YAMF: Yet Another MDMA FAQLamont Granquist
This is a Work In ProgressTODO:
- Psychological/Psychiatric Risks
- Neuropharmacology (receptor binding plus research Rudnick and Wall articles)
- Non-neurotoxic analogs (MDAI, MMAI)
Why Another FAQ?I felt like it. That's about the only good reason. I felt like writing a FAQ in my own particular style with some of my own particular axes that I'd like to grind. I'd like to think that this suppliments some of the other FAQs out there, and I don't aim to replace that information. I'd actually suggest you read the other FAQs first, since they tend to get bogged down less in technical details and tend to be more readable. They also are probably more generally relevant for the average person.
In general this FAQ deliberately aims to have it's focus on MDMA risks and on gory technical details. The "sociological" aspects (not involving risks) will deliberately not be emphasized.
Chemistry of MDMA
O //\ /\ NHCH3 / \// \/ \ / / | || | CH2 | || | \ | || CH3 \ /\\ / O \\/ MDMAMDMA, 3,4-methylenedioxymethamphetamine, C11H15NO2.
The melting point of MDMA depends on the hydration of the salt. Shulgin states: "It is apparent that with uncertain hydration, the melting point is not an acceptable criterion of identity or of purity."[ 1]. The various melting points are:
- 155 deg C (freebase @ 20 mm/Hg)
- >110-120 deg C (freebase @ 0.4 mm/Hg)
- 147-148 to 158-159 deg C (anhydrous HCl)
- soften 132 deg C, 135-139 deg C (1/4 hydrate HCl)
- soften 92 deg C, 138-145 deg C (hemihydrate HCl)
- soften 50 deg C, 90-132 deg C (3/4 hydrate HCl)
- soften 80 deg C, 107-133 deg C (monohydrate HCl)
Chemical Names for MDMAThanks to the chemists, there are about a dozen different chemical nomenclatures for MDMA. Other chemicals have similar nomenclature difficulties, but since this is an MDMA I'm only going to be concerned with MDMA. The following is a fairly comprehensive list which includes DEA and Chemical Abstracts numerology for MDMA:
- MDM (older references)
- N,alpha-dimethyl-3,4-methylenedioxyphenethylamine (Pre-1972, Chem Abs.)
- N,alpha-dimethyl-1,3-benzodioxole-5-ethanamide (Current, Chem Abs.)
- N,alpha-dimethyl-homopiperonylamine (Archaic, Chem Abs.)
- N-methyl-1-(3,4-methylenedioxyphenyl)-2-propanamine (occasionally)
- 2-methylamino-1-(3,4-methylenedioxyphenyl)-propane (uncommon)
- N-methyl-beta-(3,4-methylenedioxyphenyl)-isopropylamine (uncommon)
- N,alpha-dimethyl-beta-(3,4-methylenedioxyphenyl)-ethylamine (uncommon)
- EA-1475 (Edgewood Arsenal)
- DEA Control #7287: MDMA HCl (racemic)
- DEA Control #7405: MDMA
- DEA Control #7406: MDMA (racemic)
- Chem Abs: [66142-89-0] S-(+)-MDMA
- Chem Abs: [69558-32-3] S-(+)-MDMA HCl
- Chem Abs: [81262-70-6] R-(-)-MDMA
- Chem Abs: [69558-31-2] R-(-)-MDMA HCl
- Chem Abs: [69610-10-2] MDMA (racemic)
- Chem Abs: [64057-70-1] MDMA HCl (racemic)
MDMA in Relationship to other SubstancesMy pick for the 12 most important psychoactive (mostly) chemicals related to MDMA are shown below:
O //\ /\ NH2 O //\ /\ NHCH3 O //\ /\ NHCH2CH3 / \// \/ \ / / \// \/ \ / / \// \/ \ / / | || | / | || | / | || | CH2 | || | CH2 | || | CH2 | || | \ | || CH3 \ | || CH3 \ | || CH3 \ /\\ / \ /\\ / \ /\\ / O \\/ O \\/ O \\/ MDA MDMA MDE/MDEA O //\ /\ NHCH3 O //\ /\ NHCH3 CH3O //\ /\ NH2 / \// \/ \ / / \// \/ \ / \// \/ \/ / | || | / | || | | || CH2 | || | CH2 | || | | || \ | || CH2CH3 \ | || CH3 | || \ /\\ / \ /\\ / /\\ /\ O \\/ O \\/ Br \\/ OCH3 | OCH3 MBDB MMDA 2C-B CH3O //\ /\ NH2 CH3O //\ /\ NH2 CH3O //\ /\ NH2 \// \/ \/ \// \/ \ / \// \/ \ / | || | || | | || | | || | || | | || | | || | || CH3 | || CH3 /\\ / /\\ /\ /\\ /\ O \\/ CH3 \\/ OCH3 Br \\/ OCH3 CH3 | OCH3 Mescaline DOM DOB //\ /\ NH2 HO //\ /\ NH /\\ /\ NH2 // \/ \ / \// \/ \/ / \\_____/ \/ | || | | || || | || | || | | || || | || | || CH3 | || || | || \\ / /\\ / \ //\ / \\/ HO \\/ \// \ / N Amphetamine Dopamine(DA) Serotonin(5-HT)A by no means complete list of synonyms for the above includes:
- MDA = "Love Drug", 3,4-methylenedioxyamphetamine
- MDMA = "Ecstasy","X","E","Adam", N-methyl-MDA, 3,4-methylenedioxymethamphetamine, N-methyl-3,4-methylenedioxyamphetamine
- MDE/MDEA = "Eve", 3,4-methylenedioxyethamphetamine, 3,4-methylenedioxyethylamphetamine, N-ethyl-3,4-methylenedioxyamphetamine
- MBDB = "Eden", Methyl-J, 2-methylamino-1-(3,4-methylenedioxyphenyl)butane, N-methyl-(1,3-benzodioxol-5-yl)-2-butanamine
- MMDA = 3-methyoxy-4,5-methylenedioxyamphetamine
- 2C-B = "CBr", "Bromomescaline", 2,5-dimethoxy-4-bromo-phenethylamine
- Mescaline/M = 3,4,5-trimethoxyphenethylamine
- DOM = "STP", 4-methyl-2,5-dimethoxyamphetamine
- DOB = 4-bromo-2,5-dimethoxyamphetamine
- Amphetamine = Alpha-Methyl-PHenEThylAMINE
- Dopamine/DA = 3,4-dihydroxy-phenethylamine
- Serotonin/5-HT = 5-hydroxy-tryptamine
Considering MDMA the prototype, then MDA tends to be more psychedelic with more of a tendency to induce visual hallucinations. MDA is also more 'speedy' with more jaw-clenching and other side-effects. MDA also takes about 1.5 times as long to hit and to come down off of as MDMA. MDE has a similar chronology to MDMA (perhaps shorter), but is somewhat more stoning than MDMA, but has equal or less side-effects as MDMA. MDE may be responsible for the "Heroin in Ecstasy" myths that abound. MBDB seems to be the closest in effects to MDMA, however it does not appear often on the illegal market (particularly outside of amsterdam). MMDA seems to be similar to MDA in that it produces stronger visual hallucinations than MDMA, however MMDA seems to be totally unknown on the illegal market.
The structures of Serotonin and Dopamine are included to provide a comparison to those endogenous neurotransmitters (neither of which would be active if ingested). With the exception of Serotonin all of the chemical structures above are of phenthylamines. It is not surprising that they tend to affect the Dopamine system in the brain fairly strongly. Amphetamine is the prototypical dopaminergic agent in this class. Methamphetamine, Ritalin (methylphenidate), Cylert (pemoline), 4-methylaminorex (U4-E-Uh), ephedrine and pseudophedrine are all CNS stimulants which are related to phenethylamine.
Many of the chemicals listed, however, tend to more strongly affect Serotonin than they do Dopamine which would not be immediately obvious from a comparison of their chemical structures. The substances Mescaline, DOM, and DOB are all "classical hallucinogens" with effects similar to d-LSD. DOM made an appearance on the illegal market in the 60's. DOB is the second most potent psychedelic seen on the illegal market (500 microgram active dose) and is sometimes substituted for d-LSD, although it has a substantially longer time of action than d-LSD. Mescaline is the active component of peyote. Very often d-LSD or DOB "microdot" tablets are sold as "Mescaline" (which is only active at levels above 200 mg).
In between the MDMA-like "entactogens" and the DOB/DOM-like "classical psychedelics" is 2C-B. This compound is related to DOB by the removal of a single methyl group on the side chain (although one does not synthesize 2C-B in this fashion). It has effects somewhat similar to LSD but contains a certain "warmth" that LSD lacks. It does not produce hallucination as strong as LSD or psilocybin and it is not as euphoric as MDMA.
For further information, including synthesis instructions for many of these chemicals please see the hypertext version of Phenethylamines I Have Known and Loved ( http://www.erowid.org/pihkal/)
Making Bad Choices while on MDMAThis is quite possible to do. Particularly with regards to having sex with people who you will later regret having sex with. You may also say things to people you'd later wish to retract. You may also make a choice to take those last 6 MDMA tablets in your stash over the course of the night. These are all bad choices, which can be facilitated by that "everything is alright with the world" attitude that people get on MDMA.
MDMA breaks down barriers and gives one a general feeling of security allowing one in some cases a wider choice of options. However at the same time some barriers in the world are functional and entirely necessary. For example, sometimes it isn't good to suddenly tell people the truth the whole truth and nothing but the truth.
Of course bad choices for a given person can be good choices for another person. Suggesting that spontaneity and willingness to try new things should be suppressed while taking MDMA in some sense tends to defeat the purpose of taking MDMA. However, there is a line between MDMA-facilitated experimentation and recklessness.
A good suggestion is to think about your limits beforehand and then work to stick to those limits while you are on MDMA. Should you feel like reconsidering while you are on MDMA the best idea is to think it over again after you've come down and reassess your limits while you're not taking MDMA. Then try it when you're taking MDMA again. Take things gradually.
And most importantly don't drop X for the first time with someone who you think just wants to get you into bed and with whom you don't want to. This is probably the largest risk with MDMA (not the neurotoxicity or "heat stroke" or any other risk), and with a little bit of forethought it is entirely preventable. The first times you do MDMA do it around people you trust until you get the hang of it.
Contraindications by/for MDMA
- Heart/Circulatory Disease: MDMA places a load on the heart which may precipitate heart attacks or strokes. For older users a medical check-up is recommended before using MDMA.
- Liver Disease: MDMA is known to be hepatotoxic for some users, and may place an additional load on the liver which users with already compromised livers may not be able to tolerate. Consult your doctor.
- Driving Cars: MDMA is probably nowhere near as imparing as alcohol or even marijuana, but it is still imparing. At least one traffic fatality likely due to MDMA and uncomplicated by the presence of other drugs has been reported.
- Not Drinking Enough Water: excessive dehydration is a factor in MDMA "heat stroke" and death.
- Drinking Excessive Amounts of Water: by this it is meant on the order of gallons which can cause water intoxication and eventually death. This has actually occured in two different cases in the UK and Australia [see Proper Hydration], apparently after the subjects became acutely anxious of having a MDMA "heat stroke" reaction.
- Excessive Excersize/Activity: this is also a factor in MDMA "heat stroke" and death.
- Overheating/Not Cooling Off: a hopefully obvious factor in MDMA "heat stroke" and death.
- Opiates: mixing uppers and downers is not good. MDMA's stimulant effect may mask opiate effects and make overdose easier.
- Excessive Alcohol Use: Same as opiates, plus alcohol will increase dehydration and overheating.
- Amphetamines: increases neurotoxic risk of MDMA, increases overheating and activity, etc. Tweak, in general, sucks.
- MAOIs: prescription MAOIs such as phenelzine (Nardil) and tranylcypromine (Parnate) are major contraindications for MDMA as taking MDMA while on these drugs may cause a fatal hypertensive crisis. Taking a reversible MAOI like harmaline or moclobemide (Aurorex) may cause the same problem and should similarly be avoided.
1. Crifasi-J, Long-C, "Traffic fatality related to the use of methylenedioxymethamphetamine," J. Forensic Sci. 1996 Nov 41(6):1082-4.
Proper HydrationThis has occured in at least two cases which recieved attention in the mainstream media. One case was of Leah Betts in the UK, and the other was of Anna Woods in Australia. Both cases generated a tremendous amount of media attention, with the usual inaccuracies and the usual quotations from the parents of how "outraged" they are at anyone who steps away from the Party Line of considering MDMA to be only slightly more dangerous than tobacco.
The fact is that MDMA does cause SIADH (syndrome of inappropriate anti-diuretic hormone secretion), but this is only a problem if a person also concomitantly ingests several liters of water. Dr John Henry of Guy's Hospital, London states:
Some people may wish to label this death as a case of water intoxication in an attempt to exonerate the drug as a cause of death. However, although water intoxication was the mode of death the excess fluid ingestion would not have occurred if the drug had not been taken, and secondly the drug aggravates excessive water ingestion by causing SIADH.However, what Dr. Henry misses is that it was inaccurate information about MDMA which caused the excess fluid ingestion, not a direct chemical action of MDMA itself. I am not certain why this obvious fact seems to have escaped Dr. Henry. However, Dr. Henry makes medically sound recommendations on appropriate hydration:
The Department of Health in this country has included in its publicity the words 'water is an antidote to dancing, not an antidote to ecstasy.' People are recommended now to drink one pint of water or isotonic fluid per hour if they are dancing vigorously and not more than one cup of fluid per hour if they are not dancing vigorously. This modification of the original harm limitation message may help to avoid the two potentially fatal extremes of hyperthermic collapse (heatstroke) and hyponatraemia (water intoxication).1. http://www.cs.adelaide.edu.au/users/barrie/rave/Rave.letter4 http://www.ecstasy.org/dangers.html http://www.ecstasy.org/russell.html http://www.pcb.co.za/users/ravesafe/water.htm
2. http://www.erowid.org/chemicals/mdma/mdma_health5.shtml (this contains the coroner's report for Anna Wood).
3. Gibson-M., "The Ecstasy and the Agony," The Daily Telegraph, Sidney, Australia, May 24, 1996. http://www.ozemail.com.au/~coreweb/shine/art3.htm
NeurotoxicityMDMA is unambiguously neurotoxic in lab animals in high doses. Typical dose regimens which elicit neurotoxicity are 20 mg/kg (rats) or 5 mg/kg (primates) given twice daily for four days either i.m. (intramuscularly) or s.c. (subcutaneously). Humans typically use MDMA p.o (per oral) and at levels of about 2.5 mg/kg or less. Subcutaneous administration of MDMA tends to increase toxicity 2-3 times over p.o. Extrapolation of animal studies to human use is difficult, since humans typically use a less toxic route of administration, take somewhat less per dose and take a smaller cumulative dose.
One study of MDMA administered to primates most closely modelled human use and used doses of 2.5 mg/kg given every 2 weeks for 4 months (2.5 mg/kg x 8) which found no evidence of neurotoxicity. A single- dose study found a decrease in serotonin (5-HT) and it's major metabolite 5-hydroxyindoleacetic acid (5-HIAA) in rhesus monkeys at 5 mg/kg but not 2.5 mg/kg. Another study gave rhesus monkeys 2.5 mg/kg twice daily for four days and found depletions of 5-HT and 5-HIAA, but without any evidence of neurotoxicity from [3H]paroxetine binding to the 5-HT reuptake transporter. The finding that depletions of 5-HIAA could occur in the absense of 5-HT neurotoxicity creates problems in interpreting the results of CSF 5-HIAA reductions in human users, which remains the strongest evidence of putative MDMA neurotoxicity in humans.
Other results of human studies in MDMA users are at odds with the conclusion that MDMA is a human neurotoxin. McCann, et al. in the same study which analyzed CSF 5-HIAA, found that MDMA users tended to have better impulse control and lower hostility while lower serotonin levels are thought to be correlated with increased hostility. A study of sleep patterns of MDMA users found that MDMA users had normal sleep patterns, but with a statistically significant decrease in stage 2 sleep, leading to an overall improvement in sleep quality -- more importantly these results are not at all in accordance with studies on sleep patterns of humans given the 5-HT supressor para-chlorophenylalanine (PCPA) or with animals having lesioned 5-HT systems.
Prospective studies (giving users MDMA in a controlled environment with baseline testing and then checking for indications of neurotoxicity) rather than retrospective studies (after the fact with no baseline) are only just getting underway at the Harbor-UCLA medical center (other studies are starting in England, Switzerland and Germany). Initial retrospective results of the UCLA study indicate that MDMA may increase cerebral blood flow . This may be indicative of benficial rather than neurotoxic changes in the brain:
We are aware of a variety of neuro-psychiatric disorders associated with measurements of low blood flow, including Alzheimer's Disease, HIV Dementia, Major Depressive Disorders and Chronic Cocaine Abuse. However, there are no known clinical disorders or drugs which induce long-term elevations of rates of cerebral blood flow. -- Charles S. Grob.
There have been reports of adverse psychiatric effects in the literature particularly anxiety attacks, paranoia and depression. However, some cases present the onset of psychiatric symptoms after a single typical dose which suggests a psychological rather than biological/neurotoxic mechanism. Also, some cases of paranoia reported appear to have occured after repeated daily abuse and probably represent a manifestation of amphetamine psychosis, possibly in part due to adulteration or substitution by amphetamines.
The diet drug d-fenfluramine (Redux) causes similar effects on the 5-HT system, and it has been suggested that the lack of adverse psychiatric effects to chronic ingestion of d-fenfluramine implies that MDMA is probably without adverse effects. However, it appears that the mechanism behind MDMA and d-fenfluramine neurotoxicity are not the same, and this may make extrapolation from one drug to the other problematic.
To summarize the clinical data, the available evidence tends to suggest that in human users a (probably reversable) decrease in 5-HT may occur (possibly via suppression of the enzyme tryptophan hydroxylase) but that 5-HT neurons remain functionally intact. However, neurotoxic levels in humans are probably "attainable" and the exact amount of MDMA required to elicit a neurotoxic response in humans is unknown.
The exact mechanism of MDMA neurotoxicity in animals is not presently known , but it seems to require dopamine activity, oxidation, and access to the 5-HT transporter. Increasing dopamine activity via ingestion of methamphetamine, l-tyrosine, phenylalanine or l-dopa would tend to increase MDMA neurotoxicity. This is a concern since phenylalanine is in diet soft drinks and products sweeted with aspartame(tm) and is also in many "smart drinks" sold at raves and of course methamphetamine is a concern since MDMA is often cut with crystal. On the other hand ascorbate (vitamin C) and l-cystine which are anti-oxidants have been shown to prevent MDMA induced neurotoxicity in animals, as has the administration of a SSRI antidepressant (Prozac, Zoloft, Paxil, Luvox, etc.). Studies indicate that taking either an anti-oxidant or a SSRI up to 5 hours after taking MDMA will prevent neurotoxicity in animals.
It may be sensible irregardless of if MDMA is neurotoxic in humans for users to take an antioxidant (e.g. 2-4 g vitamin C, orange juice) along with some 5-HT precursors (l-trytophan or 5-hydroxytryptophan (5-HTP), bananas, milk).
1. Ricaurte, GA, DeLanney, LE, Irwin, I, Langston, JW. "Toxic Effects of MDMA on Central Serotonergic Neurons in the Primate: Importance of Route and Frequency of Drug Administration," Brain Research, Vol 446, P165-168, 1988.
2. Ricarute, GA, personal communication on the findings of an unpublished study.
3. Insel, TR, Battaglia, G, Johannessen, JN, Marra, S, DeSouza, EB, "3,4-Methylenedioxymethamphetamine (Ecstasy) Selectively Destroys Brain Serotonin Terminals in Rhesus Monkeys," Journal of Pharmacology and Experimental Therapeutics, Vol 249(1), P 713-720, 1989.
4. McCann, UD, Ridenour, A, Shaham, Y, Ricaurte, GA. "Serotonin neurotoxicity after (+/-) 3,4-methylenedioxy-methamphetamine (MDMA, Ecstasy): a controlled study in humans," Neuropsychopharmacology, Vol 10(2), P 129-138, 1994.
5. Allen, RP, McCann, UD, Ricaurte, GA, "Persistent effects of (+-) 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) on human sleep," Sleep, Vol 16(6), P 560-564.
6. MAPS Newslatter Vol 6, No 3, Summer 1996. http://www.maps.org/news-letters/v06n3/
7. MAPS Newsletter Vol 5, No 4, Summer 1995. http://www.maps.org/news-letters/v05n4/05402mdm.html. Grob-C-S, Poland-R-E Chang-L, Ernst-T, "Psychobiologic effects of 3,4-methylenedioxymethamphetamine in humans: methodological considerations and preliminary observations," Behav. Brain Res., 1996 73(1-2), P 103-7.
8. McCann-U-D, Ricaurte-G-A, "MDMA ('ecstasy') and panic disorder: induction by a single dose," Biol. Psychiatry 1992 Nov 15 32(10):950-3.
9. McGuire-P-K, Cope-H, Fahy-T-A, "Diversity of psychopathology associated with use of 3,4-methylenedioxymethamphetamine ('Ecstasy')," Br. J. Psychiatry, 1994 Sep 165(3):391-5.
10. Colado-M-I, O'Shea-E, Granados-R, Murray-T-K, Green-A-R, "In vivo evidence for free radical involvement in the degeneration of rat brain 5-HT following administration of MDMA ('ecstasy') and p-chloroamphetamine but not the degeneration following fenfluramine," Br. J. Pharmacol., 1997 Jul 121(5):889-900.
11. Seiden-L-S, Sabol-K-E, "Methamphetamine and methylenedioxymethamphetamine neurotoxicity: possible mechanisms of cell destruction," NIDA Res. Monogr. 1996 163:251-76.
12. Gudelsky-G-A, "Effect of ascorbate and cysteine on the 3,4-methylenedioxymethamphetamine-induced depletion of brain serotonin," J. Neural Transm., 1996 103(12), P 1397-404. McCann-U-D, Ricaurte-G-A, "Reinforcing subjective effects of (+/-) 3,4-methylenedioxymethamphetamine ('ecstasy') may be separable from its neurotoxic actions: clinical evidence." J. Clin. Psychopharmacol. 1993 Jun 13(3):214-7. Schmidt-C-J, Kehne-J-H, "Neurotoxicity of MDMA: neurochemical effects.", Ann. N.Y. Acad. Sci. 1990 600:665-80. Steranka-L-R, Rhind-A-W, "Effect of cysteine on the persistent depletion of brain monoamines by amphetamine, p-chloroamphetamine and MPTP," Eur. J. Pharmacol. 1987 Jan 13 133(2):191-7. Battaglia-G, Yeh-S-Y, De-Souza-E-B, "MDMA-induced neurotoxicity: parameters of degeneration and recovery of brain serotonin neurons," Pharmacol. Biochem. Behav. 1988 Feb 29(2):269-74.
Chemistry/SynthesisMDMA is a semi-synthetic compound, which is most commonly synthesized from the essential oil safrole. It is not difficult as chemical syntheses go, but knowledge of basic organic chemistry synthesis techniques is essential. The following is just an overview of the basic routes. For details and alternatives please see the references listed.
The most common MDMA precursors are shown below.
O //\ /\ O //\ /\\ O //\ /\ O / \// \/ \ / \// \/ \\ / \// \/ \// / | || || / | || | / | || | CH2 | || || CH2 | || | CH2 | || | \ | || CH2 \ | || CH3 \ | || CH3 \ /\\ / \ /\\ / \ /\\ / O \\/ O \\/ O \\/ safrole isosafrole MDP-2-PThe synthesis of MDMA usually starts with isosafrole which can be obtained from sassafrass root bark extracts by purification and then isomerization of safrole into isosafrole via heat + KOH. Isosafrole is then converted into MDP-2-P (aka 3,4-methylenedioxyphenyl-2-propanone aka 3,4-methylenedioxyphenylacetone aka 3,4-methylenedioxybenzyl methyl ketone) There is a simple method using hydrogen peroxide and formic acid which will accomplish this, although with somewhat reduced yields . A higher yield method uses a palladium bromide catalyst .
The MDP-2-P is then converted to MDMA most easily via reductive amination with either NaBH3CN (sodium cyanoborohydride) or aluminum amalgam . The NaBH3CN synthesis may be slightly easier, but the Al Amalgam method does not use a potentially watched chemical like NaBH3CN.
A particularly simple and dirty way to synthesize MDMA is from safrole via the 2-bromopropane.
The Leukart reaction has been popularized in such books as Valentine Michael Smith's, Psychedelic Chemistry, but produces low yields and is more difficult than either the aluminum amalgam or NaBH3CN methods. The method printed in Psychedelic Chemistry also contains 2 typos, one of which is potentially dangerous, see .
For an overview of alternative routes see .
1. Shulgin and Shulgin, PiHKAL, #109. http://www.erowid.org/pihkal/pihkal109.html. Fujisawa, T. and Deguchi, Y., "Concerning the Commercial Utilization of Safrole", J. Pharm. Soc. Japan, 74 975 (1954), CA 49:10958i (1955).
2. Nakai, M. and Enomiya, T., "Process for Producing Phenylacetones", U.S. Patent #4,638,094, dated January 20, 1987.
3. Shulgin and Shulgin, PiHKAL, #100, #105, #106, #109, #114 (substitute an equimolar amount of methylamine for the amine (e.g. ethylamine in #106) to obtain MDMA). http://www.erowid.org/pihkal/pihkal106.html. Braun, U., Shulgin, A.T. and Braun, G., "Centrally Active N- Substituted Analogs of 3,4-Methylenedioxyphenylisopropylamine (3,4-Methylenedioxyamphetamine)", J. Pharm. Sci. 69 192-195 (1980).
4. Shulgin and Shulgin, PiHKAL, #109. http://www.erowid.org/pihkal/pihkal109.html.
5. Fester, Secrets of Methamphetamine Manufacture. Anon: "Verfahren zur Darstellung von Alkyloxyaryl-, Dialkyloxyaryl- und Alkylendioxyarylaminopropanen bzw. deren am Stickstoff monoalkylierten Derivaten", German Patent, 274,350; Filed December 24, 1912, issued May 16, 1914, Assigned to E. Merck in Darmstadt. Biniecki, S. and Krajewski, E. "Preparation of DL-1-(3,4-Methylenedioxy)-2-(methylamino)propane and DL-1-(3,4-dimethoxyphenyl)- 2-(methylamino)propane," Acta Polon. Pharm. 17 421-425 (1960), CA 55:14350e (1961).
7. Dal Cason-TA. "An Evaluation of the Potential for Clandestine Manufacture of 3,4-Methylenedioxyamphetamine (MDA) Analogs and Homologs." Journal of Forensic Sciences. Vol 35(3):675-697. May 1990.