• N&PD Moderators: Skorpio | thegreenhand

Ketamine salts solubility

Right, but this is a pretty restrictive operationalization of "cognitive enhancer", and the measure they chose, encoding of new long term memories, is something that classical stimulants seem to hinder. Then again, classical stimulants seem to show cognitive enhancement only with very specific measures (centering on vigilance and STM management), not translating well to everyday learning and cognitive processing.

ebola
 
encoding of new long term memories, is something that classical stimulants seem to hinder

I'm going to be fascinated to see what effects PRL-8-53 has on that, once it hits the RC noots market soon: en.wikipedia.org/wiki/PRL-8-53

Too bad it has barely been formally studied, but it certainly appears to have the most effect on people with somewhat naturally impaired memories.
 
Psychol Res Behav Manag. 2013 Aug 27;6:65-74. doi: 10.2147/PRBM.S47526.
Influence of methylphenidate treatment assumptions on cognitive function in healthy young adults in a double-blind, placebo-controlled trial.
Mommaerts JL, Beerens G, Van den Block L, Soetens E, Schol S, Van De Vijver E, Devroey D.
Department of Family Medicine, Vrije Universiteit Brussel, Belgium.


So in laymans terms: Ritalin is just an active placebo. Not a smart drug.

I'm not saying the conclusion is wrong. But if you were going to write an academic article on the matter you'd need a lot more evidence. What I'm saying is that doesn't prove its more likely than not Ritalin is just an active placebo.
 
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5-(2-Aminopropyl)indole (5-IT): a psychoactive substance used for recreational purposes is an inhibitor of human monoamine oxidase (MAO)

5-(2-Aminopropyl)indole (5-IT) is a psychoactive compound that has recently been associated with several fatal and non-fatal intoxications in a number of European countries. There are indications that acute effects may include symptoms of monoaminergic (e.g. serotonin) toxicity and one mechanism involved in the increase of serotonin levels includes the inhibition of monoamine oxidase. This study investigated the effect of 5-IT on human MAO-A and -B isozymes using kynuramine as the substrate. Substrate conversion to 4-hydroxyquinoline was monitored by high-performance liquid chromatography coupled to diode array detection. This method was employed to determine the extent of MAO inhibition (IC50 and Ki) and it was found that 5-IT was a selective, competitive and reversible inhibitor of MAO-A. 5-IT revealed a relatively potent ability to inhibit MAO-A (IC50 = 1.6 μM and Ki = 0.25 μM) while MAO-B inhibition was not observed (0–500 μM 5-IT). Under identical experimental conditions, other established inhibitors of MAO-A and antidepressants provided the following IC50 values: clorgyline 16 nM, harmaline 20 nM, toloxatone 6.7 μM and moclobemide >500 μM. These data indicated that 5-IT was less potent than clorgyline and harmaline but more potent than toloxatone and moclobemide under the in-vitro conditions studied. The inhibition of MAO-A suggests that 5-IT by itself or in combination with other substances may be able to potentiate serotonergic/monoaminergic effects and further studies are needed to clarify its relevance to the adverse effects reported for 5-IT.

The does explain its lethality in higher doses. However, the typical dose of harmaline is 150mg, yet in this study harmaline is reported as ~100x more potent. So in theory, productive MAO inhibition is not going to really manifest until at least the 500mg mark. Am I missing something?
 
It looks like those who took it to binge levels were in for a world of hurt/death. Too bad. :( Goes to show that maybe people need to approach very new compounds with Shulginesque dosing schedules until more research comes out.

ebola
 
Pharmacokinetic and pharmacodynamic effects of methylphenidate and MDMA administered alone or in combination
Cédric M. Hysek, Linda D. Simmler, Nathalie Schillinger, Nicole Meyer, Yasmin Schmid, Massimiliano Donzelli, Eric Grouzmann and Matthias E. Liechti
The International Journal of Neuropsychopharmacology
DOI: http://dx.doi.org/10.1017/S1461145713001132 (About DOI), Published online: 08 October 2013
Methylphenidate and 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy’) are widely misused psychoactive drugs. Methylphenidate increases brain dopamine and norepinephrine levels by blocking the presynaptic reuptake transporters. MDMA releases serotonin, dopamine and norepinephrine through the same transporters. Pharmacodynamic interactions of methylphenidate and MDMA are likely. This study compared the pharmacodynamic and pharmacokinetic effects of methylphenidate and MDMA administered alone or in combination in healthy subjects using a double-blind, placebo-controlled, crossover design. Methylphenidate did not enhance the psychotropic effects of MDMA, although it produced psychostimulant effects on its own. The haemodynamic and adverse effects of co-administration of methylphenidate and MDMA were significantly higher compared with MDMA or methylphenidate alone. Methylphenidate did not change the pharmacokinetics of MDMA and vice versa. [...] In conclusion, the combined use of methylphenidate and MDMA does not produce more psychoactive effects compared with either drug alone, but potentially enhances cardiovascular and adverse effects. The findings may be of clinical importance for assessing the risks of combined psychostimulant misuse.

Yay for human studies on psychoactives!
 
maybe for the same reason that 2C-H isn't active? Fluorine can act more like Hydrogen than like a halogen, i believe.
 
those pesky neutron stars amirite?

How does that work? Stars that only consist of neutrons? And there's enough of those stars to make their number bigger than the total number of atoms, even counting those in non-neutrino stars? That sounds so far-fetched it must be true. ;]

But really?
 
qZ2ndgW.jpg

this is completely false, if anyone didn't realize

like saying "there are more brick houses on this street than there are bricks"
 
Yeah I was aware it was a joke image, though yea if there were more neutron stars that there were atoms then it would be correct.
 
Haha, Transform's reply got me. Nice one though. As long as it sounds deep enough, most people will simply believe it without questioning. =)
 
Just had a nice read through this thread. Love the jokes!

I'm not very versed in chemistry/pharmacology like others here, though I really love it. I study it as more of a hobby... would be my main focus if music wasn't my passion. Sound design is fascinating! The science of sound, then I get to make it into art! Though I'd say science is art too on a base level.

Anyways, just wanted to chime in here. I really enjoy reading this forum.
 
It just hit me, amineptine is in fact the most phallic drug molecular I've seen yet:
Amineptine3Dan.gif


Too bad it isn't a PDE5 inhibitor =D
 
Lanicemine: a low-trapping NMDA channel blocker produces sustained antidepressant efficacy with minimal psychotomimetic adverse effects
Molecular Psychiatry advance online publication 15 October 2013; doi: 10.1038/mp.2013.130
G Sanacora, M A Smith, S Pathak, H-L Su, P H Boeijinga, D J McCarthy and M C Quirk
Ketamine, an N-methyl-D-aspartate receptor (NMDAR) channel blocker, has been found to induce rapid and robust antidepressant-like effects in rodent models and in treatment-refractory depressed patients. However, the marked acute psychological side effects of ketamine complicate the interpretation of both preclinical and clinical data. Moreover, the lack of controlled data demonstrating the ability of ketamine to sustain the antidepressant response with repeated administration leaves the potential clinical utility of this class of drugs in question. Using quantitative electroencephalography (qEEG) to objectively align doses of a low-trapping NMDA channel blocker, AZD6765 (lanicemine), to that of ketamine, we demonstrate the potential for NMDA channel blockers to produce antidepressant efficacy without psychotomimetic and dissociative side effects. Furthermore, using placebo-controlled data, we show that the antidepressant response to NMDA channel blockers can be maintained with repeated and intermittent drug administration. Together, these data provide a path for the development of novel glutamatergic-based therapeutics for treatment-refractory mood disorders.
 
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