new ketones based alcohol, no ethanol, is this for real!?

[Fertile]

You misunderstand - in no toxicology test will any research body accept 'well it's less toxic than heavy alcohol use;. The test is an absolute.

Now, if it can be shown that just 1 kavalactone is responsible for the increased risk, as long as it's not vital for subjective effects then it can be omitted. It's just that I do not see any studies in which each of the actives are tested.

But as things stand, it's very easy for a government body to simply ban the product. It seems to me like it could be a good, safe alternative but a medicine (for example) would not be licenced if it had the potential to cause liver damage. Just what that damage IS would say a lot. I mean, there are MANY medicines out there that carry such risks and for those, regular liver function tests are carried out.... but this is hardy practical.

Chemically they are only modestly complex, the pain being that several are chiral. In fact, it looks like several of them can actually swap from R to S and maybe that is the source of toxicity i.e. when fresh and natural, it's safe but stored for a long time, it's not.

Believe me, I would LOVE this to be legal but it has to be a natural compound (or at least it has to be found naturally) but long experience has taught me that the BEST way to stay under the wire is happy, healthy customers.

I mean, wouldn't it be lovely if one could extract khat and make it into a vape! Vape technology is maturing but people simply will not pay huge sums and so you need to keep a close eye on costs.

 

[Neuroborean]

You misunderstand - in no toxicology test will any research body accept 'well it's less toxic than heavy alcohol use;. The test is an absolute.

Now, if it can be shown that just 1 kavalactone is responsible for the increased risk, as long as it's not vital for subjective effects then it can be omitted. It's just that I do not see any studies in which each of the actives are tested.

But as things stand, it's very easy for a government body to simply ban the product. It seems to me like it could be a good, safe alternative but a medicine (for example) would not be licenced if it had the potential to cause liver damage. Just what that damage IS would say a lot. I mean, there are MANY medicines out there that carry such risks and for those, regular liver function tests are carried out.... but this is hardy practical.

Chemically they are only modestly complex, the pain being that several are chiral. In fact, it looks like several of them can actually swap from R to S and maybe that is the source of toxicity i.e. when fresh and natural, it's safe but stored for a long time, it's not.

Believe me, I would LOVE this to be legal but it has to be a natural compound (or at least it has to be found naturally) but long experience has taught me that the BEST way to stay under the wire is happy, healthy customers.

I mean, wouldn't it be lovely if one could extract khat and make it into a vape! Vape technology is maturing but people simply will not pay huge sums and so you need to keep a close eye on costs.

What I'm saying is this:

"

ava and liver damage​

The suggestion that kava damages the liver, first surfaced in early 2000 following reports in Western Europe that 83 patients taking kava tablets died (Schmidt et al., 2005). This led to what is commonly known as the European Kava Ban. At the time of the ban, European doctors were estimated to have been prescribing 70 million (tablet) doses of kava daily, with most of this supplied for alleviating anxiety symptoms (Schmidt et al., 2005: 186). The withdrawal of kava from the European markets led to a 12-year court battle which was not resolved until 2014 by the Federal Court of Germany. The final ruling by the Court was that it was unlikely kava had caused the reported deaths, and that liver damage from kava was so rare it was negligible. The Court rejected claims of liver damage caused by kava, and specified that these assertions were a gross misrepresentation of the possible effects (Kuchta et al., 2015; Schmidt, 2014).

Kava and liver damage – The medical evidence​

Showman et al. (2015) provide a valuable review of the kava hepatotoxicity claim and counter claim literature (60–61) which includes potential ‘Mechanisms of toxicity’ (61–63). They summarize that although there is evidence of a link between ‘kava and liver toxicity demonstrated in vivo and in vitro, in the history of Western kava use, toxicity is still considered relatively rare. Only a fraction of the handful of cases reviewed for liver toxicity could be, with any certainty, linked to kava consumption and most of those involved the co-ingestion of other medications/supplements. That means that the incident rate of liver toxicity due to kava is one in 60–125 million patients’ (65).
Singh (2014) discusses additional potential mechanisms of toxicity; adulterants added to kava to artificially boost weight to increase sale profit. This can include ‘sawdust, flour, and the dregs from the extraction of sugarcane’ (42). As Aporosa warned in a recent radio interview, exporters who engage in this type of unethical practice are playing a risky game, one that could have widespread implications should the adulterant contain bacteria, ‘salmonella for instance, and if someone gets sick … this could threaten kava importation’ as it will be ‘kava’ that will be cited as the health threat and not the adulterant (Kumar et al., 2018, interview: 45 seconds).3"


And about your paper:

"Linked to concerns of kava hepatotoxicity is an increase in gamma-glutamyl transpeptidase (GGT) levels in the blood following kava use. In their article, Moulds and Malani (2003) first addressed this matter in 2003 when they asked rhetorically: ‘How relevant is the finding that some … heavy kava drinkers have raised serum GGT levels?’, responding: ‘raised GGT levels do not necessarily imply “subclinical” liver toxicity’ (452). When questioned by the author in 2009 about their subclinical liver toxicity comment, former Dean of Fiji School of Medicine, Professor Robert Moulds, commented that the abnormalities can be a concern among doctors who may not be conversant with liver function tests of kava drinkers, pointing to his colleagues article: ‘while elevated GGT and white blood cells [lymphocytes] were abnormal [to those unfamiliar with kava's effects on the liver], this does not mean that this abnormality is of concern’ (Malani, 2002: 7). Mantesso (2016) also confirms that, kava ‘may throw out the liver function a little bit, altering liver enzymes. Now that's not necessarily saying it's causing liver damage.’ Moreover, Evans (2009) explains that ‘nonsteroidal anti-inflammatory drugs, lipid-lowering drugs, antibiotics, histamine blockers (used to treat excess stomach acid production), antifungal agents, seizure medication, antidepressants, and hormones such as testosterone’, can elevate GGT levels, although these continue to be routinely prescribed (24)."

The fact that EVEN the WHO are trying to help for making it fully legal surely means is not rat poison or seriously harmful as cathinones or even alcohol.
Later in the paper:

"To assist in safeguarding kava quality, the World Health Organization (WHO) and UN have developed a Kava Codex Alimentarius Quality Standard which should be in place by 2020. Commenting on this Codex, Vanuatu kava expert Dr Vincent Lebot stated Tonga, Fiji, Samoa and Vanuatu were also seeking to register the word ‘kava’ as a traditional beverage associated with

healthy and safe raw materials used to prepare the beverage … kava is banned in the EU and banned in Australia and we believe this is due to a major misunderstanding regarding what kava is … We want to promote kava for what it is, a very healthy traditional beverage … If some companies elsewhere want to extract the active ingredients and prepare some capsules or whatever, this is not called kava any more. Like if you put caffeine in a capsule, you cannot call it coffee; if you put in dry raisin peel, you cannot call it wine, and same for tea. Kava is kava; it is the traditional beverage prepared by cold water extraction of the ground organs of the plant Piper Methysticum, and nothing else. We want to protect the geographical origins and the healthy quality kava plants we use here on an original basis. (Blades, 2018; also see Procyk and Lebot, 2013)"


I would love to find khat, never tried, probably I need to find a vendor of seeds or live plants and get it, I love agriculture and plants so it should be not very difficult for me, hope so. Nothing better than have your own sources, (being your own source). BTW, I think khat has quite a bunch of science against it, I don't if it's bad science or what, but seems to happen that it has bad reputation, similar to betel nut...

 

[izo]

Well liver damage has been recorded in the natives who harvest it themselves.

i read that liver damage occured in users of a pharmaceutical extract sold in pharmacies over here, therefore it got pulled of the shelves. i also read many times that these extract produced no central effects, contrary to real kava.

 

[Fertile]

What I'm saying is this:

"

ava and liver damage​

The suggestion that kava damages the liver, first surfaced in early 2000 following reports in Western Europe that 83 patients taking kava tablets died (Schmidt et al., 2005). This led to what is commonly known as the European Kava Ban. At the time of the ban, European doctors were estimated to have been prescribing 70 million (tablet) doses of kava daily, with most of this supplied for alleviating anxiety symptoms (Schmidt et al., 2005: 186). The withdrawal of kava from the European markets led to a 12-year court battle which was not resolved until 2014 by the Federal Court of Germany. The final ruling by the Court was that it was unlikely kava had caused the reported deaths, and that liver damage from kava was so rare it was negligible. The Court rejected claims of liver damage caused by kava, and specified that these assertions were a gross misrepresentation of the possible effects (Kuchta et al., 2015; Schmidt, 2014).

Kava and liver damage – The medical evidence​

Showman et al. (2015) provide a valuable review of the kava hepatotoxicity claim and counter claim literature (60–61) which includes potential ‘Mechanisms of toxicity’ (61–63). They summarize that although there is evidence of a link between ‘kava and liver toxicity demonstrated in vivo and in vitro, in the history of Western kava use, toxicity is still considered relatively rare. Only a fraction of the handful of cases reviewed for liver toxicity could be, with any certainty, linked to kava consumption and most of those involved the co-ingestion of other medications/supplements. That means that the incident rate of liver toxicity due to kava is one in 60–125 million patients’ (65).
Singh (2014) discusses additional potential mechanisms of toxicity; adulterants added to kava to artificially boost weight to increase sale profit. This can include ‘sawdust, flour, and the dregs from the extraction of sugarcane’ (42). As Aporosa warned in a recent radio interview, exporters who engage in this type of unethical practice are playing a risky game, one that could have widespread implications should the adulterant contain bacteria, ‘salmonella for instance, and if someone gets sick … this could threaten kava importation’ as it will be ‘kava’ that will be cited as the health threat and not the adulterant (Kumar et al., 2018, interview: 45 seconds).3"


And about your paper:

"Linked to concerns of kava hepatotoxicity is an increase in gamma-glutamyl transpeptidase (GGT) levels in the blood following kava use. In their article, Moulds and Malani (2003) first addressed this matter in 2003 when they asked rhetorically: ‘How relevant is the finding that some … heavy kava drinkers have raised serum GGT levels?’, responding: ‘raised GGT levels do not necessarily imply “subclinical” liver toxicity’ (452). When questioned by the author in 2009 about their subclinical liver toxicity comment, former Dean of Fiji School of Medicine, Professor Robert Moulds, commented that the abnormalities can be a concern among doctors who may not be conversant with liver function tests of kava drinkers, pointing to his colleagues article: ‘while elevated GGT and white blood cells [lymphocytes] were abnormal [to those unfamiliar with kava's effects on the liver], this does not mean that this abnormality is of concern’ (Malani, 2002: 7). Mantesso (2016) also confirms that, kava ‘may throw out the liver function a little bit, altering liver enzymes. Now that's not necessarily saying it's causing liver damage.’ Moreover, Evans (2009) explains that ‘nonsteroidal anti-inflammatory drugs, lipid-lowering drugs, antibiotics, histamine blockers (used to treat excess stomach acid production), antifungal agents, seizure medication, antidepressants, and hormones such as testosterone’, can elevate GGT levels, although these continue to be routinely prescribed (24)."

The fact that EVEN the WHO are trying to help for making it fully legal surely means is not rat poison or seriously harmful as cathinones or even alcohol.
Later in the paper:

"To assist in safeguarding kava quality, the World Health Organization (WHO) and UN have developed a Kava Codex Alimentarius Quality Standard which should be in place by 2020. Commenting on this Codex, Vanuatu kava expert Dr Vincent Lebot stated Tonga, Fiji, Samoa and Vanuatu were also seeking to register the word ‘kava’ as a traditional beverage associated with

healthy and safe raw materials used to prepare the beverage … kava is banned in the EU and banned in Australia and we believe this is due to a major misunderstanding regarding what kava is … We want to promote kava for what it is, a very healthy traditional beverage … If some companies elsewhere want to extract the active ingredients and prepare some capsules or whatever, this is not called kava any more. Like if you put caffeine in a capsule, you cannot call it coffee; if you put in dry raisin peel, you cannot call it wine, and same for tea. Kava is kava; it is the traditional beverage prepared by cold water extraction of the ground organs of the plant Piper Methysticum, and nothing else. We want to protect the geographical origins and the healthy quality kava plants we use here on an original basis. (Blades, 2018; also see Procyk and Lebot, 2013)"


I would love to find khat, never tried, probably I need to find a vendor of seeds or live plants and get it, I love agriculture and plants so it should be not very difficult for me, hope so. Nothing better than have your own sources, (being your own source). BTW, I think khat has quite a bunch of science against it, I don't if it's bad science or what, but seems to happen that it has bad reputation, similar to betel nut...

Many thanks for your EXCELLENT work. Just what I needed. Do you know, perchance, what dose of the kavalactones are involved to get the sought for subjective effects.

Izo - I don't think anyone is purposefully poisoning or even cutting the stuff. It sounds like the stuff either isn't stable (and protecting would be fun) OR it's packaged in a manner that produces a hepatotoxic compound. After all, one thing I think we ALL see is that water is removed to reduce mass.

Lactone undergoes hydrolysis is acidic conditions. It undergoes a different hydrolysis in neutral or alkali condition. It also undergoes decomposition when heated. It is this latter option that seems the MOST likely. After all, one could apply quite a small amount of heating if performed under a hard vaccum.

I am lucky to have access to a vacuum pump that will produce a hard (7 millibar) vacuum on a volume of 200L. I think it reasonable to suggest that this is, without a doubt, sufficient.

Now, let us consider why these kavalactones are active. It looks comples but GABAa affinity is most certainly 1 action. I note that all 6 are liopphilic and THAT is useful when designing a route to extract the actives.

6 hosted at ImgBB

Image 6 hosted in ImgBB

ibb.co

What they all have is a conjugated ketone moiety stabilized with a -OCH3. Now, let me ask a simple question. If O-demethylation occurs, what happens? Well, I would argue dehydration with the double-bond seen in methystictin & 5,6-dedihydrokavain forming. I cannot point to it and say 'behold, toxin' but it does result in the 4 chiral compounds becoming achiral. And, as you know, I've always been keen to point out that chiral compounds are, in fact, a mixture of 2 different compounds.

Now, liver toxicity seems to be connected to alcohol consumption so let's consider CYP2E1. It's complex because:

Toxicity of Kava Kava

Kava is a traditional beverage of various Pacific Basin countries. Kava has been introduced into the mainstream U.S. market principally as an anti-anxiety preparation. The effects of the long-term consumption of kava have not been documented adequately. ...

www.ncbi.nlm.nih.gov

And so one has to wonder if ethanol or indeed another common food/drink produces the toxic species. Most certainly the rupture of the MD bridge opens a whole spate of possible toxins. I think the evidence suggests that alcohol and kavalactones is BAD,

What is VERY telling is that the peoples native to the areas in which kava lactones occur are much less likely to suffer organ damage. This isn't as new idea and indeed whole classes of medicine have reached phase II or even phase III trials before their toxicity was identified.

If it were an increased risk then people could be warned and take appropriate action but we are seeing total liver failure.

Kava Kava - LiverTox - NCBI Bookshelf

Just to be clear, toxicity is RARE and as I have said, a good medicine with such a risk would simply require frequent liver function tests and yet a herbal medicine cannot possibly hope for people to take such tests. As such, it's vital to find the toxic species. A ray of light is that sources suggest that it is the preparation of Kava that is responsible for the toxicity.

That is why it's important to discover which of these compounds (or metabolites thereof) that pose a risk. Believe you me, it's going to require preparative chromatography to isolate each compound. Now, conveniently this can be carried out on the Kg scale and any company with the kit can do it quite quickly but I am left with aa specific question.

Just how much Kava Kava (specifically how much of each lactone) represents a dose? If it's hundreds of mg then game over but if it's active at 20-30mg then it's worth going through the pain to extract a safe and effective product.

There are quite a number of herbal compounds (used in traditional herbal medicine and/or Chinese herbam medicine) that the law seems to ignore. I mean, khat is an obvious one but one could go utterly crazy an use Phalaris, Delosperma, Acacia, Desmodium, Mimosa, Virola, and Psychotria plant sources. In fact, I am seriously wondering if one could feed these plants (2S)-2-amino-3-(7-methyl-1H-indol-3-yl)propanoic acid so that in the fullness of time they would produce 7,N,N-TMT.

I did get to sample this last compounds and although the taste was even worse than the usual, it DID have a more friendly feel because, I guess, it's also quite a potent serotonin releaser and so ones mood after it subsided was VERY positivr.

And daft stuff like khat and arecoline from Betel Nut.

As far as I can tell, as long as something natural is covered by THM or CHM conventions, the law will not intercede. I mean, the Chinese use pseudoephedrine and yet I haven't seen a single case of them being arrested for doing so.

So all I seek is something 1)safe 2)legal 3)non dependance forming.

It would be lovely to supply 7-OH mitragynine but that tertiary -OH will dehydrate readily and esters are inactive.

WHY is 7-OH mitragynine so active. I don't know. Well, Page 246 of Opiate Chemistry & Receptors shows that the ring-system with the N is active and my guess is that the o-O-CH3 & 7-OH interact. If one looks at the 6-OCH3 and the secondary -OH next to it in etorphine, that hydrogen-bond is vital. Remove the 6 -OCH3 and potency is 1/12 of the parent. But it's so unstable. That is why the picrate is the addition salt. A haloacid with haloganate, other strong acids with dehydrate and so one needs an acid that will not donate but will form a stable salt. I mean, picric acid is 2,4,6-trinitrophenol and you cannot get much more potent.

Why oh why are these things so complex ;-)

 

[S.J.B.]

No, this is a related compound. The problem with the stuff Cook et al came up with was duration and selectivity.

I used a triazolo ring (so no a1 affinity) and a 2-pyridiyl as the pendant aromatic (to prevent metabolism - it's excreted unchanged). I didn't go for a chiral 3 substituent or an ester moiety. It's the ester that results in short duration.

I did talk to Cook and he didn't cover the same ground as me. After all, our aims were different. My work was for Imperial Collage London and since it's patented, I suggest it isn't covered by Cooks's work.

The compound you've drawn is exactly the compound SH-TRI-108 which is shown on page 649 of the thesis I linked. Here is a later Cook paper in which it appears.

Care to share the patent you're referring to?

 

[allone]

the best ethanol replacement ive found has by far been ghb. its many times more euphoric than alcohol, no hangover, no calories more importantly. but cant go overboard on dosing or w/ds come quick with rebound anxiety and its hell. ive tried 1.4bdo and found it feels very dirty in the body and left me with a headache after one dose, no where near as clean feeling as ghb. its worth the search

ok, how do i get GHB??

 

[Fertile]

It's value is so low that mostly people just make it themselves.

GHB Synthesis FAQ

www.designer-drug.com

 

[Neuroborean]

Many thanks for your EXCELLENT work. Just what I needed. Do you know, perchance, what dose of the kavalactones are involved to get the sought for subjective effects.

Izo - I don't think anyone is purposefully poisoning or even cutting the stuff. It sounds like the stuff either isn't stable (and protecting would be fun) OR it's packaged in a manner that produces a hepatotoxic compound. After all, one thing I think we ALL see is that water is removed to reduce mass.

Lactone undergoes hydrolysis is acidic conditions. It undergoes a different hydrolysis in neutral or alkali condition. It also undergoes decomposition when heated. It is this latter option that seems the MOST likely. After all, one could apply quite a small amount of heating if performed under a hard vaccum.

I am lucky to have access to a vacuum pump that will produce a hard (7 millibar) vacuum on a volume of 200L. I think it reasonable to suggest that this is, without a doubt, sufficient.

Now, let us consider why these kavalactones are active. It looks comples but GABAa affinity is most certainly 1 action. I note that all 6 are liopphilic and THAT is useful when designing a route to extract the actives.

6 hosted at ImgBB

Image 6 hosted in ImgBB

ibb.co

What they all have is a conjugated ketone moiety stabilized with a -OCH3. Now, let me ask a simple question. If O-demethylation occurs, what happens? Well, I would argue dehydration with the double-bond seen in methystictin & 5,6-dedihydrokavain forming. I cannot point to it and say 'behold, toxin' but it does result in the 4 chiral compounds becoming achiral. And, as you know, I've always been keen to point out that chiral compounds are, in fact, a mixture of 2 different compounds.

Now, liver toxicity seems to be connected to alcohol consumption so let's consider CYP2E1. It's complex because:

Toxicity of Kava Kava

Kava is a traditional beverage of various Pacific Basin countries. Kava has been introduced into the mainstream U.S. market principally as an anti-anxiety preparation. The effects of the long-term consumption of kava have not been documented adequately. ...

www.ncbi.nlm.nih.gov

And so one has to wonder if ethanol or indeed another common food/drink produces the toxic species. Most certainly the rupture of the MD bridge opens a whole spate of possible toxins. I think the evidence suggests that alcohol and kavalactones is BAD,

What is VERY telling is that the peoples native to the areas in which kava lactones occur are much less likely to suffer organ damage. This isn't as new idea and indeed whole classes of medicine have reached phase II or even phase III trials before their toxicity was identified.

If it were an increased risk then people could be warned and take appropriate action but we are seeing total liver failure.

Kava Kava - LiverTox - NCBI Bookshelf

Just to be clear, toxicity is RARE and as I have said, a good medicine with such a risk would simply require frequent liver function tests and yet a herbal medicine cannot possibly hope for people to take such tests. As such, it's vital to find the toxic species. A ray of light is that sources suggest that it is the preparation of Kava that is responsible for the toxicity.

That is why it's important to discover which of these compounds (or metabolites thereof) that pose a risk. Believe you me, it's going to require preparative chromatography to isolate each compound. Now, conveniently this can be carried out on the Kg scale and any company with the kit can do it quite quickly but I am left with aa specific question.

Just how much Kava Kava (specifically how much of each lactone) represents a dose? If it's hundreds of mg then game over but if it's active at 20-30mg then it's worth going through the pain to extract a safe and effective product.

There are quite a number of herbal compounds (used in traditional herbal medicine and/or Chinese herbam medicine) that the law seems to ignore. I mean, khat is an obvious one but one could go utterly crazy an use Phalaris, Delosperma, Acacia, Desmodium, Mimosa, Virola, and Psychotria plant sources. In fact, I am seriously wondering if one could feed these plants (2S)-2-amino-3-(7-methyl-1H-indol-3-yl)propanoic acid so that in the fullness of time they would produce 7,N,N-TMT.

I did get to sample this last compounds and although the taste was even worse than the usual, it DID have a more friendly feel because, I guess, it's also quite a potent serotonin releaser and so ones mood after it subsided was VERY positivr.

And daft stuff like khat and arecoline from Betel Nut.

As far as I can tell, as long as something natural is covered by THM or CHM conventions, the law will not intercede. I mean, the Chinese use pseudoephedrine and yet I haven't seen a single case of them being arrested for doing so.

So all I seek is something 1)safe 2)legal 3)non dependance forming.

It would be lovely to supply 7-OH mitragynine but that tertiary -OH will dehydrate readily and esters are inactive.

WHY is 7-OH mitragynine so active. I don't know. Well, Page 246 of Opiate Chemistry & Receptors shows that the ring-system with the N is active and my guess is that the o-O-CH3 & 7-OH interact. If one looks at the 6-OCH3 and the secondary -OH next to it in etorphine, that hydrogen-bond is vital. Remove the 6 -OCH3 and potency is 1/12 of the parent. But it's so unstable. That is why the picrate is the addition salt. A haloacid with haloganate, other strong acids with dehydrate and so one needs an acid that will not donate but will form a stable salt. I mean, picric acid is 2,4,6-trinitrophenol and you cannot get much more potent.

Why oh why are these things so complex ;-)

Are you a chemist?
don't get me wrong but I read all this stuff and I hope you're a chemist or bio-molecular engineer, otherwise you're a very wise guy to learn all that on your own, but it's not specially easy to follow for those who are not yet into that level of biochemical rumbliness

 

[Skorpio]

ok, how do i get GHB??

Drug dealers. Please don't ask how to source drugs here.

 

[izo]

Kava kava: examining new reports of toxicity

Before 1998, extracts of kava kava, Piper methysticum, were considered to be very safe alternatives to anxiolytic drugs and to possibly exert a wide r…

www.sciencedirect.com

 

[Fertile]

Kava kava: examining new reports of toxicity

Before 1998, extracts of kava kava, Piper methysticum, were considered to be very safe alternatives to anxiolytic drugs and to possibly exert a wide r…

www.sciencedirect.com

Has anyone actually extracted the kavalactones to get some idea of the dose range? I have to admit that the chemistry behind this class is beyond me. I'm one of those people who begins with the basic nitrogen and works outwards. Metabolites would also be very useful.

1 hosted at ImgBB

Image 1 hosted in ImgBB

ibb.co

 

[Fertile]

1 hosted at ImgBB

Image 1 hosted in ImgBB

ibb.co

Well, it has to be said that those diones do not look to friendly. No O-demethylation which is interesting.

But as I said, if 25mg is a dose, that's one thing, if it's 400mg then it's quite another.

 

[allone]

Drug dealers. Please don't ask how to source drugs here.

drug dealers sell cocaine and heroin, or xanax and extasy pills mostly. i dont think drug dealers, any of the ones that are popular can carry such obscure shit. hence why i asked, where to find it for real??

 

[Skorpio]

drug dealers sell cocaine and heroin, or xanax and extasy pills mostly. i dont think drug dealers, any of the ones that are popular can carry such obscure shit. hence why i asked, where to find it for real??

I was being glib. Let me be blunt: it is against the rules of bluelight to ask where to find drugs.

 

[Fertile]

I was being glib. Let me be blunt: it is against the rules of bluelight to ask where to find drugs.

We have mods to decide when someone has overstepped the mark. Since my information is CLEARLY in the public domain, it hardly constitutes passing on 'secret' information.

But by all means, make an official complaint.

You have most certainly passed on references that DO constitute information almost nobody knows of.... so in reality, you have aided the development of novel compounds far, far more than this thread.

As a rule - those who can, do. Those who can't complain.

 

[new2drugs]

wow so many negative views on this. maybe thats why it hasnt caught up in the market and its sold nowhere.
but anyway, im desperately looking for altenarnatives to alcohol. and if you guys cannot help and bring me some suggestions, i have no choice but to go after this. :/

already ordered sampler btw. will see how it goes.
but seriously, instead of being so critical, try to help out a fucka out here, bring me alternatives! thanks. or just stfu

This Scientist Claims He's Created an "Alcohol" That Doesn't Give You a Hangover

Has science finally produced the perfect high?

www.menshealth.com

Few years time I'm waiting on this mate. I also need an alternative to alcohol.

Their botanical one (sentia) doesn't do anything for me

 

[new2drugs]

The one I designed (and is now patented AFAIK) was sold to Dr. Nutt. But, as I said, pyeyzolam is good at emulating 'drunk' but not at emulating 2 glasses of wine. That problem has now been solved but the solution has NOT been sold. It's important when producing an alcohol mimic for it to mimic all levels and so it took quite some time just to get it down to 2 compounds... getting it down to 1 is the key.

What do you mean the product has now solved. By David Nutt?