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Ketamine salts solubility

fastandbulbous

fastandbulbous

Bluelight Crew
Joined
Jul 29, 2004
Messages
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Can anybody give a link to, or supply data pertaining to the solubility of salts of ketamine in various solvents (water, ethanol etc) and to the appearance of the crystals formed by various salts when recrystallized from water?

Thanks in advance
 
I believe you are trying to create a ketamine drink. If not, disregard this explanation.

I have personally tried this numerous times and achieved equally intense if not more intense effects than during insufflation.

Fill up a standard 8 oz. glass of hot water about 1/4 way full. Then fill the remaining glass with orange juice. Erowid reports that Ketlar brand ketamine was soluable in water but the orange juice helps mask the flavor.

The amount of ketamine that you use is entirely up to you.

http://www.erowid.org/chemicals/ketamine/ketamine_data_sheet.shtml
 
This isn't what you want, but I've observed ketamine hcl crystals growing in water and they produced long (1-2cm), white needle-like crystals, a large forest of them from the bottom of the bottle.

PS - I'm assuming it was HCl (street ketamine...)
 
I believe you are trying to create a ketamine drink.
Click to expand...

Incorrect - next contestant!

It's actually because I had some recrystallizing out of sterile soln (or at least I think it's ketamine)
 
The Merck 13th CD edition lists minimal solubility data:

Ketamine FB: Properties: Crystals from pentane-ether, mp 92-93°.

pKa 7.5. pH of 10% aq soln 3.5.

Ketamine HCl from the Merck: White crystals, mp 262-263°. Soly in water: 20 g/100 ml.


I may have another data ref somewhere. I'll get back if I can find anything


Edit: CRC 85th lists the ketamine salt but only includes the mp, no solubility data.

Clarke's: HCl: Soluble 1 in 4 of water, 1 in 14 of ethanol and 1 in 6 of methanol; sparingly soluble in chloroform; practically insoluble in ether.
 
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specialspack said:
This isn't what you want, but I've observed ketamine hcl crystals growing in water and they produced long (1-2cm), white needle-like crystals, a large forest of them from the bottom of the bottle.

PS - I'm assuming it was HCl (street ketamine...)
Click to expand...

i used to get that happening a few years back,when i used to purchase half-litre bottles of it,there was always crystals growing at the bottom of the bottle.keeping it in the fridge would encourage it and one bottle i had had a crystal growing almost all the way to the top.this crystal,which you would get at the end,seemed to make a much longer lasting trip than the other ket in the bottle.instead of evaporating the crystal,you could just smash it up and snort it.i only ever saw this in ketamine from 99-2001.since then all the k i have seen in large bottles has had no crystal in it,no matter how cold the fridge.it was also the best k that i ever had.i still dont know what caused it,one particular brand maybe?
 
Nuke again,

This was recommended recently and I think could be a positive addition to ADD.

In this thread we will contribute short summaries of recent articles related to drugs, licit or illicit, such as biochemistry, psychopharmacology or botany. I'd encourage you to simply head to the websites of your favourite journals and browse their indexes or just to search on pubmed about topics that interest you.

I think the following format will lend well to keeping the contents of this thread organized:

1.) Title of work
2.) Authors
3.) Journal and issue number
4.) DOI reference with URL link to the article
5.) Abstract in quotes
6.) Your hopefully minimum one paragraph review commenting on your reading of the full-text article and anything exciting or fascinating you found within it.
7.) Optional: Attached pictures of some of the figures from the article

If you are having trouble accessing full-texts of papers, I would recommend you head to the local university with a flash drive and pick up whatever you want.

I would like to keep all articles within the range of the past 24 months, to keep everything recent.
--------------------------------------
Rules for sharing journal articles by Epsilon Alpha:

Several mods and users have brought up the idea of having a procedure of sharing of journal articles, and me and two of the other ADD mods have discussed this topic. As such, this is an experimental procedure to see how full text requests work out. Please leave comments/suggestions in this thread, we will do our best to make this as effective as we can; this is an experiment after all ;)

Rules
1) Do not post direct links to the paper, you can post that you are willing to send PM's of a specific paper(s) though.
2) Do not discuss the paper in the thread, make a separate thread or a relevant existing one to do so. This is to maintain an easily navigable request forum.
3) If you also would like the full text to a previously requested paper please PM the user who claims to have the fulltext or the user who requested it rather than post in the thread, however if you do not receive an answer within a reasonable time frame (~1 week) you can post a reply.
Click to expand...

Request Format
Please link the pubmed or respective hosting service as well as post the abstact in a quote.
Example:
Chronic treatment with curcumin enhances methamphetamine locomotor sensitization and cue-induced reinstatement of methamphetamine self-administration.

Zhao C, Lou Z, Zimmer B, Yu Z, Li P, Ma B, Sun Y, Huang K, Zhou W, Liu Y.
Source
Ningbo University School of Medicine, 818 Fenghua Road, Ningbo, Zhejiang 315211, PR China.
Abstract
OBJECTIVES:
Curcumin, a major active component of Curcuma longa, possesses antidepressant effects that are mediated by the 5-HT system. However, little is known about the effect of curcumin on the behavioral consequences of methamphetamine (METH).
METHODS:
The subjects were male, adult Sprague-Dawley rats. In Experiment 1, the effects of 20 and 40 mg/kg curcumin (i.p.) on response rates and breakpoints of 0.06 mg/kg/infusion METH were evaluated. In Experiment 2, rats were self-administering METH for 10 days followed by a 14-day abstinence period. During the abstinence period, the animals were treated with DMSO, 20 or 40 mg/kg curcumin. All rats were then tested for extinction responding and cue-induced reinstatement. In Experiment 3, rats were treated with DMSO, 20, or 40 mg/kg curcumin 15 min before a METH-induced locomotor activity test for 14 consecutive days. In Experiment 4, rats were pretreated with DMSO or curcumin (20 mg/kg or 40 mg/kg) for 13 days and were subsequently tested for METH-induced locomotor activity on the 14th day. In Experiment 5, three groups were tested for locomotor activity after an injection of DMSO, 20, or 40 mg/kg curcumin. The test was repeated for 14 days.
RESULTS:
Curcumin produced little effect on response rates and breakpoints maintained by METH. Chronic treatment of only 40 mg/kg curcumin during the abstinence phase enhanced cue-induced reinstatement of METH self-administration. Chronic administration of curcumin increased METH-induced sensitization of locomotor activity at the lower (20 mg/kg) but not higher (40 mg/kg) dose. However pretreatment of curcumin alone showed no significant effect on acute locomotor responses to METH and locomotor responses per se.
CONCLUSIONS:
Curcumin enhanced, rather than inhibited the behavioral effects of METH.
Copyright © 2012 Elsevier Inc. All rights reserved.
PMID: 22750063 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/22750063
Click to expand...
 
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this sounds great.
I lack expertise in the field, but i have uni journal access and would happily provide anyone with full texts.
 
Got the first and third article.
My uni lacks a subscription to Clinical Chemistry (It had a subscription, but it expired in 2005, apparently. the fuck).

How can I most easily distribute these? Clearly, they're too large for attachments on here.

ebola
 
I read it last year when it came out, it was a very good review.
 
@Smyth: Impossible to access the linked thread at ScienceMadness. Care to post a copy of the essential parts here?
 
Illicit gamma-hydroxybutyrate (GHB) and pharmaceutical sodium oxybate (Xyrem®): Differences in characteristics and misuse
Lawrence P. Cartera, Daniel Pardib, Jane Gorslinec and Roland R. Griffithsd
Drug and Alcohol Dependence 2009.04.012
http://dx.doi.org/10.1016/j.drugalcdep.2009.04.012
There are distinct differences in the accessibility, purity, dosing, and misuse associated with illicit gamma-hydroxybutyrate (GHB) compared to pharmaceutical sodium oxybate. Gamma-hydroxybutyrate sodium and sodium oxybate are the chemical and drug names, respectively, for the pharmaceutical product Xyrem® (sodium oxybate) oral solution. However, the acronym GHB is also used to refer to illicit formulations that are used for non-medical purposes. This review highlights important differences between illicit GHB and sodium oxybate with regard to their relative abuse liability, which includes the likelihood and consequences of abuse. Data are summarized from the scientific literature; from national surveillance systems in the U.S., Europe, and Australia (for illicit GHB); and from clinical trials and post-marketing surveillance with sodium oxybate (Xyrem). In the U.S., the prevalence of illicit GHB use, abuse, intoxication, and overdose has declined from 2000, the year that GHB was scheduled, to the present and is lower than that of most other licit and illicit drugs. Abuse and misuse of the pharmaceutical product, sodium oxybate, has been rare over the 5 years since its introduction to the market, which is likely due in part to the risk management program associated with this product. Differences in the accessibility, purity, dosing, and misuse of illicit GHB and sodium oxybate suggest that risks associated with illicit GHB are greater than those associated with the pharmaceutical product sodium oxybate.
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nice review paper.
 
6.) Your hopefully minimum one paragraph review commenting on your reading of the full-text article and anything exciting or fascinating you found within it.

everyone seems to be skipping this step
 
Well, my article of interest has almost hit the 24 month mark, but I still find it fascinating.

Preclinical and clinical findings indicate that a GABA(B) receptor agonist baclofen decreases cocaine use. The present study investigated the effects of the GABA(B) receptor antagonist (2S)-(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50911), the agonists baclofen and 3-aminopropyl(methyl)phoshinic acid (SKF 97541) and the allosteric positive modulator 3,5-bis(1,1-dimethylethyl-4-hydroxy-beta,beta-dimethylbenzenepropanol (CGP 7930) in cocaine-and food-maintained responding under a fixed ratio 5 schedule of reinforcement in male Wistar rats. The effects of the GABA(B) receptor ligands on cocaine (10 mg/kg)-induced discriminative stimulus in a two-lever, water-reinforced fixed ratio 20 task and on basal locomotor activity were also assessed. Baclofen (2.5-5 mg/kg), SKF 97541 (0.1-0.3 mg/kg) and CGP 7930 (30-100 mg/kg) decreased the cocaine (0.5 mg/kg/injection)-maintained responding; SCH 50911 (3-10 mg/kg) was inactive in this respect. Baclofen (5 mg/kg) and SKF 97541 (0.3 mg/kg), but not CGP 7930 or SCH 50911 attenuated the food-maintained responding. The inhibitory effects of the GABA(B) receptor agonists and the modulator were blocked by SCH 50911. SKF 97541 (0.1 mg/kg) or CGP 9730 (30-100 mg/kg) did not produce a significant shift in the cocaine (1.25-10 mg/kg) dose-response curve in a drug discrimination procedure, while baclofen (1.5 mg/kg) or SCH 50911 (10 mg/kg) attenuated the effects of separate doses of cocaine. Baclofen (5 mg/kg) and CGP 7930 (100 mg/kg) significantly reduced basal horizontal activity. We found that pharmacological stimulation of GABA(B) receptors by direct agonists or allosteric positive modulation reduces cocaine reinforcement while this property of cocaine is not related to tonic activation of GABA(B) receptors. The GABA(B) receptor stimulation-induced reduction of cocaine reinforcement was separated from its discriminative stimulus effects. Moreover, a dissociation between effects of direct GABA(B) receptor agonists and a GABA(B) allosteric positive modulator on cocaine vs. food-maintained responding was demonstrated.
Click to expand...

Filip, et. al. "Effects of GABA(B) receptor antagonist, agonists and allosteric positive modulator on the cocaine-induced self-administration and drug discrimination."
European Journal of Pharmacology, 2007 Nov 28;574(2-3):148-57.
PMID: 1769806
70448788.jpg


I'm particularly interested by Baclofen and related GABA-B agonist or positive allosteric modulators because they seem to be the first anti-craving medications, as they don't seem to affect subjective effects on cocaine. The authors explain at the end of the article that this is due to the inhibition of dopamine neurons in the VTA. I also found another reference of GABA-B localization (PMID: 14961561) that said GABA-B receptors are heavily expressed in the striatum and globus pallidus, which IIRC, are also involved with addiction. I'm excited that this could be a new area of research and focus for helping addicts, either alone or in combination with low-harm replacement therapies (methadone, bupe, etc.). I know there have been some conflicting human trials recently though, with one multi-center review saying that there was no benefit for using baclofen for cocaine addicts. I haven't looked into that review yet, but the authors suggest that the dose wasn't high enough. I'm just waiting for larger studies to come out, since most of the trials seem to enroll 40 or less people.

At the end of the article, the author mentions something about the GABA-B antagonist, SCH 50911 also reducing cocaine self-administration, which was confusing to me. Everywhere else in the article it seems as if SCH 50911 had no effect on cocaine SA, or it blocked the effects of baclofen on cocaine SA. Can anyone help explain this?

Also, I need a little help decrypting what they're talking about with the reduced food administration with the agonists. So baclofen and the positive allosteric modulators reduce food intake, but in the discussion it says that:

In contrast to the above findings, baclofen or CGP 44532 at
doses that reduced cocaine self-administration were without
significant effects on food-maintained responding on a discrete
trial procedure (Brebner et al., 1999; Roberts and Andrews, 1997)
or a multiple schedule of drug and food (Shoaib et al., 1998)in
rats.
Click to expand...

Can anyone explain how these produces are different from the fixed ratio schedules that did show a reduction in food SA?
 
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