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Tenamfetamine

PubChem CID
1614
Structure
Tenamfetamine_small.png
Tenamfetamine_3D_Structure.png
Molecular Formula
Synonyms
  • Tenamfetamine
  • 3,4-methylenedioxyamphetamine
  • 4764-17-4
  • Methylenedioxyamphetamine
  • 3,4-Methylenedioxy-amphetamine
Molecular Weight
179.22 g/mol
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Dates
  • Create:
    2005-03-25
  • Modify:
    2025-01-18
Description
3,4-Methylenedioxyamphetamine is a member of benzodioxoles.
TENAMFETAMINE is a small molecule drug with a maximum clinical trial phase of II.
An amphetamine derivative that inhibits uptake of catecholamine neurotransmitters. It is a hallucinogen. It is less toxic than its methylated derivative but in sufficient doses may still destroy serotonergic neurons and has been used for that purpose experimentally.

1 Structures

1.1 2D Structure

Chemical Structure Depiction
Tenamfetamine.png

1.2 3D Conformer

2 Names and Identifiers

2.1 Computed Descriptors

2.1.1 IUPAC Name

1-(1,3-benzodioxol-5-yl)propan-2-amine
Computed by Lexichem TK 2.7.0 (PubChem release 2021.10.14)

2.1.2 InChI

InChI=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
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.3 InChIKey

NGBBVGZWCFBOGO-UHFFFAOYSA-N
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.4 SMILES

CC(CC1=CC2=C(C=C1)OCO2)N
Computed by OEChem 2.3.0 (PubChem release 2024.12.12)

2.2 Molecular Formula

C10H13NO2
Computed by PubChem 2.2 (PubChem release 2021.10.14)

2.3 Other Identifiers

2.3.1 CAS

2.3.2 Deprecated CAS

51497-09-7

2.3.3 European Community (EC) Number

2.3.4 UNII

2.3.5 ChEBI ID

2.3.6 ChEMBL ID

2.3.7 DrugBank ID

2.3.8 DSSTox Substance ID

2.3.9 HMDB ID

2.3.10 KEGG ID

2.3.11 Metabolomics Workbench ID

2.3.12 NCI Thesaurus Code

2.3.13 Nikkaji Number

2.3.14 Pharos Ligand ID

2.3.15 Wikidata

2.3.16 Wikipedia

2.4 Synonyms

2.4.1 MeSH Entry Terms

  • 3,4 Methylenedioxyamphetamine
  • 3,4-Methylenedioxyamphetamine

2.4.2 Depositor-Supplied Synonyms

3 Chemical and Physical Properties

3.1 Computed Properties

Property Name
Molecular Weight
Property Value
179.22 g/mol
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
XLogP3
Property Value
1.6
Reference
Computed by XLogP3 3.0 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Donor Count
Property Value
1
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Acceptor Count
Property Value
3
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Rotatable Bond Count
Property Value
2
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Exact Mass
Property Value
179.094628657 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Monoisotopic Mass
Property Value
179.094628657 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Topological Polar Surface Area
Property Value
44.5 Ų
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Heavy Atom Count
Property Value
13
Reference
Computed by PubChem
Property Name
Formal Charge
Property Value
0
Reference
Computed by PubChem
Property Name
Complexity
Property Value
174
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Isotope Atom Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Atom Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Undefined Atom Stereocenter Count
Property Value
1
Reference
Computed by PubChem
Property Name
Defined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Undefined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Covalently-Bonded Unit Count
Property Value
1
Reference
Computed by PubChem
Property Name
Compound Is Canonicalized
Property Value
Yes
Reference
Computed by PubChem (release 2021.10.14)

3.2 Experimental Properties

3.2.1 Color / Form

Almost colorless oil
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 995

3.2.2 Boiling Point

157 °C at 22 mm Hg; 80-90 °C at 0.2 mm Hg
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 995

3.2.3 LogP

1.64
HANSCH,C & LEO,AJ (1985)
log Kow = 1.64
Hansch,C, Leo,AJ; Medchem Project. Issue no. 26. Claremont, CA: Pomona College (1985)
1.64

3.2.4 Decomposition

When heated to decomposition it emits toxic fumes of /Nitrogen oxides/.
Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2438

3.2.5 Dissociation Constants

pKa
9.67 (at 25 °C)
PERRIN,DD (1965)
pKa = 9.67 (conjugate acid)
Perrin DD; Dissociation constants of organic bases in aqueous solution. IUPAC Chem Data Ser, Buttersworth, London (1965)

3.2.6 Kovats Retention Index

Standard non-polar
1443 , 1443 , 1434 , 1470 , 1495 , 1472 , 1480 , 1464.6 , 1472 , 1460 , 1460
Semi-standard non-polar
1508.8 , 1484 , 1483 , 1496.3 , 1469.2 , 1457.4
Standard polar
2204 , 2204

3.2.7 Other Experimental Properties

Crystals from isopropanol/ether, mp 187-188 °C ... also reported as mp 180-181 °C ... Easily soluble in water, alcohol /Hydrochloride/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 995

3.3 Chemical Classes

Stimulant
S120 | DUSTCT2024 | Substances from Second NORMAN Collaborative Dust Trial | DOI:10.5281/zenodo.13835254

3.3.1 Drugs

Pharmaceuticals -> Synthetic Cannabinoids or Psychoactive Compounds
S58 | PSYCHOCANNAB | Synthetic Cannabinoids and Psychoactive Compounds | DOI:10.5281/zenodo.3247723
Pharmaceuticals -> Illicit drugs
S56 | UOATARGPHARMA | Target Pharmaceutical/Drug List from University of Athens | DOI:10.5281/zenodo.3248837
3.3.1.1 Human Drugs
Pharmaceuticals
S72 | NTUPHTW | Pharmaceutically Active Substances from National Taiwan University | DOI:10.5281/zenodo.3955664

4 Spectral Information

4.1 1D NMR Spectra

4.1.1 1H NMR Spectra

Instrument Name
Varian A-60
Source of Sample
Aldrich Chemical Company, Inc., Milwaukee, Wisconsin
Copyright
Copyright © 2009-2024 John Wiley & Sons, Inc. All Rights Reserved.
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4.1.2 13C NMR Spectra

Copyright
Copyright © 2016-2024 W. Robien, Inst. of Org. Chem., Univ. of Vienna. All Rights Reserved.
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4.2 Mass Spectrometry

4.2.1 GC-MS

1 of 9
View All
NIST Number
352965
Library
Main library
Total Peaks
94
m/z Top Peak
44
m/z 2nd Highest
136
m/z 3rd Highest
135
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2 of 9
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NIST Number
386207
Library
Main library
Total Peaks
79
m/z Top Peak
44
m/z 2nd Highest
136
m/z 3rd Highest
135
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4.2.2 MS-MS

1 of 9
View All
Spectra ID
Ionization Mode
Positive
Top 5 Peaks

77.0384 100

95.049 99.84

105.0446 67.95

79.0541 63.18

51.0229 57.64

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2 of 9
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Spectra ID
Ionization Mode
Positive
Top 5 Peaks

79.0541 100

77.0384 70.25

95.049 69.43

103.0541 58.47

105.0446 46.25

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4.2.3 LC-MS

1 of 34
View All
Authors
Kevin S. Jewell; Björn Ehlig; Arne Wick
Instrument
TripleTOF 6600 SCIEX
Instrument Type
LC-ESI-QTOF
MS Level
MS2
Ionization Mode
POSITIVE
Ionization
ESI
Collision Energy
110
Fragmentation Mode
CID
Column Name
Zorbax Eclipse Plus C18 2.1 mm x 150 mm, 3.5 um, Agilent
Retention Time
5.295 min
Precursor m/z
180.1019
Precursor Adduct
[M+H]+
Top 5 Peaks

50.0148 999

51.0219 792

39.0228 284

37.0075 280

62.0152 235

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License
dl-de/by-2-0
2 of 34
View All
Authors
Kevin S. Jewell; Björn Ehlig; Arne Wick
Instrument
TripleTOF 6600 SCIEX
Instrument Type
LC-ESI-QTOF
MS Level
MS2
Ionization Mode
POSITIVE
Ionization
ESI
Collision Energy
30
Fragmentation Mode
CID
Column Name
Zorbax Eclipse Plus C18 2.1 mm x 150 mm, 3.5 um, Agilent
Retention Time
5.295 min
Precursor m/z
180.1019
Precursor Adduct
[M+H]+
Top 5 Peaks

105.0693 999

135.0435 718

133.0638 420

79.0536 267

77.0378 195

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License
dl-de/by-2-0

4.3 UV Spectra

4.3.1 UV-VIS Spectra

Copyright
Copyright © 2008-2024 John Wiley & Sons, Inc. All Rights Reserved.
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4.4 IR Spectra

4.4.1 FTIR Spectra

Technique
CAPILLARY CELL: NEAT
Source of Sample
Aldrich Chemical Company, Inc., Milwaukee, Wisconsin
Copyright
Copyright © 1980, 1981-2024 John Wiley & Sons, Inc. All Rights Reserved.
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4.4.2 ATR-IR Spectra

Instrument Name
Bio-Rad FTS
Technique
ATR-Film (MeCl2) (DuraSamplIR II)
Source of Spectrum
Forensic Spectral Research
Source of Sample
Lipomed AG
Catalog Number
Free base of MDA-79-HC-1LM
Lot Number
Free base of 94.3B10.2L1
Copyright
Copyright © 2014-2024 John Wiley & Sons, Inc. All Rights Reserved.
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6 Chemical Vendors

7 Drug and Medication Information

7.1 Drug Transformations

3,4-Methylenedioxyamphetamine is a known transformation product of 3,4-Methylenedioxy-N-ethylamphetamine and 3,4-Methylenedioxy-N-methylamphetamine.
S66 | EAWAGTPS | Parent-Transformation Product Pairs from Eawag | DOI:10.5281/zenodo.3754448

7.2 Clinical Trials

7.2.1 ClinicalTrials.gov

7.3 Therapeutic Uses

Adrenergic Uptake Inhibitors; Hallucinogens; Serotonin Agents
National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)

8 Pharmacology and Biochemistry

8.1 MeSH Pharmacological Classification

Adrenergic Uptake Inhibitors
Drugs that block the transport of adrenergic transmitters into axon terminals or into storage vesicles within terminals. The tricyclic antidepressants (ANTIDEPRESSIVE AGENTS, TRICYCLIC) and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic transport. Many of these drugs also block transport of serotonin. (See all compounds classified as Adrenergic Uptake Inhibitors.)
Hallucinogens
Drugs capable of inducing illusions, hallucinations, delusions, paranoid ideations, and other alterations of mood and thinking. Despite the name, the feature that distinguishes these agents from other classes of drugs is their capacity to induce states of altered perception, thought, and feeling that are not experienced otherwise. (See all compounds classified as Hallucinogens.)
Serotonin Agents
Drugs used for their effects on serotonergic systems. Among these are drugs that affect serotonin receptors, the life cycle of serotonin, and the survival of serotonergic neurons. (See all compounds classified as Serotonin Agents.)

8.2 Absorption, Distribution and Excretion

... This paper describes for the first time an evaluation of the concentrations of methylenedioxymethamphetamine (MDMA) and 3,4-methylenedioxyamphetamine (MDA) found in five fatalities admitted to hospital where both antemortem and postmortem blood samples were available. Admission MDMA and MDA concentrations ranged between 0.55 and 4.33 mg/L and 0 and 0.10 mg/L, respectively, in antemortem serum/plasma. Postmortem blood MDMA and MDA concentrations ranged between 0.47 and 28.39 mg/L and 0.02 and 1.33 mg/L, respectively. Postmortem concentrations were higher than corresponding antemortem concentrations in all 5 cases with postmortem/antemortem ratios between 1.1 and 6.6 for MDMA and 1.5 and 13.3 for MDA. Differences in concentrations were also observed between anatomical sites, with central sites (e.g., heart) having much higher concentrations than peripheral sites (e.g., femoral). Overall, MDMA and MDA appear to exhibit postmortem redistribution and concentrations measured in postmortem specimens (even from peripheral sites) are not directly comparable with antemortem findings close to or prior to death.
Elliott SP; J Anal Toxicol 29 (5): 296-300 (2005)
Data ... reported /here/ include postmortem distribution of methylenedioxymethamphetamine (MDMA) and methylenedioxyamphetamine (MDA) in heart blood, gastric content, urine, and bile specimens from 20 fatal cases; other drugs found in the heart blood from these 20 cases; and the distribution of MDMA and MDA in 25 antemortem urine and 6 hair specimens. The MDA/MDMA concentration ratio observed in a limited number of hair specimens (n=6) are consistent and appear to be higher than those found in other specimens. Compared to other commonly abused drugs (e.g., cocaine and heroin), the "drug/metabolite" concentration ratio (MDMA/MDA) in hair is not significantly different from the ratios derived from other specimens, such as urine and blood. This observation is consistent with the relative drug/metabolite incorporation rates reported for cocaine/benzoylecgonine, tetrahydrocannabinol/tetrahydrocannabinoic acid, and MDMA/MDA.
Liu RH et al; J Anal Toxicol 30 (8): 545-50 (2006)

8.3 Metabolism / Metabolites

The phase I and II metabolites of the designer drugs methylenedioxyamphetamine (MDA), R,S-methylenedioxymethamphetamine (MDMA), R,S-methylenedioxyethylamphetamine (MDE), R, S-benzodioxazolylbutanamine (BDB) and R, S-N-methyl-benzodioxazolylbutanamine (MBDB) were identified by gas chromatography-mass spectrometry (GC-MS) or liquid chromotography-mass spectrometry (LC-MS) in urine and liver microsomes of humans and rats. Two overlapping pathways could be postulated: (1) demethylenation followed by catechol-O-methyl-transferase (COMT) catalyzed methylation and/or glucuronidation/sulfatation; (2) N-dealkylation, deamination and only for MDA, MDMA, MDE oxidation to the corresponding benzoic acid derivatives conjugated with glycine. Demethylenation was mainly catalyzed by CYP2D1/6 or CYP3A2/4, but also by CYP independent mechanisms. In humans, MDMA and MBDB could also be demethylenated by CYP1A2. N-demethylation was mainly catalyzed by CYP1A2, N-deethylation by CYP3A2/4. ...
Maurer HH et al; Toxicol Lett 112-113: 133-42 (2000)
The two major metabolites of (+/-)3,4-methylenedioxyamphetamine (MDA), alpha-methyldopamine (alpha-MeDA) and 3-O-methyl-alpha-methyldopamine (3-O-Me-alpha-MeDA), were administered to rats intracerebroventricularly and into brain parenchyma. In addition, their precursors, (alpha-MeDOPA and 3-O-Me-alpha-MeDOPA, respectively) were administered systemically, individually and in combination. None of these treatments produced a lasting depletion of brain serotonin (5-HT). These findings suggest that neither of MDA's major metabolites mediate its toxic effects on 5-HT neurons and that either a minor metabolite is responsible or that alternate mechanisms are involved.
McCann UD, Ricaurte GA; Brain Res 545 (1-2): 279-82 (1991)
3,4-Methylenedioxyamphetamine (MDA) and 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) are ring-substituted amphetamine derivatives with stimulant and hallucinogenic properties. The recreational use of these amphetamines, especially MDMA, is prevalent despite warnings of irreversible damage to the central nervous system. MDA and MDMA are primarily serotonergic neurotoxicants. Because (1) neither MDA nor MDMA produces neurotoxicity when injected directly into brain, (2) intracerebroventricular (i.c.v.) administration of some major metabolites of MDA and MDMA fails to reproduce their neurotoxicity, (3) alpha-methyldopamine (alpha-MeDA) and N-methyl-alpha-MeDA are metabolites of both MDA and MDMA, (4) alpha-MeDA and N-methyl-alpha-MeDA are readily oxidized to the corresponding ortho-quinones, which can undergo conjugation with glutathione (GSH), and (5) quinone thioethers exhibit a variety of toxicologic activities, /the investigators/ initiated studies on the potential role of thioether metabolites of alpha-MeDA and N-methyl-alpha-MeDA in the neurotoxicity of MDA and MDMA. /These/ studies have revealed that the thioether conjugates stimulate the acute release of serotonin, dopamine, and norepinephrine and produce a behavioral response commensurate with the "serotonin syndrome." Direct injection of the conjugates into rat brain also produces long-term depletions in serotonin (5-HT) concentrations, elevations in GFAP expression, and activation of microglial cells. The data are consistent with the view that thioether metabolites of alpha-MeDA and N-methyl-alpha-MeDA contribute to the neurotoxicity of the parent amphetamines.
Momks TJ et al; Ther Drug Monit 26 (2): 132-6 (2004)
3,4-Methylenedioxyamphetamine (MDA) and 3,4-methyl-enedioxymethamphetamine (MDMA, ecstasy) are widely abused amphetamine derivatives that target the serotonin system. The serotonergic neurotoxicity of MDA and MDMA seems dependent on their systemic metabolism. 5-(Glutathion-S-yl)-alpha-methyldopamine [5-(GSyl)-alpha-MeDA] and 2,5-bis(glutathion-S-yl)-alpha-methyldopamine [2,5-bis(GSyl)-alpha-MeDA], metabolites of MDA and MDMA, are also selective serotonergic neurotoxicants and produce behavioral and neurochemical changes similar to those seen with MDA and MDMA. 5-(GSyl)-alpha-MeDA and 2,5-bis(GSyl)-alpha-MeDA are more potent than MDA and MDMA (K(i) = 69, 50, 107, and 102 microM, respectively) at inhibiting 5-hy-droxytryptamine (serotonin) transport into SK-N-MC cells transiently transfected with the human serotonin transporter (hSERT). Moreover, 5-(GSyl)-alpha-MeDA and 2,5-bis(GSyl)-alpha-MeDA simultaneously stimulated dopamine (DA) transport into the hSERT-expressing cells, an effect attenuated by fluoxetine, indicating that stimulated DA transport was hSERT-dependent. Finally, 5-(GSyl)-alpha-MeDA and 2,5-bis(GSyl)-alpha-MeDA, and to a lesser extent MDA and MDMA, induced a concentration and time-dependent increase in reactive oxygen species (ROS) in both hSERT and human dopamine transporter-transfected cells. Fluoxetine attenuated the increase in ROS generation in hSERT-expressing cells. The results are consistent with the view that the serotonergic neurotoxicity of MDA and MDMA may be mediated by the metabolism-dependent stimulation of DA transport into hSERT-expressing cells and ROS generation by redox active catechol-thioether metabolites and DA.
Jones DC et al; J Pharmacol Exp Ther 311 (1): 298-306 (2004)
Metabolites of 3,4-methylenedioxyamphetamine in the urine of dogs and monkeys were separated by gas-liquid chromatography as their trifluoroacetyl and/or n-butyl ether derivatives and identified by comparison of the chromatographic and mass spectrometric behavior of these derivatives with those of synthetic compounds. The metabolites identified in dog and monkey urine were alpha-methyldopamine, 3-O-methyl-alpha-methyldopamine, and 3,4-dihydroxybenzyl methyl ketone. The monkey urine also contained 3,4-methylenedioxybenzyl methyl ketone and 3,4-methylenedioxybenzoic acid present as a glucuronide and/or sulfate conjugate, whereas the dog urine had 3-methoxy-4-hydroxybenzoic acid present as a conjugate other than glucuronide and sulfate. The phenolic metabolites in both species were present free and as glucuronide and/or sulfate conjugates.
Midha KK et al; Drug Metab Dispos 6 (6): 623-30 (1978)

8.4 Mechanism of Action

Phenylethylamines act on the peripheral and central nervous system by alpha- and beta-adrenergic stimulation. These compounds may also have varying degrees of serotonergic and dopaminergic activity, depending on structural similarity to mescaline. /Phenylethylamines/
Haddad, L.M. (Ed). Clinical Management of Poisoning and Drug Overdose 3rd Edition. Saunders, Philadelphia, PA. 1998., p. 574
The effect of various analogues of the neurotoxic amphetamine derivative, MDA (3,4-methylenedioxyamphetamine) on carrier-mediated, calcium-independent release of 3H-5-HT and 3H-DA from rat brain synaptosomes was investigated. Both enantiomers of the neurotoxic analogues MDA and MDMA (3,4-methylenedioxymethamphetamine) induce synaptosomal release of 3H-5-HT and 3H-DA in vitro. The release of 3H-5-HT induced by MDMA is partially blocked by 10(-6) M fluoxetine. The (+) enantiomers of both MDA and MDMA are more potent than the (-) enantiomers as releasers of both 3H-5-HT and 3H-DA. ... Possible long-term serotonergic neurotoxicity was assessed by quantifying the density of 5-HT uptake sites in rats treated with multiple doses of selected analogues using 3H-paroxetine to label 5-HT uptake sites. In the neurotoxicity study of the compounds investigated, only (+)MDA caused a significant loss of 5-HT uptake sites in comparison to saline-treated controls. ...
McKenna DJ et al; Pharmacol Biochem Behav 38 (3): 505-12 (1991)
The effect of the R(-) and S(+) isomers of 3,4-methylenedioxyamphetamine (MDA) and its N-methyl analog 3,4-methylenedioxymethamphetamine (MDMA) on [3H]inositol monophosphate accumulation was studied in cells expressing either 5-HT2A or 5-HT2C receptors. The isomers of MDA produced a concentration dependent increase in phosphatidyl inositol (PI) hydrolysis at the 5-HT2A receptors, with the R(-) isomer of MDA being more potent than the S(+) at the 5-HT2A receptor. The R(-) and S(+) isomers of MDMA were significantly less efficacious at the 5-HT2A receptor as compared to MDA; S(+)MDMA had no effect. At the 5-HT2C receptor, both R(-) and S(+)MDA were equipotent at stimulating PI hydrolysis, with the S(+) isomer of MDMA being more efficacious at the 5-HT2C receptor compared with the R(-) isomer. In all cases at both the 5-HT2A and 5-HT2C receptors, the affinities of the isomers of MDMA and MDA were at least 2-3 orders of magnitude less than 5-HT. Despite the weak effect of these compounds at the 5-HT2A and 5-HT2C receptors, these substituted amphetamines do possess intrinsic activity which may contribute to their neurotoxic effects when administered at high doses.
Nash JF et al; Neurosci Lett 177 (1-2): 111-5 (1994)

8.5 Transformations

9 Use and Manufacturing

9.1 Uses

EPA CPDat Chemical and Product Categories
The Chemical and Products Database, a resource for exposure-relevant data on chemicals in consumer products, Scientific Data, volume 5, Article number: 180125 (2018), DOI:10.1038/sdata.2018.125
This is a /DEA/ Schedule I controlled substance.
21 CFR 1308.11(d) (USDEA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of March 20, 2008: https://www.ecfr.gov
... Destroys serotonergic neurons and has been used for that purpose experimentally.
Wishart DS et al; DrugBank: a comprehensive resource for in silico drug discovery and exploration. Nucleic Acids Res. 2006 1;34. Available from, as of Feb 11, 2008: https://redpoll.pharmacy.ualberta.ca/drugbank/

9.1.1 Use Classification

Pharmaceuticals -> Illicit drugs and related compounds -> Transformation products
S66 | EAWAGTPS | Parent-Transformation Product Pairs from Eawag | DOI:10.5281/zenodo.3754448
Pharmaceuticals
S72 | NTUPHTW | Pharmaceutically Active Substances from National Taiwan University | DOI:10.5281/zenodo.3955664

9.2 Methods of Manufacturing

Prepn: C. Mannich, W. Jacobsogn, Ber. 43, 189 (1910); U. Baum et al., J. Pharm Sci 69, 192 (1980)
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 995

9.3 General Manufacturing Information

This is a controlled substance (hallucinogen) 21CFR1308.11
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 995
Synth amphetamine derivative with stimulant and hallucinogenic properties
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 995

10 Identification

10.1 Analytic Laboratory Methods

Analyte: 3,4-methylenedioxyamphetamine; matrix: bulk material; procedure: capillary electrophoresis with ultraviolet detection at 210 nm and 230 nm
Walker JA et al; J Forensic Sci 41: 824-829 (1996). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: 3,4-methylenedioxyamphetamine; matrix: bulk material; procedure: high-performance liquid chromatography with ultraviolet detection at 254 nm
Law B et al; J Chromatogr 301: 165-172 (1984). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: 3,4-methylenedioxyamphetamine; matrix: bulk material; procedure: capillary electrophoresis with ultraviolet detection at 200 nm
Varesio E et al; Electrophoresis 18: 931-937 (1997). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)

10.2 Clinical Laboratory Methods

HPLC determination in whole blood ... GC/MS determination in hair.
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 995
Analyte: 3,4-methylenedioxyamphetamine; matrix: tissue (hair), urine; procedure: capillary electrophoresis with ultraviolet detection at 200 nm; limit of detection: 37 ng/mL
Tagliaro F et al; Electrophoresis 19: 42-50 (1998). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: 3,4-methylenedioxyamphetamine; matrix: urine; procedure: high-performance liquid chromatography with photodiode array ultraviolet detection at 198 nm; limit of detection: 30 ng/mL
Helmlin HJ, Brenneisen R; J Chromatogr 593: 87-94 (1992). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: 3,4-methylenedioxyamphetamine; matrix: blood (serum), tissue (hair), urine; procedure: capillary electrophoresis with ultraviolet detection at 200 nm
Frost M et al; Electrophoresis 18: 1026-1034 (1997). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: 3,4-methylenedioxyamphetamine; matrix: blood (plasma), saliva, tissue (brain), urine; procedure: high-performance liquid chromatography with ultraviolet detection at 235 nm
Bonate PL et al; J Liq Chromatogr 18: 3473-3494 (1995). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)

11 Safety and Hazards

11.1 Hazards Identification

11.1.1 GHS Classification

Pictogram(s)
Acute Toxic
Signal
Danger
GHS Hazard Statements

H300 (100%): Fatal if swallowed [Danger Acute toxicity, oral]

H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]

H319 (100%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H335 (100%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]

Precautionary Statement Codes

P261, P264, P264+P265, P270, P271, P280, P301+P316, P302+P352, P304+P340, P305+P351+P338, P319, P321, P330, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501

(The corresponding statement to each P-code can be found at the GHS Classification page.)

ECHA C&L Notifications Summary

Aggregated GHS information provided per 38 reports by companies from 1 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown.

11.1.2 Hazard Classes and Categories

Acute Tox. 2 (100%)

Skin Irrit. 2 (100%)

Eye Irrit. 2 (100%)

STOT SE 3 (100%)

11.2 Accidental Release Measures

11.2.1 Disposal Methods

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

11.3 Regulatory Information

11.3.1 FDA Requirements

/DEA/ Schedule I shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation, which contains any quantity of the following hallucinogenic substances, or which contains any of its salts, isomers, and salts of isomers whenever the existence of such salts, isomers, and salts of isomers is possible within the specific chemical designation (for purposes of this paragraph only, the term "isomer" includes the optical, position and geometric isomers). 3,4-Methylenedioxyamphetamine (DEA Code Number: 7400) is included on this list.
21 CFR 1308.11(d) (USDEA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of February 27, 2008: https://www.ecfr.gov

12 Toxicity

12.1 Toxicological Information

12.1.1 Acute Effects

12.1.2 Interactions

Designer drugs of the amphetamine type (eg, ... MDA) ... have gained popularity and notoriety as rave drugs. ... A variety of adverse effects have been associated with the use/abuse of this class of drugs in humans, including a life-threatening serotonin syndrome, hepatotoxicity, neurotoxicity, and psychopathology.
Maurer HH et al; Ther Drug Monit 26 (2): 127-31 (April 2004)
Lethality to both isolated and aggregated mice was determined for graded ip doses of d-amphetamine, dl-4-methoxyamphetamine (PMA), dl-2,5-dimethoxyamphetamine (DMA), dl-2,5-dimethoxy-4-bromoamphetamine (DOB), dl-2,5-dimethoxy-4-methylamphetamine (DOM) and dl-3,4-methylenedioxyamphetamine (MDA). Haloperidol (2.0 mg/kg), propranolol (10 mg/kg) and phenoxybenzamine (30 mg/kg) were tested for ability to antagonize the lethal effects of amphetamine and its derivatives. Considerable protection against amphetamine lethality was produced by haloperidol in both isolated and aggregated mice and by phenoxybenzamine in isolated mice, but propranolol was ineffective. An equivalent degree of protection was not achieved by use of any of the three agents before PMA, DMA or DOB. Protection against DOM was achieved only with phenoxybenzamine and only for isolated mice. Extensive protection against MDA was supplied by both phenoxybenzamine and propranolol for either condition of housing. ...
Davis WM et al; Res Commun Chem Pathol Pharmacol 21 (1): 27-36 (1978)

12.1.3 Antidote and Emergency Treatment

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160
Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160
Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160-1
Maintain an open airway and assist ventilation if necessary. Treat agitation, seizures, coma, and hyperthermia if they occur. benzodiazepines are usually satisfactory for treatment of agitation, although butyrophenones may also be used. Continuously monitor the temperature, other vital signs, and ECG for a minimum of 6 hours. There is no specific antidote. Hypertension is best treated by sedation and, if this is not effective, a parenteral vasodilator such as phentolamine or nitroprusside. Treat tachycardia with propranolol or esmolol. ... Decontamination: administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly. Consider whole-bowel irrigation and repeat doses of charcoal after ingestion of drug filled packets ("body stuffers"). Enhanced elimination: Dialysis and hemoperfusion are not effective. Repeat-dose charcoal has not been studied. ... /Amphetamines/
Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2007., p. 75
Treatment is aggressive and supportive with careful attention to temperature, blood pressure and seizure control. ...
Buchanan JF, Brown CR; Med Toxicol Adverse Drug Exp 3 (1): 1-17 (1988)

12.1.4 Human Toxicity Excerpts

/SIGNS AND SYMPTOMS/ ... In overdose the differences between methamphetamine, 3,4-methylenedioxyamphetamine (MDA), and 3,4-methylenedioxymethamphetamine (MDMA) blur and the clinical presentation is similar to that of amphetamine overdose characterized by tachycardia, hypertension, hyperthermia, diaphoresis, mydriasis, agitation, muscle rigidity, and hyper-reflexia. Death usually results from arrhythmias, hyperthermia or intracerebral haemorrhage. Treatment is aggressive and supportive with careful attention to temperature, blood pressure and seizure control. ...
Buchanan JF, Brown CR; Med Toxicol Adverse Drug Exp 3 (1): 1-17 (1988)
/SIGNS AND SYMPTOMS/ Central nervous system effects may be secondary to both sympathetic stimulation and altered perception. Therapeutic or recreational doses may induce feelings of warmth and are purported to promote communication and empathy. Higher doses may induce hallucinations, agitation, delirium, hyperreflexia, or rigidity. Seizures may occur and can reflect either direct CNS stimulation or hypertension induced cerebrovascular hemorrhage. Sympathetic stimulation may induce a state of hyperthermia and agitated delirium. Direct sympathetic stimulation and increased metabolic heat production may be the primary pathophysiologic event; however, in many cases, increased muscular activity may be contributory as well. /Phenylethylamines/
Haddad, L.M. (Ed). Clinical Management of Poisoning and Drug Overdose 3rd Edition. Saunders, Philadelphia, PA. 1998., p. 574
/SIGNS AND SYMPTOMS/ Cardiovascular effects generally reflect sympathetic stimulation. Systolic and diastolic hypertension can be seen. Plus can be variably affected. Tachycardia can be seen; however if alpha-adrenergic effects predominate, hypertension with reflex bradycardia can occur. /Phenylethylamines/
Haddad, L.M. (Ed). Clinical Management of Poisoning and Drug Overdose 3rd Edition. Saunders, Philadelphia, PA. 1998., p. 574
/CASE REPORTS/ ... In this case /investigators/ detail a divided dose of 850 mg of MDA ingested within 2 hr and 15 min /which/ was sufficient to cause the death of a 24-year-old male, 4 hr after the final dose. The symptoms of MDA intoxication exhibited by the decedent prior to death closely mimic those of acute amphetamine poisoning: profuse sweating, violent and irrational behavior, and stereotypically compulsive behavior. While the methaqualone may have contributed to the demise of the decedent ... the MDA itself was sufficient to cause death. ...
Poklis A et al; J Forensic Sci 24 (1): 70-5 (1979)
/CASE REPORTS/ ...The following symptoms were found in a patient /following Methylenedioxyamphetamine exposure/: sympathomimetic effects, coma, seizures, hyperreflexia, and hyperthermia. The patient's condition was initially stabilized and then deteriorated with uncontrollable hyperthermia, hematologic abnormalities, and coma that culminated in death. ... The concept that this drug is primarily a hallucinogen with mild toxicity is erroneous.
Simpson DL, Rumack BH; Arch Intern Med 141 (11): 1507-9 (1981)

12.1.5 Non-Human Toxicity Excerpts

/LABORATORY ANIMALS: Acute Exposure/ ... A single 1.8 mg/kg dose of MDA produced 30 to 64% increases in the 5-HT content of frontal cortex from 30 to 120 min after injection and a decrease in 5-HT turnover from 30 min to 8 hr, but had no effect in hippocampus, caudate nucleus, or hypothalamus /of rabbits/. A single 3.6 mg/kg dose of MDA also reduced the turnover of 5-HT in frontal cortex, but this was accompanied by a decrease in 5-HIAA with no increase in 5-HT. The 1.8 and 3.6 mg/kg doses of MDA had no significant or consistent effects on the contents of DA, DOPAC, HVA, and NE in any brain area examined. Chronic administration of MDA (3.6 mg/kg/day for 4 days) failed to produce any evidence of a neurotoxic action on 5-HT neurons. Higher doses could not be employed because the LD50 of MDA was approximately 5 mg/kg. This study has demonstrated that behaviorally effective and nonneurotoxic doses of MDA produce increases in the content and decreases in turnover of 5-HT in frontal cortex that resemble those of other hallucinogens such as LSD and DOM.
Romano AG et al; Pharmacol Biochem Behav 49 (3): 599-607 (1994)
/LABORATORY ANIMALS: Acute Exposure/ ... In rats, /3,4-methylenedioxyamphetamine (MDA) and 3,4-methylenedioxymethamphetamine (MDMA)/ cause large reductions in brain levels of serotonin (5-HT). This study employs immunocytochemistry to characterize the neurotoxic effects of these compounds upon monoaminergic neurons in the rat brain. Two weeks after systemic administration of MDA or MDMA (20 mg/kg, sc, twice daily for 4 d), there is profound loss of serotonergic (5-HT) axons throughout the forebrain; catecholamine axons are completely spared. Regional differences in drug toxicity are exemplified by partial sparing of 5-HT axons in hippocampus, lateral hypothalamus, basal forebrain, and in some areas of neocortex. The terminals of 5-HT axons are selectively ablated, while axons of passage and raphe cell bodies are spared. Thickened preterminal fibers exhibit increased staining due to damming-up of neurotransmitter and other axonal constituents. Fine 5-HT axon terminals are extremely vulnerable to these drugs, whereas terminal-like axons with large varicosities survive, raising the possibility that some 5-HT axons may be resistant to the neurotoxic effects. At short survivals, visualization of greatly swollen, fragmented 5-HT axons provides anatomic evidence for degeneration of 5-HT projections. The results establish that MDA and MDMA produce structural damage to 5-HT axon terminals followed by lasting denervation of the forebrain. Both drugs have similar effects, but MDA produces a greater reduction of 5-HT axons than does MDMA at the same dosage. ...
O'Hearn E et al; J Neurosci 8 (8): 2788-803 (1988)
/LABORATORY ANIMALS: Acute Exposure/ A high intravenous (i.v.) dose of MDA (20 mg/kg) to mongrel dogs elevated body temperature, heart rate, mean arterial pressure and other cardiovascular parameters initially, but only the 1st two remained high. Other functions soon became quite depressed, and death shortly ensued. Arterial pO2 decreased, but pH and pCO2 showed a biphasic response after an initial decrease ...
Davis WM et al; Gen Pharmacol 17 (2): 179-83 (1986)
/LABORATORY ANIMALS: Acute Exposure/ Body temperature and spontaneous home cage activity were monitored continuously in six male rhesus monkeys via radiotelemetric devices. The subjects were challenged intramuscularly with 0.56-2.4 mg/kg MDMA, 0.56-2.4 mg/kg MDA and 0.1-1.0 mg/kg METH. All three amphetamines significantly elevated temperature; however the timecourse of effects differed. The acute effect of METH lasted hours longer than MDA or MDMA and a disruption of nighttime circadian cooling was observed as long as 18 hours after 1.0 mg/kg METH and 1.78-2.4 mg/kg MDA, but not after MDMA. Activity levels were only reliably increased by 0.32 mg/kg METH. It is concluded that while all three substituted amphetamines produce hyperthermia in rhesus monkeys, the effects do not depend on elevated locomotor activity and exhibit differences between compounds. The results highlight physiological risks posed both by recreational use of the amphetamines and by current trials for clinical MDMA use.
Crean RD et al; Neuroscience 142(2): 515-525 (2006)
For more Non-Human Toxicity Excerpts (Complete) data for 3,4-METHYLENEDIOXYAMPHETAMINE (7 total), please visit the HSDB record page.

12.1.6 Non-Human Toxicity Values

LD50 Mouse oral 13,300 ug/kg
Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2438
LD50 Mouse ip 82,300 ug/kg
Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2438
LD50 Mouse ip 68 mg/kg /hydrochloride/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 996
LD50 Mouse iv 31,100 ug/kg
Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2438
For more Non-Human Toxicity Values (Complete) data for 3,4-METHYLENEDIOXYAMPHETAMINE (7 total), please visit the HSDB record page.

12.1.7 Populations at Special Risk

... Phenylisopropylamines as a class interact with CYP2D6 as substrates and/or inhibitors. Their use may cause metabolic interactions with other drugs that are CYP2D6 substrates, and the potential for polymorphic oxidation via CYP2D6 may be a source of interindividual variation in their abuse liability and toxicity.
Wu D et al; Biochem Pharmacol 53 (11): 1605-12 (1997)

12.2 Ecological Information

12.2.1 Environmental Water Concentrations

While data specific to 3,4-methylenedioxyamphetamine were not located(SRC, 2008), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2). Studies have indicated that several polar pharmaceutically active compounds can leach through soils(1).
(1) Heberer T; Tox Lett 131: 5-17 (2002)
(2) Koplin DW et al; Environ Sci Toxicol 36: 1202-211 (2002)

13 Associated Disorders and Diseases

14 Literature

14.1 Consolidated References

14.2 NLM Curated PubMed Citations

14.3 Springer Nature References

14.4 Thieme References

14.5 Chemical Co-Occurrences in Literature

14.6 Chemical-Gene Co-Occurrences in Literature

14.7 Chemical-Disease Co-Occurrences in Literature

15 Patents

15.1 Depositor-Supplied Patent Identifiers

15.2 WIPO PATENTSCOPE

15.3 Chemical Co-Occurrences in Patents

15.4 Chemical-Disease Co-Occurrences in Patents

15.5 Chemical-Gene Co-Occurrences in Patents

16 Interactions and Pathways

16.1 Chemical-Target Interactions

16.2 Drug-Drug Interactions

17 Biological Test Results

17.1 BioAssay Results

18 Classification

18.1 MeSH Tree

18.2 NCI Thesaurus Tree

18.3 ChEBI Ontology

18.4 KEGG: Target-based Classification of Drugs

18.5 ChemIDplus

18.6 ChEMBL Target Tree

18.7 UN GHS Classification

18.8 EPA CPDat Classification

18.9 NORMAN Suspect List Exchange Classification

18.10 EPA DSSTox Classification

18.11 EPA Substance Registry Services Tree

18.12 MolGenie Organic Chemistry Ontology

19 Information Sources

  1. CAS Common Chemistry
    LICENSE
    The data from CAS Common Chemistry is provided under a CC-BY-NC 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc/4.0/
  2. ChemIDplus
    ChemIDplus Chemical Information Classification
    https://pubchem.ncbi.nlm.nih.gov/source/ChemIDplus
  3. DrugBank
    LICENSE
    Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode)
    https://www.drugbank.ca/legal/terms_of_use
  4. EPA DSSTox
    (+/-)-3,4-(Methylenedioxy)amphetamine
    https://comptox.epa.gov/dashboard/DTXSID40859958
    CompTox Chemicals Dashboard Chemical Lists
    https://comptox.epa.gov/dashboard/chemical-lists/
  5. European Chemicals Agency (ECHA)
    LICENSE
    Use of the information, documents and data from the ECHA website is subject to the terms and conditions of this Legal Notice, and subject to other binding limitations provided for under applicable law, the information, documents and data made available on the ECHA website may be reproduced, distributed and/or used, totally or in part, for non-commercial purposes provided that ECHA is acknowledged as the source: "Source: European Chemicals Agency, http://echa.europa.eu/". Such acknowledgement must be included in each copy of the material. ECHA permits and encourages organisations and individuals to create links to the ECHA website under the following cumulative conditions: Links can only be made to webpages that provide a link to the Legal Notice page.
    https://echa.europa.eu/web/guest/legal-notice
  6. FDA Global Substance Registration System (GSRS)
    LICENSE
    Unless otherwise noted, the contents of the FDA website (www.fda.gov), both text and graphics, are not copyrighted. They are in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from FDA. Credit to the U.S. Food and Drug Administration as the source is appreciated but not required.
    https://www.fda.gov/about-fda/about-website/website-policies#linking
  7. Hazardous Substances Data Bank (HSDB)
  8. Human Metabolome Database (HMDB)
    LICENSE
    HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications.
    http://www.hmdb.ca/citing
    3,4-Methylenedioxyamphetamine
    http://www.hmdb.ca/metabolites/HMDB0041931
  9. ChEBI
  10. Open Targets
    LICENSE
    Datasets generated by the Open Targets Platform are freely available for download.
    https://platform-docs.opentargets.org/licence
  11. ChEMBL
    LICENSE
    Access to the web interface of ChEMBL is made under the EBI's Terms of Use (http://www.ebi.ac.uk/Information/termsofuse.html). The ChEMBL data is made available on a Creative Commons Attribution-Share Alike 3.0 Unported License (http://creativecommons.org/licenses/by-sa/3.0/).
    http://www.ebi.ac.uk/Information/termsofuse.html
  12. ClinicalTrials.gov
    LICENSE
    The ClinicalTrials.gov data carry an international copyright outside the United States and its Territories or Possessions. Some ClinicalTrials.gov data may be subject to the copyright of third parties; you should consult these entities for any additional terms of use.
    https://clinicaltrials.gov/ct2/about-site/terms-conditions#Use
  13. Comparative Toxicogenomics Database (CTD)
    LICENSE
    It is to be used only for research and educational purposes. Any reproduction or use for commercial purpose is prohibited without the prior express written permission of NC State University.
    http://ctdbase.org/about/legal.jsp
  14. Therapeutic Target Database (TTD)
  15. IUPAC Digitized pKa Dataset
    benzene, 1-(2-amino)propyl-3,4-methylenedioxy-
    https://github.com/IUPAC/Dissociation-Constants
  16. EPA Chemical and Products Database (CPDat)
  17. NIST Mass Spectrometry Data Center
    LICENSE
    Data covered by the Standard Reference Data Act of 1968 as amended.
    https://www.nist.gov/srd/public-law
    3,4-Methylenedioxyamphetamine
    http://www.nist.gov/srd/nist1a.cfm
  18. Japan Chemical Substance Dictionary (Nikkaji)
  19. KEGG
    LICENSE
    Academic users may freely use the KEGG website. Non-academic use of KEGG generally requires a commercial license
    https://www.kegg.jp/kegg/legal.html
    Target-based classification of drugs
    http://www.genome.jp/kegg-bin/get_htext?br08310.keg
  20. MassBank Europe
  21. MassBank of North America (MoNA)
    LICENSE
    The content of the MoNA database is licensed under CC BY 4.0.
    https://mona.fiehnlab.ucdavis.edu/documentation/license
  22. Metabolomics Workbench
  23. NCI Thesaurus (NCIt)
    LICENSE
    Unless otherwise indicated, all text within NCI products is free of copyright and may be reused without our permission. Credit the National Cancer Institute as the source.
    https://www.cancer.gov/policies/copyright-reuse
  24. SpectraBase
    alpha-methyl-3,4-(methylenedioxy)phenethylamine
    https://spectrabase.com/spectrum/IjcU9FNGDtQ
    alpha-METHYL-3,4-(METHYLENEDIOXY)PHENETHYLAMINE
    https://spectrabase.com/spectrum/K4PGBxxgIv6
    alpha-methyl-3,4-methylenedioxyphenethylamine
    https://spectrabase.com/spectrum/HZ5oenHuCO1
    3,4-METHYLENEDIOXYAMPHETAMINE;MDA
    https://spectrabase.com/spectrum/J2knqlcHlx0
  25. NORMAN Suspect List Exchange
    LICENSE
    Data: CC-BY 4.0; Code (hosted by ECI, LCSB): Artistic-2.0
    https://creativecommons.org/licenses/by/4.0/
    (+/-)-3,4-(Methylenedioxy)amphetamine
    NORMAN Suspect List Exchange Classification
    https://www.norman-network.com/nds/SLE/
  26. Pharos
    LICENSE
    Data accessed from Pharos and TCRD is publicly available from the primary sources listed above. Please respect their individual licenses regarding proper use and redistribution.
    https://pharos.nih.gov/about
  27. Springer Nature
  28. Thieme Chemistry
    LICENSE
    The Thieme Chemistry contribution within PubChem is provided under a CC-BY-NC-ND 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc-nd/4.0/
  29. Wikidata
    3,4-methylenedioxyamphetamine
    https://www.wikidata.org/wiki/Q223020
  30. Wikipedia
  31. Medical Subject Headings (MeSH)
    LICENSE
    Works produced by the U.S. government are not subject to copyright protection in the United States. Any such works found on National Library of Medicine (NLM) Web sites may be freely used or reproduced without permission in the U.S.
    https://www.nlm.nih.gov/copyright.html
    3,4-Methylenedioxyamphetamine
    https://www.ncbi.nlm.nih.gov/mesh/68015104
    Adrenergic Uptake Inhibitors
    https://www.ncbi.nlm.nih.gov/mesh/68018759
  32. PubChem
  33. GHS Classification (UNECE)
  34. EPA Substance Registry Services
  35. MolGenie
    MolGenie Organic Chemistry Ontology
    https://github.com/MolGenie/ontology/
  36. PATENTSCOPE (WIPO)
  37. NCBI
CONTENTS