential oils such as safrole or piperonal.		MDA is typically ] from ]s such as ] or ]. Common approaches from these ] include:
			* Reaction of safrole's ] ] with a ] containing ] followed by ].<ref>{{cite journal | vauthors = Muszynski E | title = | 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=]|date=2011|publisher=Transform Press|location=Berkeley, CA|isbn=978-0-9630096-3-0|page=165|edition=1}}</ref>
	:]
			]
			* ] of safrole to yield ] (MDP2P) followed by ]<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> or via ] of its ].<ref name="Mannich">{{cite journal | vauthors = Mannich C, Jacobsohn W, Mannich HC |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>
			* ] of piperonal with ] followed by ].<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>{{cite book| vauthors = Shulgin A, Shulgin A |title=PiHKAL: A Chemical Love Story|year=1991|publisher=Transform Press|location=Lafayette, CA|isbn=978-0-9630096-0-9|url=https://books.google.com/books?id=O8AdHBGybpcC&q=9780963009609}}</ref>
			*] 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 ], which was then subjected to a Leuckart reaction.
			* The "two dogs" or "dopeboy" ] method, starting with ] as a precursor. First, an oxime is created using hydoxylamine. Then, a ] is performed with nickel acetate to form the amide. Then a ] is done to form the freebase amine of MDA. Then it is purified with an ].<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-methyl<wbr />enedioxy<wbr />methamphetamine 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>
			===Derivatives===
			MDA constitutes part of the core structure of the ] ].
	==History==		==History==
	MDA was first ] by G. Mannish and W. Jacobson in 1910. It was first ingested in July 1930 by ] who later licensed the drug to ].<ref>The First MDA trip and the measurement of ‘mystical experience’ after MDA, LSD, and Psilocybin http://psychedelicresearch.org/?p=45</ref> MDA was first used in ] in 1939, and ] began in 1941 in the exploration of possible therapies for ]. From 1949 to 1957, more than 500&nbsp;human subjects were given MDA in an investigation of its potential use as an ] and/or ] by ]. The ] also experimented with the drug, code named EA-1298, while working to develop a ] or incapacitating agent. ]<ref>The History Channel documented details of his death here http://www.youtube.com/watch?v=ySw-0uY4CUA See minute 2:38 onward.</ref> died in January 1953 after being intravenously injected with 450&nbsp;mg of the drug. MDA was patented as a ] by H. D. Brown in 1958, as an ] by ] in 1960, and as an ] under the trade name "Amphedoxamine" in 1961. MDA began to appear on the ] scene around 1963 to 1964. It was then inexpensive and readily available as a ] from several scientific supply houses. Several researchers, including ] and ], have explored MDA in the field of ].{{cn|date=January 2015}}		MDA was first synthesized by ] and W. Jacobsohn in 1910.<ref name=Mannich /> It was first ingested in July 1930 by ] who later licensed the drug to ].<ref>{{cite web|title=The First MDA trip and the measurement of 'mystical experience' after MDA, LSD, and Psilocybin|url=http://psychedelicresearch.org/?p=45|archive-url=https://archive.today/20120713055811/http://psychedelicresearch.org/?p=45|archive-date=13 July 2012|date=18 July 2008|publisher=Psychedelic research}}</ref> MDA was first used in ] in 1939, and ] began in 1941 in the exploration of possible therapies for ]. From 1949 to 1957, more than five hundred human subjects were given MDA in an investigation of its potential use as an ] and/or ] by ]. The ] also experimented with the drug, code named EA-1298, while working to develop a ] or incapacitating agent. ] died in January 1953 after being intravenously injected, without his knowledge or consent, with 450&nbsp;mg of the drug as part of ]. MDA was patented as an ] by ] in 1960, and as an ] 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 ] from several scientific supply houses. Several researchers, including ] and Richard Yensen, have explored MDA in the field of ].<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 ] (INN) ''tenamfetamine'' was recommended by the ] (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 ] (DOB), brolamfetamine, was recommended.<ref name="WHO1986" /> These events suggest that MDA and DOB were under development as potential ]s at the time.<ref name="WHO1986" />
			==Society and culture==
			]
			===Name===
			When MDA was under development as a potential pharmaceutical drug, it was given the ] (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 ].<ref name="Poisons Standard">Poisons Standard (October 2015) </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" />
			====United States====
			MDA is a ] in the US.
			==Research==
			In 2010, the ability of MDA to invoke mystical experiences and alter vision in healthy volunteers was studied. The study concluded that MDA is a "potential tool to investigate mystical experiences and visual perception".<ref name="BaggottSiegristGalloway2010" />
			A 2019 double-blind study administered both MDA and MDMA to healthy volunteers. The study found that MDA shared many properties with MDMA including ] and ] effects, but generally lasted longer and produced greater increases in psychedelic-like effects like complex imagery, ], and ].<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>
			===Adverse effects===
			MDA can produce ] effects in rodents,<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> which might in part be due to ] into MDA followed by subsequent ].<ref name="de_la_Torre_2004" /> In addition, MDA activates a response of the ], though this subsides after use.<ref name="Herndon_2014" />
			==See also==
			* ]
			* ]
			* ]
			* ]
	==References==		== References ==
	{{Reflist|2}}		{{Reflist}}
	==External links==		== External links ==
	*		*
	*		*
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