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Ketamine salts solubility

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I am mostly interested in organic chemistry and my interest in pharmacology is a result of this and my interest in how our whole world works like. I've recently started studying chemistry again. I had a 3-year break due to various health problems and I didn't manage to get a master's degree. I even started studying IT during the break, but I quit it when I realised chemistry is my biggest passion and I want to learn it because it simply makes me happy. I don't really care about the money I could earn in the future, it's not a factor at all, but I'm definitely not a person who would accept an underpayment. I seriously consider staying at some university but I still have plenty of time and perhaps I will have a better opportunity to research. As I was thinking about it a few days ago, it made me kind of scared when I realised I actually hadn't planned studying chemistry again. It would be such a shame because studying IT didn't make me happy at all, it was such a tiresome duty. I'm really glad I've started changing my life so I can live the way I've always wanted. The past doesn't matter but the knowledge got through past experiences.

Why are you nervous to reveal what you study? :>
 
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adder said:
Why are you nervous to reveal what you study? :>
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Because this is a recreational drug use board, although hopefully its fairly obvious to an outside observer that I am here for the information alone (don't even use anything but alcohol any more).
 
All right, that's fine. :) Although I used to be very addicted to opioids and benzodiazepines, and I am still on Suboxone, I don't study chemistry to work in shady business. Chemistry is such a broad science that there is a lot of interesting stuff completely unrelated to psychoactive substances one may do with it. I explain this to every person who looks at me suspiciously when I mention I study chemistry.
 
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Because this is a recreational drug use board, although hopefully its fairly obvious to an outside observer that I am here for the information alone (don't even use anything but alcohol any more).
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This is a harm reduction forum

Nothing technically shady about that ;)
 
This thread has been dormant for a while so here is some new developments in the 5-HT2A field:

Bill Fantegrossi has tested the purportedly 100-fold selective 5-HT2A agoanist 25CN-NBOMe in mice
Hallucinogen-like effects of 2-([2-(4-cyano-2,5-dimethoxyphenyl) ethylamino]methyl)phenol (25CN-NBOH), a novel N-benzylphenethylamine with 100-fold selectivity for 5-HT2A receptors, in mice.

RATIONALE:2-([2-(4-cyano-2,5-dimethoxyphenyl)ethylamino]methyl)phenol (25CN-NBOH) is structurally similar to N-benzyl substituted phenethylamine hallucinogens currently emerging as drugs of abuse. 25CN-NBOH exhibits dramatic selectivity for 5-HT2A receptors in vitro, but has not been behaviorally characterized.OBJECTIVE: 25CN-NBOH was compared to the traditional phenethylamine hallucinogen R(-)-2,5-dimethoxy-4-iodoamphetamine (DOI) using mouse models of drug-elicited head twitch behavior and drug discrimination. METHODS: Drug-elicited head twitches were quantified for 10 min following administration of various doses of either DOI or 25CN-NBOH, with and without pretreatments of 0.01 mg/kg 5-HT2A antagonist M100907 or 3.0 mg/kg 5-HT2C antagonist RS102221. The capacity of 25CN-NBOH to attenuate DOI-elicited head twitch was also investigated. Mice were trained to discriminate DOI or M100907 from saline, and 25CN-NBOH was tested for generalization. RESULTS: 25CN-NBOH induced a head twitch response in the mouse that was lower in magnitude than that of DOI, blocked by M100907, but not altered by RS102221. DOI-elicited head twitch was dose-dependently attenuated by 25CN-NBOH pretreatment. 25CN-NBOH produced an intermediate degree of generalization (55 %) for the DOI training dose, and these interoceptive effects were attenuated by M100907. Finally, 25CN-NBOH did not generalize to M100907 at any dose, but ketanserin fully substituted in these animals. CONCLUSIONS: 25CN-NBOH was behaviorally active, but less effective than DOI in two mouse models of hallucinogenic effects. The effectiveness with which M100907 antagonized the behavioral actions of 25CN-NBOH strongly suggests that the 5-HT2A receptor is an important site of agonist action for this compound in vivo.
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Dave Nichols made a bunch N-benzyl tryptamines and compared them to N-benzyl phenethylaminesa
N-Benzyl-5-methoxytryptamines as Potent Serotonin 5-HT2 Receptor Family Agonists and Comparison with a Series of Phenethylamine Analogues

A series of N-benzylated-5-methoxytryptamine analogs was prepared and investigated, with special emphasis on substituents in the meta position of the benzyl group. A parallel series of several N-benzylated analogs of 2,5-dimethoxy-4-iodophenethylamine (2C-I) also was included for comparison of the two major templates (i.e., tryptamine and phenethylamine). A broad affinity screen at serotonin receptors showed that most of the compounds had highest affinity at the 5-HT2 family receptors. Substitution at the para-position of the benzyl group resulted in reduced affinity, whereas substitution in either the ortho or meta position enhanced affinity. In general, introduction of a large lipophilic group improved affinity, whereas functional activity often followed the opposite trend. Tests of the compounds for functional activity utilized intracellular Ca2+ mobilization. Function was measured at the human 5-HT2A, 5-HT2B, and 5-HT2C receptors, as well as at the rat 5-HT2A and 5-HT2C receptors. There was no general correlation between affinity and function. Several of the tryptamine congeners were very potent functionally (EC50 values from 7.6 to 63 nM), but most were partial agonists. Tests in the mouse head twitch assay revealed that many of the compounds induced the head twitch, and there was a significant correlation between this behavior and functional potency at the rat 5-HT2A receptor.
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Martin Hansen made a bunch of new N-heterocyclic phenethylamines
Synthesis and pharmacological evaluation of N-benzyl substituted 4-bromo-2,5-dimethoxyphenethylamines as 5-HT2A/2C partial agonists

N-benzyl substitution of phenethylamine 5-HT2A receptor agonists has dramatic effects on binding affinity, receptor selectivity and agonist activity. In this paper we examine how affinity for the 5-HT2A/2C receptors are influenced by N-benzyl substitution of 4-bromo-2,5-dimethoxyphenethylamine derivatives. Special attention is given to the 2’ and 3’-position of the N-benzyl as such compounds are known to be very potent. We found that substitutions in these positions are generally well tolerated. The 2’-position was further examined using a range of substituents to probe the hydrogen bonding requirements for optimal affinity and selectivity, and it was found that small changes in the ligands in this area had a profound effect on their affinities. Furthermore, two ligands that lack a 2’-benzylsubstituent was also found to have high affinity contradicting previous held notions. Several high-affinity ligands were identified and assayed for functional activity at the 5-HT2A and 5-HT2C receptor, and they were generally found to be less efficacious agonists than previously reported N-benzyl phenethylamines.
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I've transferred into a serious agoraphobe hermit so irony not withstanding being the creator of this social environment, I'm mixed in the feeling department.

You cat's keep cooking, clasping, grasping, and flip-brewing complex compounds for catatonic catostraphic calamitous cool.

Please. You're doing gods work.
 
fitting, though, that this is perhaps the least social of all social threads.

if this thread continues filling up at the current average rate of posts since its creation, then it will not hit the end of page 40 for another 16 and a half years.
 
'Darwinian' test uncovers an antidepressant's hidden toxicity

The organismal performance assay detects subtle toxic effects by subjecting mice to a relentless, Darwinian competition for food, shelter and mates. If there is a defect in any physiological system, it is more likely to stand out if test animals have to compete for resources, scientists say.
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http://www.sciencedaily.com/releases/2014/12/141215094147.htm

i clicked that link in the article and couldn't open the actual journal. if that link works in anybodies browser could you post the full abstract?

Abstract
Paroxetine is a selective serotonin reuptake inhibitor (SSRI) that is currently available on the market and is suspected of causing congenital malformations in babies born to mothers who take the drug during the first trimester of pregnancy. We utilized organismal performance assays (OPAs), a novel toxicity assessment method, to assess the safety of paroxetine during pregnancy in a rodent model. OPAs utilize genetically diverse wild mice (Mus musculus) to evaluate competitive performance between experimental and control animals as they compete among each other for limited resources in semi-natural enclosures. Performance measures included reproductive success, male competitive ability and survivorship. Paroxetine-exposed males weighed 13% less, had 44% fewer offspring, dominated 53% fewer territories and experienced a 2.5-fold increased trend in mortality, when compared with controls. Paroxetine-exposed females had 65% fewer offspring early in the study, but rebounded at later time points, presumably, because they were no longer exposed to paroxetine. In cages, paroxetine-exposed breeders took 2.3 times longer to produce their first litter and pups of both sexes experienced reduced weight when compared with controls. Low-dose paroxetine-induced health declines detected in this study that were undetected in preclinical trials with doses 2.5–8 times higher than human therapeutic doses. These data indicate that OPAs detect phenotypic adversity and provide unique information that could be useful towards safety testing during pharmaceutical development.
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Hey, long time no see!

Its been a busy year and a half for me, been working hard at medical school and trying to travel abroad as much as possible during my breaks. How's everyone been in my absence? Over this last year I've been narrowing down the medical specialties I'm interested in pursuing, I think I've got it down to: rural family medicine, emergency medicine, and internal medicine (oncology/rheumatology). Things are going quite well on my end overall, celebrating the 3 year anniversary with the girlfriend in just over a week and just bought my first place. Heck, I've even got my sleep disorder nearly sorted out with careful lifestyle management. I'm still a little paranoid about the whole NSA thing, but I feel that they've got better things to do than scope me out. Don't think I'll be posting much as I'm extremely busy these days, but definitely will be doing some lurking to see what topics have come up over the last while!

How are you guys doing?

Best,
EA
 
What's up EA, glad to hear your studies are going so well!

How do you like the new season of Archer?
 
Thanks endo!

I'm liking it, Archer Vice was good but they shouldn't have pulled an entire season out of that concept. What do you think?
 
I've been told I'm a bit like a less crazy Krieger...I'll take it.

ebola
 
I love this season, still the best show on television, although I don't like how they had to give "ISIS" back to the terrorists :p
 
I would have thought that keeping the name ISIS would have benefited marketing of the show's merchandise. They also could have responded in-show...like have ISIS take on ISIS/ISIL in a battle over the name. I'd watch that.

To be perfectly honest, I haven't gotten into the show that much, but I think I just need to be steered toward good episodes and am currently open to suggestions.

ebola
 
^That's what I thought about the whole ISIS situation! But I guess the creators didn't want to give free press to terrorists, which...fair.

I really liked the three part pirate mini series before last season, you should check those out.
 
5-HT(2B) receptors are required for serotonin-selective antidepressant actions.
Diaz SL 2012
http://www.ncbi.nlm.nih.gov/pubmed/25342944
The therapeutic effects induced by serotonin-selective reuptake inhibitor (SSRI) antidepressants are initially triggered by blocking the serotonin transporter and rely on long-term adaptations of pre- and post-synaptic receptors. We show here that long-term behavioral and neurogenic SSRI effects are abolished after either genetic or pharmacological inactivation of 5-HT(2B) receptors. Conversely, direct agonist stimulation of 5-HT(2B) receptors induces an SSRI-like response in behavioral and neurogenic assays. Moreover, the observation that (i) this receptor is expressed by raphe serotonergic neurons, (ii) the SSRI-induced increase in hippocampal extracellular serotonin concentration is strongly reduced in the absence of functional 5-HT(2B) receptors and (iii) a selective 5-HT(2B) agonist mimics SSRI responses, supports a positive regulation of serotonergic neurons by 5-HT(2B) receptors. The 5-HT(2B) receptor appears, therefore, to positively modulate serotonergic activity and to be required for the therapeutic actions of SSRIs. Consequently, the 5-HT(2B) receptor should be considered as a new tractable target in the combat against depression.
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Fluoxetine and all other SSRIs are 5-HT2B Agonists - Importance for their Therapeutic Effects.
Peng 2014
http://www.ncbi.nlm.nih.gov/pubmed/22158014
Fluoxetine and other serotonin-specific re-uptake inhibitors (SSRIs) are generally thought to owe their therapeutic potency to inhibition of the serotonin transporter (SERT). However, research in our laboratory showed that it affects, with relatively high affinity the 5-HT2B receptor in cultured astrocytes; this finding was confirmed by independent observations showing that fluoxetine loses its ability to elicit SSRI-like responses in behavioral assays in mice in which the 5-HT2B receptor was knocked-out genetically or inhibited pharmacologically. All clinically used SSRIs are approximately equipotent towards 5-HT2B receptors and exert their effect on cultured astrocytes at concentrations similar to those used clinically, a substantial difference from their effect on SERT. We have demonstrated up-regulation and editing of astrocytic genes for ADAR2, the kainate receptor GluK2, cPLA2 and the 5-HT2B receptor itself after chronic treatment of cultures, which do not express SERT and after treatment of mice (expressing SERT) for 2 weeks with fluoxetine, followed by isolation of astrocytic and neuronal cell fractionation. Affected genes were identical in both experimental paradigms. Fluoxetine treatment also altered Ca(2+) homeostatic cascades, in a specific way that differs from that seen after treatment with the anti-bipolar drugs carbamazepine, lithium, or valproic acid. All changes occurred after a lag period similar to what is seen for fluoxetine's clinical effects, and some of the genes were altered in the opposite direction by mild chronic inescapable stress, known to cause anhedonia, a component of major depression. In the anhedonic mice these changes were reversed by treatment with SSRIs.
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greengummybear said:
'Darwinian' test uncovers an antidepressant's hidden toxicity
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Good read. I would presume being 'placated' gives less drive and similarly being even contented (by recreational or therapeutic drug use) would intuitively put a life-form 'evolved', or even "designed" (it's all the same for me), for struggle at a social- or ecological- -Darwinistic disadvantage. This was nothing where a study had to be made for me to come to that assumption. Of course, I've been using prescribed and self-sought psychoactive substances for approaching a decade now, and I know my capacity to persist in the competitive stratosphere of excelling at facets of life has been blunted. So it is of concern to me on some level. Though the over-domestication and abstracted machinery of civilization of the human species negates a lot of the pertinence had of true instincts & their pull for many kinds of ingrained feelings for accomplishments, though certainly never to the full degree of any one out of all of them.
 
^what about the fact that the offspring of SSRI treated animals fared worse than animals with drug free parents? To me it seems more likely that the SSRI had some minor physical toxicity that made the offspring less competitive compared to their peers.
 
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