Search Results for "mephedrone"

Nov 13 2012

Mephedrone Brief 11/13/2012: Yes, it was the 4-methylmethcathinone that killed him

There's a new Case Report in the Journal of Analytical Toxicology

Adamowicz P, Tokarczyk B, Stanaszek R, Slopianka M. Fatal Mephedrone Intoxication--A Case Report. J Anal Toxicol. 2012 Nov 7. [Epub ahead of print] [PubMed][DOI]

The victim was a 30 year old male, found in a stairwell in a "critical state". Emergency response was ineffectual and the individual died at the scene. The toxicology testing found his blood and vitreous humour positive for mephedrone (5.5 and 7.1 ug/mL, respectively). There was no alcohol in the individual, no positives on "routine screening analysis" nor any sign of amphetamine, methamphetamine or MDMA. The 2C-B compound initially suspected by police (based on some field assay, looks like) was not confirmed in the powder in his possession nor in tissue samples.

That's it, short and sweet. The mephedrone (aka 4-methylmethcathinone) killed him.

Additional reading on the substituted cathinone designer drugs of abuse can be found in my archive.

Related reading on MDMA-induced fatality can be found in the MDMA Archive.

2 responses so far

Dec 08 2011

Congress moves to control synthetic cannabimimetic (K2/Spice) and designer cathinone (mephedrone/MDPV) drugs

HR 1254 (pdf) has passed the House.

This Act would criminalize possession of a range of compounds which activate the endogenous cannabinoid CB1 receptor. The language covers several structural classes as well as an extended list of, e.g. the JWH-xxx compounds. In essence this is another attempt on the analog front in which the DEA is not able to move quickly enough on specific new drugs that emerge within a general neuropharmacological class.

The bill also doubles the amount of time the DEA has to generate the support for a final rule, once an emergency action has been invoked.

The House Resolution next addresses 17 compounds in the likely stimulant/empathogen class, with most of them being cathinone derivatives. Readers of this blog will be familiar with the well known 4-methylmethcathinone (mephedrone) and 3,4-methylenedioxypyrovalerone (MDPV) on this list.

One assumes that Chuck Schumer will be leading the charge on this in the Senate and that it will pass in short order...opposition to this sort of legislation is not usually robust among elected politicians.

8 responses so far

Sep 30 2010

Recreational Mephedrone Brief (09/30/10)

Mephedrone, or 4-methylmethcathinone, is a recreational drug that got very popular in the UK in recent years, no doubt due to it being legal to sell and possess up until April of this year. There is not a tremendous amount known about the pharmacology of this drug at present, however we can deduce quite a bit about where we should start looking from user experiences. I am currently intrigued by the fact that if you look at online user forums you can get Ecstasy fans describing mephedrone as being sortof like Ecstasy...only not as good, or not quite the same. In addition, a recent paper which surveyed a certain subset of users found that many of them report intranasal mephedrone to be as good or better than intranasal cocaine. You will recall, of course, that I have a great deal of blog interest in discussing MDMA-related fatalities.
ResearchBlogging.orgA Case Report that recently appeared in the Lancet helps us to connect up some dots. Sammler and colleagues report on the case of a 15 year old girl who presented to their emergency department one afternoon with "altered mental status, vomiting and nausea". She had been out drinking the night before and had also consumed a "white powdery substance". The clinical workup contained a few interesting clues:

-the cerebrospinal fluid (CSF) opening pressure during lumbar puncture in the lateral decubitus position was raised at 350 mm of water.
-Blood tests showed profound hyponatraemia at 118 mmol/L.
-Serum osmolality was low at 256 mmol/kg, whereas urine osmolality was high at 742 mmol/kg.

Well, well, well. Hyponatraemia is frequently reported in cases of MDMA-related medical emergency and death. This is very likely related to an effect on vasopressin / antidiuretic hormone release that would cause the kidneys to retain water, perhaps in combination with induced polydipsia (urge to drink) or intentional (albeit misguided) prophylactic strategies. This is likely driven by the serotonin transporter inhibition properties of MDMA, this indirect agonist effect perhaps working through the serotonin 3, 2C, 4 and/or 7 receptor subtypes to induce vasopressin release.

I have no good stats but there is a distinct impression from reading MDMA case reports that young women may be particularly liable to hyponatremia following MDMA. This is something I need to take up at some point- is there evidence for increased sensitivity of adolescent women to fluid balance dysregulation?

Returning to the topic at hand, is this just a case of MDMA-induced hyponatraemia?

Fortunately, the doctors ran the tox panels:

We suspected drug intoxication and did gas chromatography-mass spectroscopy of the patient’s urine; this was unequivocally positive for mephedrone metabolites, but was negative for opioids, methadone, barbiturates, cocaine, cannabinoids, alcohol, benzodiazepines, and amphetamines including ecstasy. Analysis of the white powder was consistent with mephedrone.

Interesting. This suggests to me, as it did to the authors, that there is a MDMA-like component to this mephedrone stuff. It may be a dopamine transporter inhibitor and/or dopamine releaser like cocaine, amphetamine, methamphetamine but the hyponatraemia suggests an additional (significant) serotonergic component of the pharmacological response to mephedrone. This would be consistent with those users who report it as being at least somewhat like Ecstasy.

As I discussed before, one prior paper reported on the subjective effects of several cathinone analog compounds using the drug-discrimination assay. The cathinone structure if very similar to amphetamine and supports parallel modifications. The question becomes whether the same modifications of the cathinone and amphetamine core structures convey similar changes in the pharmacology.

In very brief overview of the drug-discrimination procedure, you train rats to tell you if the drug you have just given it is similar to a reference drug such as amphetamine or MDMA. The prior paper found that methylenedioxycathinone (MDC) and methylenedioxymethcathinone (MDMC) fully substituted for MDMA at reasonably similar doses. MDMC also fully substituted for amphetamine whereas MDC did not; in both cases the potency was much lower-higher doses had to be employed for comparable effect to the reference amphetamine.

This is complicated, because if anything MDA is closer in subjective and behavioral effect to amphetamine than is MDMA. And if there are any data on the 4-Methylmeth modification of amphetamine, I am unaware of them. Nevertheless it provides some clue that we are not totally out of line to suspect that the 4-Methylmeth modification to cathinone adds on a serotonergic agonist component, very likely mediated by blockade of the serotonin transporter (with perhaps some releasing effect)...just like one sees with the methylenedioxymeth modification of amphetamine in the case of MDMA.

Final note: The 15 year old girl in this Case Report made a full recovery. That's a very good thing.
Sammler EM, Foley PL, Lauder GD, Wilson SJ, Goudie AR, & O'Riordan JI (2010). A harmless high? Lancet, 376 (9742) PMID: 20801405

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Sep 19 2010

Mephedrone (4-Methylmethcathinone) appearing in "Ecstasy" in the Netherlands

I have in the past discussed the fact that a substantial amount of recreational drug being sold as "Ecstasy" on the street contains psychoactive constituents other than 3,4-methylenedioxymethamphetamine (MDMA). This is old news and you can play around with one source of data for yourself at*. In addition, I have mentioned the UK explosion in use of 4-methylmethcathinone (4-MMC, aka mephedrone) over the past year (here, here, here, here).
ResearchBlogging.orgBrunt and colleagues have provided an update from the Netherlands Drug Information and Monitoring System which obtains drug samples, described in their prior paper, from recreational users at clubs and somehow turned over to police. For this paper they have included analysis from 12,331 tablets collected from 2008-2009. The first major observation is that the proportion of tablets containing zero MDMA increased sharply in late 2008 which is a big change from the ~90% MDMA-containing samples in prior years. Something on the order of 50-60% of the Ecstasy obtained in the Netherlands in 2009 didn't have any MDMA in it. Bummer, dude.
The other fascinating thing is that even though the usual suspect non-MDMA components were found (23-54% mCPP, methamphetamine/amphetamine, caffeine are common) the substituted cathinone 4-MMC/mephedrone is a new player.

A total of 995 (11.5% of the total ) tablets sourced from the DIMS system in 2009 contained only mephedrone. The authors note that this compound was also found in samples derived from over 100 police seizures. Although it is unclear how the proportions match up, at least the sample biases represented from the voluntary (?) user submissions and the police actions are grossly comparable in the sense that mephedrone tablets are appearing in the Dutch market. The paper goes on to note that 4-MMC is not yet "under the Scheduled Substances Act" so presumably it is a situation much like the UK up until April of 2010.

A final note of interest is the downturn in the proportion of non-MDMA tablets in late 2009- it will be interesting to see if this MDMA-drought was a shortlived blip or if actions such as Cambodia, Vietnam and Thailand finally getting serious about controlling the production of the safrole oil used as a precursor in MDMA manufacture is having a lasting effect on world markets.

One thing that I would personally like a little more clarity on is the degree to which the authors assert that the tablets they are analyzing were "sold as ecstasy". Given the popularity of the drug under its own name in the UK, one wonders if it is merely being marketed as mephedrone/4-MMC instead of deceptively as "Ecstasy" which I think is commonly understood to mean MDMA. There is also the usual problem with samples sourced from users in this paper- there could always be a substantial bias to submit or turn over tablets (which are likely batch-identifiable by stampings/color) of unexpected or suspicious subjective character. Likewise, it is hard to determine marketshare for a particular batch or appearance of tablet. This makes it hard to infer what the constituents are in the population of pills actually being consumed by users with high accuracy. Nevertheless these data are very welcome since across time and geographical region we can get some confidence on relative MDMA content, the appearance of new drugs, etc.

*Since I mentioned the pill testing outfit at the top, I should note that a search for mephedrone pulls up 5 different tablets, all sourced from Zurich (it is possible that the other source laboratories are not testing for 4-MMC yet). All 5 contain caffeine and two contain MDMA in addition to the 4-MMC.

Brunt TM, Poortman A, Niesink RJ, & van den Brink W (2010). Instability of the ecstasy market and a new kid on the block: mephedrone. Journal of psychopharmacology (Oxford, England) PMID: 20826554

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Aug 18 2010

Recreational Mephedrone Brief (8/18/10)

The recreational drug 4-methylmethcathinone (4-MMC; aka mephedrone, MMCAT) was legal in the UK up until mid April of this year. I had previously covered the only work in a behaving animal model that I could find, a paper using drug-discrimination techniques to evaluate the discriminative stimulus (aka, subjective) properties of several cathinone derivative compounds (but not 4-MMC) in comparison with amphetamine and MDMA. In a subsequent post I mentioned what appears to be the first well characterized death of someone due to 4-MMC, the relative dearth of scientific evidence about this compound and speculated on what I'd like to see happen if I were a Program Officer in NIDA.

I was very interested to see news accounts that investigators at John Moores University in Liverpool were going to start some laboratory studies in human volunteers. It really is unfortunate that we know very little about cathinones at all and essentially zero about 4-MMC, particularly when you compare it to research on the amphetamine class derivative compounds that are in recreational use. By the news account the JMU study was approved by the local IRB and it appeared to be heading into standard territory for looking at the subjective/affective, cognitive and physiological reactions to a drug in human subjects.

The public health department at JMU has won "ethical approval" to begin researching the drug with the help of students determined to get their weekend thrills.
While getting "high", they will be questioned by university academics throughout the night about their different states of consciousness. Tests will study their thoughts and ability to think coherently, as they are asked to describe how they feel on an "adjective bar", with "sad" or "depressed" at the bottom and "euphoric" or "very happy' at the top. Further tests include matching objects to numbers and being asked to recall logical sequences.

Well, plans have changed. A piece in click Liverpool reports

A study testing the effects of the controversial deadly drug mephedrone has been scrapped by a Liverpool university.

Liverpool John Moores University (JMU) were given the green light to research the one-time legal high after the project initially raised eyebrows in March.

Scientists planned to monitor the effects of the white powder also known as "Mcat" or "Miaow Miaow", which became popular among party-goers.

But now after months of deliberation, the university has cancelled its research following several casualties since the plant food hit shelves across the country.

A spokeswoman said: "This particular research project at the School of Natural Sciences and Psychology was discontinued following the change in the legal status of mephedrone.

Bummer. Far be it from me to question the actions of an IRB but given that the Swedish fatality occurred in late 2008 and the link to 4-MMC was clear by fall of 2009, well, I'm not certain I see where the risk/benefit has changed. Lots more people were taking it by early 2010 so the identification of a few more fatalities that were linked to 4-MMC shouldn't really change the odds. Oh well, perhaps the JMU IRB simply overlooked the Swedish death or something.

There is one minor bit of hope for those of us that want to see some research data become available.
"However, a team at the School of Pharmacy and Bimolecular Sciences is continuing its own area of research into the damaging effects of this drug."

They don't specify but I'm thinking that perhaps this means animal studies are ongoing. So we should see at least something out of this University over the next year, hopefully.

If, and admittedly this is an assumption, the JMU IRB got cold feet over reports of fatalities in the popular press, this turns our attention back to the tox reports. In the case of MDMA (see prior link) we often resort to the Case Report literature for additional clues as to the likely causal role of the recreational drug in medical emergency and fatality. I have on offer one such report for 4-MMC that has just popped up in pre-publication form.

ResearchBlogging.orgA Letter to the Editor published in Forensic Science International by Torrance and Cooper presents an analysis of blood levels of 4-methylmethcathinone in four fatalities. This is not a full Case Report so the details are a bit sketchy. The main point seems to be identifying the presence of 4-MMC and the levels observed (22, 3.3, 5.1 and 1.2 mg/L). The authors do make clear that in only two of the four cases was 4-MMC identifed by the medical examiner as being causal in the death of the decedent. The first two cases involved suspicion of 4-MMC/mephedrone from presentation. It doesn't specify but presumably friends or acquaintances of the victims identified drug taking in the interval immediately prior to the death. In the two other cases 4-MMC was not suspected or causal (one case involved an abdominal stabbing, the other is unspecified) but rather was identified in the victim via tox screening.

So the main result from this paper is the identification of a range of blood levels of 4-MMC that might be associated with fatality (3.3-22 mg/L) and the mention of the presence of other drugs

Case1 had less than 0.1mg/L of diazepam and nordiazepam and 0.34mg/L of amphetamine. In case 2,mephedrone was the only drug detected in blood with low concentrations of benzoylecgonine [cocaine metabolite-DM] and 11-nor-delta-9-tetrahydrocannabinol-9-carboxylic acid detected in urine only.

We'd prefer more of a full Case Report workup, of course. Including more details about the subjects, their use timeline and the clinical picture prior to death. But as always in science you have to build the case, brick by brick, so every little bit can be informative. We'll just have to stay tuned.
Torrance H, & Cooper G (2010). The detection of mephedrone (4-methylmethcathinone) in 4 fatalities in Scotland. Forensic science international PMID: 20685050

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Apr 08 2010

UK bans Mephedrone

The UK House of Lords has followed the riff-raff MPs in voting for a ban of the previously uncontrolled recreational drug 4-methymethcathinone (4-MMC, mephedrone, meow-meow, plant-food, etc). Prior observations from me are here and here.
This is a good opportunity to point to the report on the cathinones [ pdf ] that was created by the Advisory Council on the Misuse of Drugs. This more or less echos my points in my prior posts that while we may know a bit about cathinones the available scientific knowledge is pretty pathetic compared to the amphetamine-class drugs. And essentially nothing has been published on 4-MMC/mephedrone.

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Mar 19 2010

Scientific Research 101: Meow-Meow, "plant food", 4-MMC, mephedrone...

Published by under Science 101

I recently introduced a paper on the discriminative stimulus properties of cathinone analog drugs with reference to the recent emergence in the popular media of an analog called 4-methylmethcathinone (4-MMC), mephedrone (2-methylamino-1-p-tolylpropan-1-one), Meow-Meow, MMCAT. The name "plant food" is what 4-MMC is apparently being marketed under in the UK, given that the compound itself is not controlled but it is illegal (I surmise) to sell things as "legal ecstasy" or "legal methamphetamine" or similar. There has been one fatality attributed* to 4-MMC that I can find and a few bits of seized-drug analysis confirming that the stuff is indeed being used.
An early report of a fatality associated with consumption of the drug in Sweden resulted in placement of mephedrone on the controlled list. The followup in the Swedish press shows that the woman was reported to have consumed mephedrone (confirmed post-mortem) and smoked cannabis (no apparent confirmation; alcohol and other narcotics excluded postmortem) and then collapsed. Emergency services were unable to revive her and she died a day and a half later; symptoms of brain swelling, stroke, hyponatremia and hypokalemia were mentioned, as well as a low body temperature of 33 degrees C.
The story has heated up recently in the UK press after the death of two individuals who are, at present, suspected of taking 4-MMC/mephedrone, reportedly in combination with methadone (an opiate) and alcohol. As I mentioned before, a quick scan of PubMed finds little reported on the effects of this compound in animal models or in humans.
So the question is, scientists, what next?
Let's play virtual science, shall we?

Continue Reading »

9 responses so far

Nov 06 2015

RFAs do not narrow the NIH portfolio, quite the opposite.

Mike the Mad Biologist has taken issue with the findings of a "cross-campus, cross-career stage and cross-disciplinary series of discussions at a large public university" which "has produced a series of recommendations for addressing the problems confronting the biomedical research community in the US".

Mike the Mad has pulled out a number of the proposals and findings to address but I was struck by one on the role of "R&D contracts, Requests for Applications (RFAs) and intramural research". From page 4 of the UW report:

Fourth, the NIH should increase the proportion of its budget directed to Research Project Grants, Center Grants and Training, and it should decrease the proportion directed to R&D contracts, Requests for Applications (RFAs) and intramural research. These changes would redirect funds towards investigator-initiated research and allow funding of a greater diversity of projects. R&D contracts and RFAs place limits on the topics and approaches that can be pursued, so a shift away from them will lead to fewer intellectual constraints being placed on researchers. We emphasize that this is not a recommendation to eliminate R&D contracts or RFAs, but rather to reduce their number, which will sharpen their quality and provide the funds needed to award more investigator-initiated grants.

I disagree with the notion that RFAs are poisonous to diversity and the notion that pure "investigator-initiated" leads to fewer intellectual constraints.

The NIH peer review process is an inherently conservative one because it tends to reinforce itself. Those who are successful within the system do the primary judging of who is next to be successful. Those who become successful have to, in large degree, adapt themselves to the thinking and expectations of those who have previously been successful.

When it comes to the role of Program Officers in selecting grants for pickups and saves, well, they too are influenced by the already-successful. This is in addition to the fact that POs have long term careers and thus their orientations and biases come into play across literally decades of grant applications. To the extent that POs are judged by the performance of their grant portfolios, you can see that they are no different than the rest of us. Higher JIF, higher citations, more press attention, more high-profile scientists....all of these things dictate them selecting grants that are going to be more of the same.

Sure, this is a thumb on the scale. Lots of scientists are open to new ideas. Lots of scientists can become enamoured of scientific proposals that are outside of their immediate interests. Peer reviewers and Program Officers alike.

But there more assuredly is a thumb on the scale. And it is a constantly reinforcing cycle of conservatism to select grants for funding that are very much like ones that have previously been funded. Alike in topic, alike in PI characteristics, alike in the University which is applying.

Request for Applications (RFAs) quite often serve to fight against the narrowing of topic diversity and in favor of getting grants funded in a new area of investigation. Trust me, if they already have copious amounts of grant funding on a topic, this does not result in additional RFAs!

In some of my general oversight of RFAs over the years from some of my favorite ICs I've noticed topics like sex-differences and less-usual experimental models are often at play. Adolescent/developmental studies as well. To take a shot at my much beloved NIDA--- well, they have been, and continue to be, the National Institute on Cocaine and Heroin Abuse. Notice how whenever the current Director Nora Volkow gets interviewed on the general lay media she goes on and on about the threat of marijuana to our adolescents? Try a trip over to RePORTER to review NIDA's respective portfolios on marijuana versus cocaine or heroin.

There have been several NIDA RFAs, PARs and PASs over the years which are really about "Gee, can't we fund at least two grants on this other drug over here?". There's an old one begging for medications development for cannabis dependence (RFA-DA-04-014; 10 awards funded) and another asking for investigation of developmental effects of cannabis exposure (RFA-DA-04-016; 6 awards funded). Prenatal exposure to MDMA (RFA-DA-01-005). Etc.

The latest version of this is PAR-14-106 on synthetic drugs. You know, the bath salts and the fake weed. I've been chatting with you about these since what, 2010? The PAR was issued in 2014 (4 awards funded so far, 5 if you include R03/R21 versions).

Is this because evil NIDA wants to force everyone to start working on these topics? Constraining their intellectual freedom? Hampering the merry progress on cocaine and heroin? You might ask the same about various sex-differences FOA that have been issued over the years.

Heck no. All that stuff has continued to be funded at high rates under NIDA's normal operation. Why? well because tons and tons and tons of highly funded and highly productive researchers have focused on cocaine and heroin for their entire careers. And these are the grants that seem most important to them....the cocaine and heroin grants. They are the successful scientists who review other grants and who whisper in the ears of POs at every turn.

So the other drugs get short shrift in the funding race.

Every now and again a PO gets up the courage to mount an assault on this conservatism and get a few grants funded in his or her bee-in-the-bonnet interest. Having watched one of these develop back in the good old days, it takes time. Two POs I observed at NIDA set up mini-symposia at NIH and at meetings for several years before lo and behold an RFA was issued on that topic. This was in the days when presumably they had the spare cash to do this sort of grooming of a topic domain.

The CRAN initiative initially side-stepped the review process altogether and issued supplements for combined-drug research (think "effects of alcohol drinking on smoking behavior and vice versa").


I am sure that parallels exist at all of the other ICs.

And let me be emphatically clear on this. It isn't as though there are not individual investigators out there independently initiating grant applications on these topics. OF COURSE there are.

They just haven't been able to get funded.

I come back to this claim in the UW document that RFAs "place limits on the topics and approaches that can be pursued" and the suggestion that their diminishment will lead to "fewer intellectual constraints being placed on researchers".

This is nonsense. Targeted FOAs very often address topics which have been "investigator-initiated" many, many times but these applications have not been successful in navigating the study section process. I would be shocked if there were more than a very small number of targeted funding announcements from the NIH that were on a topic that nobody had ever applied for funding to research. Shocked.

The pool of people applying for funding is just so large and so diverse that any half-way interesting idea has been proposed by somebody at some point in time. The idea that NIH Program have come up with something that nobody in the extramural community has ever thought about is just not that credible.

17 responses so far

Jul 28 2015

Yes, it was the methylone that killed him

StructureFig-mdma-vs-cathinones450A new Case Report verifies the lethal potential of methylone (PubMed). This drug is also known as beta-keto-MDMA (bk-MDMA; Wikipedia) or 3,4-methylenedioxycathinone. In short, this is the closest cathinone cousin to MDMA, aka Ecstasy.

Barrios L, Grison-Hernando H, Boels D, Bouquie R, Monteil-Ganiere C, Clement R. Death following ingestion of methylone. Int J Legal Med. 2015 Jun 13. [Epub ahead of print]

The decedent was a 21 year old man reported to ingest methylone and cannabis. Friends placed him in a "nearby children's paddling pool" upon report of breathing difficulty and polypnea (rapid breathing, panting).

By the time emergency medical services made contact he was in cardiac arrest.

Investigators were able to procure a sample of the powder the decedent consumed, represented to him as ecstasy upon purchase.

The toxicological screening was negative for alcohol or "medication", opiates, cocaine and amphetamines (including MDMA, MDA, MBDB and MDEA). This individual was positive for THC. The screening for substances by GC/MS identified a substance with characteristics identical to the seized material which the decedent had ingested- methylone with a purity of 83.3%.

Now admittedly a cardiac arrest with labored breathing is not right down the main line of clinical findings in MDMA overdose cases. So this is a bit strange. However, "sudden collapse" or "found unresponsive" is not atypical as the triggering observation that the person on MDMA is in trouble. There are also numerous studies showing adverse effects on MDMA on aspects of cardiac function. Similarly, cardiac implications are common with methamphetamine-related deaths- both acutely and apparently as a consequence of longer term use.

So there is every reason to think that methylone might be cardiotoxic.

The finding of cardiac arrest triggered a vague memory and luckily these authors cited the paper I was remembering:

Carbone PN, Carbone DL, Carstairs SD, Luzi SA. Sudden cardiac death associated with methylone use. Am J Forensic Med Pathol. 2013 Mar;34(1):26-8. doi: 10.1097/PAF.0b013e31827ab5da.

Now in this case a 19 year old man collapsed while jogging and had a much lower blood level of methylone (0.007 mg/L) compared with the 6.64 mg/L blood levels in the Case reported by Barrios et al. No other drugs were detected, however:

No other drugs were detected in the urine or central blood, including pseudoephedrine, ephedrine, amphetamine, methamphetamine, MDMA, 3,4-methylenedioxyamphetamine, phenylpropanolamine, or cocaine and metabolites. Analysis was also negative for several other bath salts including flephedrone, n-ethylcathinone, mephedrone, methedrone, ethylone, butylone, MDPV, and naphyrone.

This was presumably not an effect of acute overdose intoxication but perhaps a lingering effect on heart function caused by the methylone consumed hours before. Hard to know without controlled studies, particularly given the exercise this person was engaged in.

Nevertheless, this new Case Report serves as a reminder that methylone, which is increasingly replacing MDMA in the US market, represents a risk for immediate and lasting adverse health consequences.
Related Reading:

It was the methylone that killed him.

Methylone, or beta-keto-MDMA, also causes fatality

Various posts on MDMA-related fatality and morbidity

2 responses so far

Mar 13 2015

Why PMA if dealers don't want to kill their clients?

Published by under MDMA

There's an interesting piece on Ecstasy in Mixmag that addresses something that is a side issue of the MDMA overdose issue that I've talked about on the blog. These issues bubble up to our conscious consideration every time there is a mysterious Ecstasy-related cluster of adverse events such as at Wesleyan University. Until there is confirmation of the drug(s) involved from toxicological testing we can only speculate as to the cause of the events.

Even though we know that MDMA itself is always a top suspect, PMA, (para-Methoxyamphetamine), is a fine Usual Suspect of a non-MDMA substance sold to users as "Ecstasy" but resulting in adverse consequences.

The Mixmag piece reminds us of the MDMA drought in the UK that launched mephedrone into the recreational pharmacopeia.

One of the easiest ways to make MDMA is to use an essential oil called safrole, which occurs naturally in the roots and bark of the yellow camphor tree, found in Cambodian rainforests and elsewhere. The UN has targeted the trade repeatedly in the last decade, with the noble aims of protecting the rainforest, which is being chopped down by the gangs that steam-distil the oil out of the bark in giant, bubbling cauldrons in jungle labs. The UN burned 33 tonnes of it in 2008, which caused a worldwide drought of MDMA and the emergence of mephedrone as both gangsters and clubbers looked for alternatives. In September 2010, 50 tonnes were burned in Thailand.

Yep, we recall.

However, this previous preferred-method for synthesizing MDMA leads on to the reason why PMA is sometimes pushed out on the market for consumers to use, unsuspectingly in many cases. Mixmag proposes this hypothesis:

PMA is made from an oil called anethole, which is legal, cheap, and easy to get hold of.

Professor David Nutt agrees that the likely scenario is that clandestine chemists use anethole in a trial run, to test new lab set-ups, and then sell the resulting PMA to unscrupulous pill pressers. Making PMA involves an identical set of chemical reactions to making MDMA – only the precursor is different. Think about it: if you had a limited amount of very expensive safrole or PMK, and you had a new lab, or a new chemist, you’d want to test your kit out. A trial run making PMA from anethole would help you practice the technique and avoid losing valuable precursors – and you’d make some money back.

They then ask any chemists reading to confirm so one must take this as speculation rather than journalistically confirmed with clandestine labs.

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