α-メチル-3,4-(メチレンジオキシ)フェネチルアミン

1.64

log Kow = 1.64

1.64

9.67 (at 25 °C)

pKa = 9.67 (conjugate acid)

1443；1443；1434；1470；1495；1472；1480；1464.6；1472；1460；1460

1508.8；1484；1483；1496.3；1469.2；1457.4

2204；2204

Danger

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]

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 (click each P-code to see the statement)

Aggregated GHS information provided per 39 reports by companies from 2 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. For more detailed information, please visit ECHA C&L website.

/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.

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.

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.

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. ...

/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. ...

/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/

/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/

/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. ...

/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.

/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.

/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. ...

/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 ...

/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.

For more Non-Human Toxicity Excerpts (Complete) data for 3,4-METHYLENEDIOXYAMPHETAMINE (7 total), please visit the HSDB record page.

... 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.

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).

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/

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/

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/

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/

Treatment is aggressive and supportive with careful attention to temperature, blood pressure and seizure control. ...

LD50 Mouse oral 13,300 ug/kg

LD50 Mouse ip 82,300 ug/kg

LD50 Mouse ip 68 mg/kg /hydrochloride/

LD50 Mouse iv 31,100 ug/kg

For more Non-Human Toxicity Values (Complete) data for 3,4-METHYLENEDIOXYAMPHETAMINE (7 total), please visit the HSDB record page.

/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.

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/

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. ...

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.

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. ...

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.

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.

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.

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.

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.

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.

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.

... 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.

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.

This is a /DEA/ Schedule I controlled substance.

... Destroys serotonergic neurons and has been used for that purpose experimentally.

Pharmaceuticals -> Illicit drugs and related compounds -> Transformation products

Pharmaceuticals

This is a controlled substance (hallucinogen) 21CFR1308.11

Synth amphetamine derivative with stimulant and hallucinogenic properties