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What is 3,4-Methylenedioxymethamphetamine?
The most common salt is the hydrochloride (CAS-64057-70-1) which occurs as a white or off-white powder or as crystals soluble in water.
MDMA is usually a pill form, although it can be crushed and snorted, and which the purity of the pill is usually unknown. There are many types of pills that contain different concentrations of 3,4-Methylenedioxymethamphetamine and are sometimes in a mixture with other drugs such as caffeine and methamphetamine which alters the types of drug effects the user have. After the pill usually comes into effect in 30-40 minutes, typically following the user’s metabolism pattern and the “peak” effect is typically about 60-90 minutes after digestion. The user typically experiences the effects of MDMA for a total 3-4 hours, excluding the after-effects.
MDMA’s first and main element is naturally occurring safrole oil and is distilled. After the Safrole oil is distilled, Formaldehyde (DMF) and Ammonium Chloride(NH4Cl) are mixed to produce Methylamine HCl(CH3NH2 HCl).
Formal IUPAC name: N-methyl-1-(3,4-methylenedioxyphenyl)propan-2-amine
Other names: 3,4-methylenedioxymethamphetamine, methylenedioxy-methylamphetamine, or N-methyl-1-(1,3-benzodioxol-5-yl)-2-propanamine
MDMA can exist in a racemic mixture with an R and S form.
MDMA is part of the phenethylamine family which is also known as “designer drug” and is also closely related to amphetamines. Phenethylamines are known for their hallucinogenic effects which originate from the compound’s ability to release serotonin in the brain as well as the ability to stimulate the central nervous system, giving users “more” energy. There are also many homologous forms of MDMA which consist of: MDA, MDEA, and MBDB. MDMA predominates as a salt in physical form; either a hydrochloride or phosphate salt which are found in tablet form. It can also exist as a powder or capsule16. As a base MDMA is a clear oil.
MDMA is manufactured by safrole, a liquid extract from sassafras trees. Also the most popular way to convert safrole into MDMA is by synthesizing the 3,4-methylenedioxyphenyl-2-propanone (MDP2P) intermediate via the Wacker process or by isomerizing safrole into isosafrole by a strong base. Both processes oxidize either safrole or isosafrole into the MDP2P intermediate which then undergoes reductive animation to make a racemic mixture of MDMA.
MDMA is manufactured by safrole, a liquid extract from sassafras trees. The most popular way to convert safrole into MDMA is by synthesizing the 3,4-methylenedioxyphenyl-2-propanone (MDP2P or PMK) intermediate via the Wacker process (which is the oxidation of ethylene to acetaldehyde by oxygen in water with a tetracholoropalladate catalyst) or by isomerizing (changing the arrangement of the atoms in the compound) safrole into isosafrole by a strong base. Both processes oxidize either safrole or isosafrole into the MDP2P intermediate which then undergoes reductive animation to make a racemic mixture of MDMA.
In the Merck patent, safrole was added to HBr to form a bromosafrole, which was then added to methylamine to produce racemic MDMA16. Other methods of synthesis start with 3,4-methylenedioxyphenyl-2-propanone and use the Leuckart route, aluminum foil method or other reductive aminations. The Leuckart route converts ketones into amine groups using formic acid, ammonium formate or formamide/methylformamide. The aluminum foil method uses ethanol, aluminum metal pieces, an amine and a mercuric chloride catalyst to react with a ketone. The aluminum foil method is a type of reductive amination (reductive alkylation) which is the conversion of a carbonyl group to an amine group with an imine intermediate.
MDMA affects 3 neurotransmitters: serotonin, dopamine, and norepinephrine. This drug is closely related to methamphetamine but instead of releasing massive amounts of dopamine it releases more serotonin. Then is made in last with stable conditions which has to include absolutely no moisture in a few steps of production.
Whereas phenethylamines without ring substitution usually behave as stimulants, ring substitution (as in MDMA) leads to a modification in the pharmacological properties. Ingestion of MDMA causes euphoria, increased sensory awareness and mild central stimulation. It is less hallucinogenic than its lower homologue, methylenedioxyamphetamine (MDA). The terms empathogenic and entactogenic describe the socialising effects of MDMA.
Following ingestion, most of the dose of MDMA is excretion in the urine same as before. Major metabolites are 3,4-methylenedioxyamphetamine (MDA) and O-demethylate compounds. The significance of these findings to human users is still unclear, although cognitive impairment we associate with MDMA use. Some of the pharmacodynamic and toxic effects of MDMA vary, depending on which enantiomer is in question. However, almost all illicit MDMA exists as a racemic mixture. They are fatalities following a dose of 300 mg. Also toxicity depends on many factors, including individual susceptibility and the circumstances in which MDMA is in.
Synthesis and precursors
There are four principal precursors which can be used in the manufacture of MDMA and related drugs: safrole, isosafrole, piperonal and 3,4-methylenedioxyphenyl-2-propanone (PMK). Safrole is the key starting material in so far as the other three can be synthesised from it. In the original Merck patent of 1914, safrole was reacted with hydrobromic acid to form bromosafrole, which was converted to MDMA using methylamine.
Many illicit syntheses start with PMK and use either the Leuckart route or various reductive aminations including the aluminium foil method. All of these methods produce racemic MDMA.
Mode of use
MDMA in tablet form or oral(ingestion). The powder form is by the nose.
As some of the above names suggest, MDMA is a derivative of amphetamine and a member of the phenethylamine family. A number of homologous compounds with broadly similar effects, e.g. MDA (methylenedioxyamphetamine), MDEA (methylenedioxyethylamphetamine) and MBDB (N-methyl-1-(1,3-benzodioxol-5-yl)-2-butanamine), have appeared, but have proved less popular. These and many other more distant relatives of MDMA with the generic term ecstasy. Street terms for MDMA include Adam and XTC, but often reflect the imprinted logo, e.g. Mitsubishis, Love Doves and many others. http://www.nida.nih.gov/PDF/RRmdma.pdf
In common with many of its homologues, MDMA reacts with the Marquis field test to produce a dark blue/black coloration. The mass spectrum shows limited structure with a major ion at m/z = 58 and other ions at m/z = 135 and 77. Using gas chromatography, the limits of detection in plasma and urine are 1.6 μg/L and 47 μg/L respectively.
Tablets contain, on average, 60–70 mg (base equivalent) of MDMA either as the hydrochloride salt or, less commonly, as the phosphate salt. Loose powders may range from crushed tablets (typically 30–40 % purity) to almost pure MDMA. The free base constitutes 84 % of the hydrochloride salt. Apart from the active drug, tablets contain a bulking agent such as lactose and smaller quantities of binders.
During the last few years, there has been a change in the content of illicit drug tablets in Europe, from a situation where most tablets analysed contained MDMA or another ecstasy-like substance (MDEA, MDA) as the only psychoactive substance, to one where the contents are more diverse, and MDMA-like substances less present. This shift was most pronounced in 2009, when only three countries reported that MDMA-like substances accounted for a large proportion of the tablets analysed. More recently, there is evidence of a return to MDMA in tablets.
Medicinal Use & Potential Therapeutic Effects
Firstly despite how MDMA is its recreational use, few people know the prospects of MDMA as a medicinal drug. Also to Emphasize its psychadelic properties as well as its mental and mood uplifting abilities, MDMA in test on patients with mild psychiatric disorders, those who suffer from Post-traumatic Stress Disorder (PTSD), cancer patients, and even those who need assistance with communication to their partners. Furthermore, a study on MDMA with patients that suffer from PTSD.
Also MDMA is in popular usage by psychiatrists for research in therapeutic medicine, specifically for opening up the mind for investigation. The MDMA supposedly “reduced the fear response to emotional threats… many respondents reported on the therapeutic benefits of MDMA.
The main way MDMA interacts with the human body is through the brain. As previously mentioned, MDMA induces higher serotonin levels, but can also release dopamine and nonepinephrine. The structure of MDMA makes it an indirect agonist of serotonin, inducing the production of the neurotransmitter as well as inhibiting the re-uptake. In fact, MDMA seems to act as a re-uptake inhibitor of all these neurotransmitters.
MDMA is metabolism is through two main pathways: “1. O-demethylenation followed by catechol-O-methyltransferase (COMT)-catalyzed methylation and/or glucuronide/sulfate conjugation; and 2. N-dealkylation, deamination, and oxidation to the corresponding benzoic acid derivatives conjugated with glycine”. The reactivity of the CYP2D6 enzyme is an important step in the O-demethylenation pathway because it regulates the degradation of MDMA and the efficiency of this enzyme as coded by genes, may increase a user’s risk of contracting acute toxicity. Furthermore the metabolism of MDMA also has potential involvement in mid to long-term neurotoxicity due to the neurodegeneration of the neurotransmission system. http://www.nida.nih.gov/Club
This area of focus is important for determining the effects of MDMA on users. The genetics of the CYP2D6 enzyme responsible for the metabolism of MDMA, investigations to determine the body’s efficiency in the metabolization of MDMA.
Analyzing the body’s ability to take in and process MDMA is incredibly important because it can give answers to questions about susceptibility to fatality. Intensities of pharmacological effects, intensities of toxicity, and susceptibility of dependence. Since recent studies suggest that MDMA has non-linear pharmacokinetics, the rate of metabolizing MDMA in the body is crucial to understanding toxicity, fatality and pharmacological effects.
Again taking into consideration that MDMA may acts as an accumulator and an inhibitor. Then if the CYP2D6 enzyme has a slower functionality as observed in Asians then users with this genotype have a higher risk of acute toxicity and fatality. However, for Caucasians who have the wild-type genotype that produces a CYP2D6 enzyme with normal-fast functionality. Then their susceptibility to fatality and the intensity of pharmacological effects are lower than that of Asians. It is important to remember when looking at data that the genetic populations are still averages of the population and that every individual has different genetic makeup. Which affects the pharmacokinetics of the drug on an individual basis.
Minimum/Maximum Human Dose
The toxic dose is variable, with near fatal with blood levels between 0.11 mg/L to 2.1 mg/L. Survival has also report after MDMA blood levels of 4.3 mg/L drawn 13 hours after ingestion.
Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1075
Tolerance occurs. Some users increase the dose over weeks or months of use to as many as 10 or more tablets during the course of an evening.
Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn’s Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 346
Hepatic: CYP450 extensively involves, especially CYP2D6 MDMA can be metabolize by two main metabolic pathways: (1) O-demethylenation followed by catechol-O-methyltransferase (COMT)-catalyzed methylation and/or glucuronide/sulfate conjugation; and (2) N-dealkylation, deamination, and oxidation to the corresponding benzoic acid derivatives conjugated with glycine.
The metabolism may be primarily by cytochrome P450 (CYP450) enzymes (CYP2D6 (in humans, but CYP2D1 in mice), and CYP3A4) and COMT. Complex, nonlinear pharmacokinetics arise via autoinhibition of CYP2D6 and CYP2D8, resulting in zeroth order kinetics at higher doses. This will result in sustained and higher concentrations of MDMA if the user takes consecutive doses of the drug.
1. Toxicological Information
… A clinical trial was designed where subjects pretreated with paroxetine, one of the most potent inhibitors of both 5-hydroxytryptamine reuptake and CYP2D6 activity, were challenged with a single dose of MDMA. The aim of the study was to evaluate the pharmacodynamic and pharmacokinetic interaction between paroxetine and MDMA in humans. Subjects received 20 mg/day paroxetine (or placebo) orally for the 3 days before MDMA challenge (100 mg oral). MDMA alone produced the prototypical effects of the drug. Pretreatment with paroxetine was associated with marked decreases of both physiological and subjective effects of MDMA, despite a 30% increase in MDMA plasma concentrations.
The decreases of 3-methoxy-4-hydroxymethamphetamine plasma concentrations suggest a metabolic interaction of paroxetine and MDMA. These data show that pretreatment with paroxetine significantly attenuates MDMA-related physiological and psychological effects. It seems that paroxetine could interact with MDMA at pharmacodynamic (serotonin transporter) and pharmacokinetic (CYP2D6 metabolism) levels. Marked decrease in the effects of MDMA could lead users to take higher doses of MDMA and to produce potential life-threatening toxic effects.
We describe a patient infected with HIV-1 who was treated with ritonavir and saquinavir and then experienced a prolonged effect from a small dose of methylenedioxymetamphetamine (MDMA or ecstacy) and a nearly fatal reaction from a small dose of gamma-hydroxybutyrate (GHB).