RCs 2-Methoxyqualone "Quaaludes"

[placebonaut]

So dosent hit very well if at all ?

it does hit but it's not that simple, and this combo I think actually dampened the effect as well.

long science bit sorry:-
Quaaludes and analogues are all quinazolinone derivatives which are inherently lipophilic, so they more readily distribute into fat tissues.

I'm 280lbs (obese), for me this means slower onset and longer duration as the drug is absorbed into fat, this means longer half-life and higher risk of accumulation. Add to this the fact that no-one knows how quickly tolerance builds with this analogue and you're left in a place where it's pointless to draw any conclusions from a subjective experience of 1 person with different biochemistry to you (especially when they've been munching on a few of these for a few weeks now).

Dicking around with the ring in analogues can change how lipophilic they are, 2-Methoxyqualone is actually slightly less lipophilic than quaalude.

soooooooo.....it definitely hits, but I'm 280lbs so I need more of it for it to hit than for someone with lower BMI. The question is how much more.....and what's the risk of dosing that high given unknown toxicology.

I'm going to take a tolerance break from all GABA related drugs, and then give this a try again at at higher dose of 660mg in 1 go.

I would expect people with lower BMI to get a better kick from this, certainly worthwhile trying it. As always do it safely and titrate up!

I also think in principle sublingual dosing should be a better ROA creating faster onset and quicker peak plasma levels. I just need to figure out the best way to take it sublingually, I'm not a fan of sticking pure ethanol under my tongue, it burns like fuck! not sure how much pure ethanol I need to get a 330mg pill into solution, and then not sure how much I can dilute it to make it practical to use , open to idea here if anyone has any suggestions?

 

[placebonaut]

for completeness adding a link to another post where I did a lot more research on things.

Pharmacology, toxicology, strength comparison of 2‑Methoxyqualone versus Quaalude

My conclusion is that my plan to take 660mg in 1 go with wine is fine for me personally given it has significantly lower toxicology that Quaalude, and is likely to be lower in strength and duration. The wine should be helping with bioavailability.

 

[placebonaut]

how time flies, I'd forgotten that it was this thread that made me register for BL!

So the price of 2-MQ has dropped significantly, which means more people are going to be taking it, shit I'm considering buying some again ffs.

with this in mind I've been using chatGPT to look at what the hypothetical pharmacology of 2-MQ might be because I've actively reduced the types of GABAgeic drugs that I take and I'm considering if 2-MQ might work occasionally alongside weekly pregabalin/gapapentin use (different receptors to ludes), and also alongside occasional benzo use post stim binge - my goal is to avoid withdrawal again and significant GABA receptor downregulation because it sucks donkey balls.

So I've asked ChatGPT to take a guess at 2-MQ pharmacology and how it might compare to methaqualone (Quaaludes) based on 1. Methaqualone research 2. The changes that 2-MQ has compared to methaqualone (C2 methoxy substitution) 3. the trip reports in this thread.

I can't say I've decided if I'm going to take it again (but most likely I will!), I'm in a different place now taking far fewer drugs so I think given the new price this might be worth another go for me personally.

YMMV, do your own fucking research before you take this shit, start low go slow etc etc - you've been warned!! I'm a fucking idiot.

anyway, thought I'd share the output as it took me hours to generate and thought it was an interesting read.

@4DQSAR would value your opinion - though clearly this is all hypothetical bollocks so take it with a shovel load of salt

@Bleaney here we go again...


Let the AI bollocks begin.....DO NOT TRUST THIS SHIT

2-Methoxyqualone: Updated Trip-Report Analysis and Pharmacological Comparison With Quaaludes​

Layman's summary​

The additional reports make 2-methoxyqualone (2-MQ) look more consistently psychoactive than the earliest reports suggested. Across the accounts, the recurring effects include warmth, contentment, relaxation, mild euphoria, sedation and a distinctly slowed or foggy mental state.
However, the reports still do not establish how potent pure 2-MQ is, how long its effects normally last, or whether its mechanism is identical to that of methaqualone (Quaaludes).
My current interpretation is that 2-MQ may retain methaqualone-like activity at GABA-A receptors, but its apparent potency and subjective effects could differ substantially. Product variability and the extensive use of other psychoactive substances remain major uncertainties.

What the trip reports add​

1. The effects appear reproducible across several reports, but their intensity varies.
The accounts now include reports of a warm, pleasant glow, contentment, mild head euphoria, body euphoria and pronounced relaxation. One user also described an experience resembling the subjective effects they associate with benzodiazepines, particularly when benzodiazepines are combined with pregabalin.
This makes it more plausible that the products contained a psychoactive substance capable of producing sedative effects. It does not, however, establish the identity or purity of the active ingredient in every batch.
2. The apparent onset is relatively rapid in some of these particular sessions.
One user reported noticeable effects around an hour after oral administration, followed by a decline in perceived intensity and renewed effects after taking more. Another reported feeling the effects within roughly half an hour in sessions involving an empty stomach, alcohol and cannabis.
These observations are compatible with relatively rapid absorption, but the timing cannot be generalised to 2-MQ alone. The other substances, formulation and differences between sessions all complicate interpretation.
3. The effects may become more sedative without producing proportionally more euphoria.
The clearest example is the report involving pregabalin, diazepam, alcohol, cannabis and 2-MQ. The user described increasing sedation, difficulty concentrating, unsteady walking, slurred speech and double vision, while finding the euphoria comparatively disappointing.
This is an important observation. Subjective enjoyment and pharmacological impairment are not interchangeable measures of drug effect.
It also means that the reports do not justify assuming that a weak euphoric effect indicates weak overall pharmacological activity.
4. The short-duration hypothesis remains plausible but unproven.
One user described a decline in the initial effects after approximately two hours, followed by renewed effects after further exposure. Another remained noticeably intoxicated several hours after taking 2-MQ in a complex drug combination.
These observations suggest that the perceived duration may depend on the intensity of the initial effects, subsequent exposure and co-administered drugs. They do not establish the elimination half-life or the duration of action of pure 2-MQ.
5. The apparent interaction with other sedatives is more complicated than simple potentiation.
The reports suggest that combining 2-MQ with other substances can substantially change the overall experience. In some sessions, users describe pleasant relaxation; in another, pronounced impairment accompanied relatively little additional euphoria.
However, this does not establish that benzodiazepines or pregabalin directly suppress 2-MQ's euphoric effects. The combination may increase sedation and cognitive impairment without producing a corresponding increase in pleasure, and the different drugs' effects cannot be cleanly separated in these reports.
6. The reports raise a significant safety concern.
The described combinations include alcohol, GBL, pregabalin, benzodiazepines and carisoprodol. These substances can produce overlapping central nervous system depression.
Unsteady walking, slurred speech and double vision are warning signs of substantial impairment, not reassuring evidence that a combination remains within a safe range. Adding further depressants can lead to loss of consciousness, respiratory depression and death.

Updated overall interpretation​

The simplest working hypothesis remains that 2-MQ may act partly through methaqualone-like GABA-A receptor modulation, with potentially different functional potency or receptor-subtype effects.
The new reports make a purely inactive-product explanation less satisfactory as an explanation for the entire collection of experiences, although variable product content remains a credible explanation for some of the differences.
They also strengthen the distinction between three separate properties:

• Euphoric potency: how strongly the substance produces a subjectively pleasant or rewarding effect.
• Sedative and impairing potency: how strongly it affects alertness, coordination, speech and cognition.
• Duration: how long its effects persist, which depends on both pharmacodynamics and pharmacokinetics.

These properties do not necessarily change in parallel.
The reports therefore suggest that 2-MQ can produce meaningful intoxication, but do not establish that it is simply a weaker, shorter-acting version of Quaaludes. The available evidence remains insufficient to determine its potency relative to methaqualone or to characterise its safety profile.

---

Detailed pharmacology​

1. Established pharmacology of methaqualone​

Methaqualone's best-established molecular target is the GABA-A receptor, an inhibitory neurotransmitter-gated ion channel.
The 2015 study A Multifaceted GABA-A Receptor Modulator: Functional Properties and Mechanism of Action of the Sedative-Hypnotic and Recreational Drug Methaqualone found positive allosteric modulation across several conventional GABA-A receptor subtypes, with more diverse effects across other receptor configurations.
A 2024 cryo-electron microscopy study subsequently visualised methaqualone at transmembrane interfaces between GABA-A receptor subunits. This provides direct structural support for a binding mechanism distinct from the canonical benzodiazepine binding site.
References:

• Methaqualone functional pharmacology — Molecular Pharmacology
• Structural insights into GABA-A receptor potentiation by Quaalude — Nature Communications

These findings provide a credible mechanistic basis for investigating 2-MQ as a possible GABA-A modulator. They do not establish its binding affinity, efficacy or receptor-subtype profile.

2. Structural implications of the C2 methoxy substitution​

2-MQ retains the broad quinazolinone scaffold and N3 ortho-tolyl substituent of methaqualone, while replacing the C2 methyl substituent with methoxy.
This substitution changes the molecule's steric and electronic properties and introduces an oxygen atom capable of accepting hydrogen bonds.
Several effects are plausible:

• Binding energetics: The altered substituent may change hydrophobic contacts and the energetic cost of transferring the compound from water into the receptor's binding pocket.
• Binding geometry: The methoxy group may change the orientation of the quinazolinone core or the interactions available to neighbouring residues.
• Functional efficacy: Even if 2-MQ binds at the same site, it may stabilise receptor conformations differently.
• Pharmacokinetics: The substitution may alter metabolism, distribution and protein binding, but the direction of these changes cannot be reliably inferred from the structure alone.

A reduced-potency hypothesis is therefore chemically reasonable, but it remains untested.

3. What the new time-course observations tell us​

The reports contain three different kinds of observations:

Observation	What it supports	What it does not establish
Noticeable effects within approximately 30–60 minutes in some sessions	A relatively rapid onset may occur under those conditions	A universal onset time or absorption rate for pure 2-MQ
Declining subjective effects after the initial period	The perceived intensity can change substantially over time	A specific elimination half-life
Renewed effects following additional exposure	Further exposure can change the overall subjective experience	Whether the original dose had been eliminated, or whether the renewed effects came entirely from 2-MQ
Persistent impairment in a multi-drug session	The overall combination can produce prolonged impairment	The independent duration of 2-MQ
Pronounced sedation with comparatively modest euphoria	Sedation and euphoria can diverge	That another drug directly blocks 2-MQ's euphoric mechanism

The reports involving multiple substances are especially difficult to interpret because alcohol, pregabalin, benzodiazepines and carisoprodol can all affect the central nervous system independently.
The observations are useful for generating hypotheses, but they cannot provide reliable pharmacokinetic parameters.

4. Does the benzodiazepine-like feeling imply the same mechanism?​

Not necessarily.
Benzodiazepines and methaqualone both affect GABA-A receptor function, but their binding sites and receptor interactions differ. A similar subjective effect does not prove identical molecular pharmacology.
The reports describe a benzodiazepine-like feeling in a setting involving other substances, including pregabalin and, in some sessions, alcohol or cannabis. Those drugs can alter the subjective effects of the overall combination.
There is also a difference between shared target involvement and cross-tolerance. Two drugs can influence the same receptor family without producing identical functional effects or identical adaptations following repeated exposure.
The most defensible conclusion is that the reported similarity is consistent with a broadly sedative mechanism, but is not specific evidence of a shared binding site.

5. Why might sedation increase without a corresponding increase in euphoria?​

There are several possible explanations.
Different pharmacological endpoints. Sedation, motor coordination, attention and subjective reward are distinct outcomes. They need not increase proportionally.
Different receptor-subtype effects. GABA-A receptor subtypes differ in their distribution and functional roles. A compound's activity across these subtypes may affect the balance of its observable effects.
Contributions from other drugs. Pregabalin, benzodiazepines and alcohol can substantially affect alertness and coordination. Their combined effects can dominate the overall experience, making the contribution of 2-MQ difficult to identify.
Impairment affecting self-assessment. Cognitive slowing and intoxication can themselves make it difficult to judge the intensity or quality of a drug's subjective effects reliably.
The reports do not distinguish these explanations. In particular, they do not establish the proposed idea that benzodiazepines and 2-MQ interact through different channel-opening mechanisms in a way that specifically suppresses euphoria.

6. What can be concluded about interactions and safety?​

The reports demonstrate why subjective intensity is an inadequate measure of the danger of a drug combination.
GABA-A modulators such as benzodiazepines, sedatives such as carisoprodol, alcohol and GHB-related substances such as GBL can produce overlapping depressant effects. Pregabalin can add further impairment and sedation.
The resulting risk is not determined simply by whether a person feels pleasantly intoxicated. Serious impairment can occur without a proportionally strong euphoric experience.
The reported gait instability, slurred speech and double vision indicate significant impairment. Such symptoms should not be treated as a cue to increase exposure or as evidence that the combination is approaching a desirable effect safely.
The report of unusually good sleep following a complex drug combination is also not evidence of improved sleep physiology or preserved normal sleep architecture. Subjective sleep quality cannot establish that respiratory function or sleep stages were unaffected.

7. Updated ranking of the mechanistic hypotheses​

The reports do not establish a molecular mechanism, but the following remains a reasonable provisional framework.

Hypothesis	Current assessment	Reasoning
GABA-A modulation resembling methaqualone	Leading hypothesis	Structural similarity and reported sedative effects make it plausible, but direct 2-MQ receptor data are lacking.
Reduced functional potency relative to methaqualone	Plausible	The C2 substitution could alter receptor interactions; the reports cannot quantify potency.
Altered receptor-subtype profile	Plausible	Could contribute to differences between sedation, euphoria and cognitive impairment.
Different absorption, metabolism or elimination	Plausible	Could contribute to the reported time course, but no comparative pharmacokinetic data establish the direction.
Variable active content or product composition	Important alternative explanation	Unverified tablet contents could account for some variation in apparent potency.
A different primary molecular target	Not excluded, but less directly supported	No direct evidence currently establishes a different primary target for 2-MQ.

These are hypotheses rather than experimentally determined probabilities. The reports cannot justify precise numerical rankings or potency estimates.

8. What evidence is still missing?​

The central unresolved questions are:

1. What compounds and concentrations are actually present in the products being described?
2. Does pure 2-MQ positively modulate GABA-A receptors, and if so, at which subtypes and binding sites?
3. Does it have lower functional potency or efficacy than methaqualone?
4. Are its reported effects shorter-lived because of pharmacodynamics, pharmacokinetics, or both?
5. What are its toxicological profile, adverse effects and interaction risks?

Analytical chemistry, receptor electrophysiology, structural studies and comparative pharmacokinetic research would be needed to answer these questions.

Final conclusion​

The expanded collection of reports suggests that 2-MQ can produce noticeable sedative, relaxing and sometimes euphoric effects. The experiences also suggest that its subjective effects can be difficult to separate from its impairing effects, particularly when several depressant drugs are involved.
A methaqualone-like GABA-A mechanism remains the leading structural hypothesis, but neither reduced potency nor shorter duration has been established experimentally. The new reports are consistent with those possibilities, while also highlighting major uncertainty about product composition and the effects of co-administered substances.
The most important practical conclusion is that a modest euphoric effect does not imply modest pharmacological impairment. Until the compound's identity, receptor pharmacology, pharmacokinetics and toxicology are properly characterised, its potency and safety should be considered unpredictable.

 

[4DQSAR]

I found a really big paper in which the researchers tried to find all of the sites methaqualone acts on and it's an odd one. It's a positive allosteric modulator at some subtypes of receptor, a negative allosteric modulator at others and a direct agonist at yet more subtypes, a superagonist at one BUT an antagonist at one or two.

With later research that included derivatives such as dimethaqulone, the conundrum is that the key para position of that pendent aromatic is the spot that at once increases potency the most BUT is also responsible for the pro-convulsant effects.

Apparently in the 1970s ER doctors would be dealing with one methaqualone overdose where the unlucky punter was spark out and in the next cubible someone who was in status epilepticus because they had also overdosed on methaqualone.

As for methoxyqualone, it's both the size and the electronic character that alters the subjective effects.

Don't forget, the researchers who discovered the sedative/hypnotic effects of methaqualone were in fact looking for a new treatment for malaria. So they HAD hundreds of related analogues to hand and settled on methaqualone.

I've said elsewhere that a post-graduate student in South Africa wrote their thesis on the various things sold as Mandrax. They had access to about 120 samples.

The 2-methyl-3-chloro was the only one that seemed as well accepted as along with methaqualone, it was one of the only two compounds found in dozens of samples. I don't think it's explicitly controlled anywhere. But I sense that methoxyqualone has turned up first because 2-methoxyaniline is cheaper than 3-chloro-2-methyl-aniline.

But being pragmatic, Mandrax has been a blight in South Africa for over fifty years so I would frankly be amazed if all of these more obscure homologues hadn't turned up at some point but simply were not accepted by the market.

It seems methaqualone is a tiny 'island of activity' since while several modifications are known so in theory their should be hundreds of diferent varients turning up... there aren't.

It appears that even the slightest change in size or electronic character is detrimental to the subjective effects.

Finally, street Mandrax (buttons) only contain 40-125mg of the actives but diphenhydramine is found in almost every sample because it slows down the metabolism of methaqualone.

 

[placebonaut]

I found a really big paper in which the researchers tried to find all of the sites methaqualone acts on and it's an odd one. It's a positive allosteric modulator at some subtypes of receptor, a negative allosteric modulator at others and a direct agonist at yet more subtypes, a superagonist at one BUT an antagonist at one or two.

yeah I was reading about this in some detail recently and was quite surprised just how may sites it was active at

With later research that included derivatives such as dimethaqulone, the conundrum is that the key para position of that pendent aromatic is the spot that at once increases potency the most BUT is also responsible for the pro-convulsant effects.

Apparently in the 1970s ER doctors would be dealing with one methaqualone overdose where the unlucky punter was spark out and in the next cubible someone who was in status epilepticus because they had also overdosed on methaqualone.

hadn't heard of this before, pretty scary shit

The 2-methyl-3-chloro was the only one that seemed as well accepted as along with methaqualone, it was one of the only two compounds found in dozens of samples. I don't think it's explicitly controlled anywhere. But I sense that methoxyqualone has turned up first because 2-methoxyaniline is cheaper than 3-chloro-2-methyl-aniline.

there was a post not to long ago on the dark net forum where a vendor was stating that cost of production is a factor in 2-MQ v methaqualone production. This makes sense in my mind as an extension of the lack of direct precursor availability driver a longer and more complex synthesis (though this is well about my pay grade to fully understand).

It appears that even the slightest change in size or electronic character is detrimental to the subjective effects.

interesting observation, care to guess as to why this is? given how broad the effects are of methaqualone on a number of sub receptor types I guess it could be a collective effect or that 1 sub type contributes to the effect significantly more than others, so a single subtype might dominate and methaqualone is simply the best at activating it, other analogues might still activate it (or indeed the other sub types) but just be less potent

Finally, street Mandrax (buttons) only contain 40-125mg of the actives but diphenhydramine is found in almost every sample because it slows down the metabolism of methaqualone.

I didn't realise the dosage was so low per pill

 

[4DQSAR]

there was a post not to long ago on the dark net forum where a vendor was stating that cost of production is a factor in 2-MQ v methaqualone production.

The two majort precursors to methaqualone are as cheap as chips BUT two are tlighly legally controlled so SAYING that is meaningless. The third not often used as it's a bit of a nightmare. A million South Africans will tell you people clearly CAN get them but the cost is NOT the same as comparing the two in Merck. A million South Africans will tell you people can obtain them, but far, far above market price.

But they were infering they HAD made methaqualone?

In South Africa, users smoke de wit pijp - vapourized methaqalone, like crack cocaine, concentrates in the brain. With this class, people smoke one, fall on their face, get up and do it all again.

I STRONLY recommend you don't do the same with whatever you were sold - without a GC-MS/NMR pair, it's just another 'mystery powder game' and the precursors are carcinogens so even only if left in the product in tiny amounts, do you want lung cancer?

 

[placebonaut]

The two majort precursors to methaqualone are as cheap as chips BUT two are tlighly legally controlled so SAYING that is meaningless.

yeah I took it to mean the cost for precursors that they could obtain

The third not often used as it's a bit of a nightmare. A million South Africans will tell you people clearly CAN get them but the cost is NOT the same as comparing the two in Merck. A million South Africans will tell you people can obtain them, but far, far above market price.

But they were infering they HAD made methaqualone?

no, they were trying to defend 2-MQ over the lack of availability of methqualone, effectively 2-MQ is as good as you're going to get because the cost to make methqualone makes it no viable given the price they'd have to charge, so eat up you 2-MQ instead

In South Africa, users smoke de wit pijp - vapourized methaqalone, like crack cocaine, concentrates in the brain. With this class, people smoke one, fall on their face, get up and do it all again.

I STRONLY recommend you don't do the same with whatever you were sold - without a GC-MS/NMR pair, it's just another 'mystery powder game' and the precursors are carcinogens so even only if left in the product in tiny amounts, do you want lung cancer?

I'm not smoking this shit

IIRC though when I looked into how 2-MQ was likely made I thought the precursors weren't likely to be carcinogens as that was 1 of the worries I had i.e. left over precursors in the pills, I thought it was o-toluidine specifically that was the concern which isn't used in 2-MQ production - think I posted it somewhere on BL ages ago but too lazy to search for it

 

[shreddedlettuce]

NOT the same as comparing the two in Merck

Pics from old non-smartphone Nokia back in the day so excuse the quality.

I think they were Merck Originals but could be mistaken.



FRONT



BACK



What is smoked in white pipes (buttons/weed/tobacco), ... is so adulterated (as mentioned by @4DQSAR), I would be surprised if there was even any real methaqualone mixed in - with all the shit they press in to make buttons/"pills"

Shared the pics for keep sake record of pharmaceutical grade from decades ago and I found it interesting to see how they packaged them too.



Sorry if off topic.
Bottom line - Dinosaur

 

[4DQSAR]

they were trying to defend 2-MQ over the lack of availability of methqualone, effectively 2-MQ is as good as you're going to get because the cost to make methqualone makes it no viable given the price they'd have to charge, so eat up you 2-MQ instead.

And there defence for not producing the seemingly accepted 'methachloroqualone'? The one homologue that data suggests IS accepted by the South African market and AFAIK isn't explicitly controlled in any nation but South Africa? Animal models suggest it is in fact a little more potent BUT models test very specific things. The rotarod test just puts them on a rotating rod and see how long it take them to fall off. It tells us something, but I am SHOCKED how many people use that as a guide to subjective human activity.

But 1 million human South Africans... that's a large if uncontrolled human trial whose data I would trust more.

Not for toxicity data but the fact that multiple laboratories were and are producing it, likely because the precursor ISN'T controlled make the de facto price lower.

 

[placebonaut]

And there defence for not producing the seemingly accepted 'methachloroqualone'? The one homologue that data suggests IS accepted by the South African market and AFAIK isn't explicitly controlled in any nation but South Africa? Animal models suggest it is in fact a little more potent BUT models test very specific things. The rotarod test just puts them on a rotating rod and see how long it take them to fall off. It tells us something, but I am SHOCKED how many people use that as a guide to subjective human activity.

But 1 million human South Africans... that's a large if uncontrolled human trial whose data I would trust more.

Not for toxicity data but the fact that multiple laboratories were and are producing it, likely because the precursor ISN'T controlled make the de facto price lower.

not quite sure of your point, do you mean it not being controlled in SA make it workable there, but it is controlled everywhere else?

 

[shreddedlettuce]

I highlighted "fourth" just for info purposes and also to address the "decline" in popularity due to the other "usual suspects" being easier to produce and cheaper etc.
It is sad that this is overlooked IMO.

If you want the full report... link below.

Source


Local surveys identify cannabis as the most widely used drug in South Africa, with Mandrax ranking fourth after methamphetamine and heroin.



Mandrax seizures in South Africa, 2009-present

Year	Location	Type of Seizure	Notes	Quantity Seized (tons)
2009	Cape Town	Powder	Linked to international syndicates	1.7
2010	Durban	Powder	Found in shipping containers	1.5
2013	Johannesburg	Tablets	Lab producing Mandrax tablets raided	1.2
2017	Port Elizabeth	Powder	Hidden in cargo containers	1.6
2020	Ballito, Durban	Powder	Warehouse raid; one of SA’s largest	3.9
2023	Cape Town	Powder + precursors	Linked to Nigerian syndicates	1
2026	Beitbridge Border Post	Powder	Concealed in truck compartments	0.7

 

[4DQSAR]

not quite sure of your point, do you mean it not being controlled in SA make it workable there, but it is controlled everywhere else?

I just meant that if we can agree to call it methachloroqualone, well, it appears to be the ONLY homologue that turned up almost as much AS real methaqualone in Mandrax buttons so likely it's the most subjectively similar to or better than methaqualone. In the crude animal models it was around 50% more active so while the precursor might cost more, you would get more buttons from a given weight of the stuff.

It was patented so evidently someone thought it had the potential to make them money.

US3162634A

Table 1, example 7. I have a feeling I've read it isn't twice as potent as the patent so the TI MAY be a bit better, but not twice that of methaqualone. But it's a patent so of course they will choose the metrics that pose their candidates in their best light,

As for prevelence, Mandrax seems to have an older user demographic and because of the extreme synthetic simplicity and how the precursor supply chain works MAY obscure the real levels of usage.

Seizure rates only shows us how many people were dumb enough to get caught. I say this because people like Greg Fleet mentioned that when they got into heroin, it was unfashionable so the only places where for a premium price buyers got solid quality were almost exclusively inhabited by older users. Like a coffee bar where the only clue was that all of the spoons had a small hole neatly drilled through them. A non-user may wander in and not even notice the behind-the-counter trade.

I don't say the above is true, only that law enforcement also has a budget so they have to choose priorities and not being in people's faces and people not dying (at least within the establishment) will mean undercounting is a definite possibility. If it's true that people go on 'missions' as they do with crack, while a button may only cost R40, If someone does in ten in an evening, that must be profitable.

I would look at hospitlizations and fatalities but even then, a user only gets to be old if they know their own limits.

 

[shreddedlettuce]

It seems that they are being mis-advertised as Quaaludes

My bad, don't know why, but missed this part when reading OP properly.


Didn't mean to derail the thread, ADHD moment I guess... , ok not a guess, definite ADHD moment that I feel I needed to correct.

A nice reminder as to why I don't post in RC threads .................... because I have sweet FA knowledge with them. 0% literally.

Damn Title needs a "?" (nah, all good).. but just wanted to say

a user only gets to be old if they know their own limits.

that this sentence resonated with me and hope it does for all, so simple yet vital no matter the substance/vice etc and one is never too old to admit it.

 

[4DQSAR]

Quāālude.

The macrons aren't just for show, they specify a long vowel sound. Now the fact that Rorer extended one macron across two letter 'a's is so people don't change tone - which would sound odd IS pretty clever.

I was quite impressed not that a US company would contact 'quiet interlude' but that the graphic designer put some thought into how to ensure both clinicians and the public would agree how to pronounce the name.

But it's a sad truth that 'Rorer and rape her' became a (very) tasteless joke and may be why William H. Rorer Inc. stopped producing the medication. A similar joke with the word 'Lemmon' in it remains extant.

 

[placebonaut]

I was quite impressed not that a US company would contact 'quiet interlude' but that the graphic designer put some thought into how to ensure both clinicians and the public would agree how to pronounce the name.

it is a bit of marketing genius isn't it, I was always quite impressed with that

But it's a sad truth that 'Rorer and rape her' became a (very) tasteless joke

fucking hell, never heard that before, sick.

and may be why William H. Rorer Inc. stopped producing the medication.

I thought the reason (urban myth?) was because it made up less than 2% of their sales but caused 98% of their headaches

A similar joke with the word 'Lemmon' in it remains extant.

I don't get it!

 

[4DQSAR]

@placebonaut - I hate to break it to you but people LIE. William H. Rorer certainly wouldn't break a sweat making the stuff and profits are profits.

All I can tell you is the moment William H. Rorer stopped producing Quāālude, the Lemmon Pharmacal Company began making them. They even made the tablets bear the same 714 marking (methaqualone being compound 714 in that original 1950s research program in India). But here's a thing - try finding a photograph of a 100 count bottle of Lemmon Phramcutical Company Mequin™. They understood that Roror got a bad name so kept their own production on the QT.

Hence my attempted meta-joke.