Ketamine salts solubility

thegreenhand · May 1, 2020

sekio said:
The Therapeutic Effect of Adding Dextromethorphan to Clonidine for Reducing Symptoms of Opioid Withdrawal: A Randomized Clinical Trial
Ayyoub Malek, Shahrokh Amiri, and Bohlool Habibi Asl
ISRN Psychiatry. 2013; 2013: 546030. Published online 2013 Jun 20. doi: 10.1155/2013/546030
Background. Dextromethorphan is a noncompetitive N-methyl D-aspartate receptor antagonist that is clinically feasible for relieving the opioid withdrawal symptoms. This study compares the efficacy of a combination therapy with dextromethorphan and clonidine to treatment with clonidine alone.
Methods and Materials. In this double-blind randomized clinical trial, patients were selected from inpatients of detox and rehabilitation ward of Razi Hospital, Tabriz, Iran. They were randomly allocated to two groups receiving either clonidine (0.4–1.2 mg/day) or clonidine and dextromethorphan (300 mg/day). Withdrawal symptoms were evaluated in the first day of admission and again 24, 48, and 72 hours later.
Results. Thirty male patients completed the trial in each group. Withdrawal symptoms began to decrease in the second day in patients receiving dextromethorphan and clonidine while patients receiving clonidine experienced the more severe symptoms in 72 hours. Analysis of variance of the symptom severity score revealed a significant group × time interaction (F = 14.25; P < 0.001), so that patients receiving dextromethorphan plus clonidine had milder symptoms during three days in all of the measurements compared to clonidine group.
Conclusion. Combination therapy of dextromethorphan and clonidine would result in milder opioid withdrawal symptoms compared to clonidine alone with a reduction beginning at the second day.

Looks like getting to a 1st/low 2nd plateau dose for a few days is actually helpful in opioid w/d, despite what one might think
I guess if you can keep the cough syrup/pills down then you should give it a go, 300mg is not that high

Is this purely because of its action as a delta-opioid agonist? Essentially, just flattening the curve of the taper. I wonder if there’s any specific benefit to DXM over another opioid

thegreenhand · May 1, 2020

AlphaMethylPhenyl · May 4, 2020

sekio said:
Did you know the average house where methamphetamine is smoked indoors could have two grams or more of meth adsorbed into the drywall?

(Don't tell the tweakers this though, next thing they'll be ripping gyprock off of the crack dens and boiling it in crockpots)

I wonder then what it is that makes some psychoactive substances absorb into the wall, whereas, at least in the case of tobacco smoke, I thought it was just the tar and other on-pleasant chemicals that condenses on the walls to form the declared "third-hand smoke".

polymath · May 4, 2020

I have to clean the windows of my home quite often because e-cigarette vapor condenses on them. The earlier low-power vaporizer I had didn't cause this problem.

sekio · May 6, 2020

I have to clean the windows of my home quite often because e-cigarette vapor condenses on them.

Yuck.

Pain. 1986 Dec;27(3):277-90.
Compulsive thalamic self-stimulation: a case with metabolic, electrophysiologic and behavioral correlates.
Portenoy RK, Jarden JO, Sidtis JJ, Lipton RB, Foley KM, Rottenberg DA.
A 48-year-old woman with a stimulating electrode implanted in the right thalamic nucleus ventralis posterolateralis developed compulsive self-stimulation associated with erotic sensations and changes in autonomic and neurologic function. Stimulation effects were evaluated by neuropsychologic testing, endocrine studies, positron emission tomographic measurements of regional cerebral metabolic rate for glucose, EEG and evoked potentials. During stimulation, vital signs and pupillary diameter increased and a left hemiparesis and left hemisensory loss developed. Verbal functions deteriorated and visuospatial processing improved. Plasma growth hormone concentrations decreased, and adrenocorticotrophic hormone and cortisol levels rose. With stimulation, glucose metabolism increased in both thalami and both hemispheres, reversing baseline right-sided hypometabolism and right-left asymmetries. EEG and both somatosensory and brain-stem auditory evoked potentials remained unchanged during stimulation, while visual evoked potentials revealed evidence of anterior visual pathway dysfunction in the left eye. This case establishes the potential for addiction to deep brain stimulation and demonstrates that widespread behavioral and physiological changes, with concomitant alteration in the regional cerebral metabolic rate for glucose, may accompany unilateral thalamic stimulation.

Soon after insertion of the nVPL electrode, the patient noted that stimulation also produced erotic sensations. This pleasurable response was heightened by continuous stimulation at 75% maximal amplitude, frequently augmented by short bursts at maximal amplitude. Though sexual arousal was prominent, no orgasm occurred with these brief increases in stimulation intensity. Despite several episodes of paroxysmal atrial tachycardia and the development of adverse behavioral and neurological symptoms during maximal stimulation, compulsive use of the stimulator developed. At its most frequent, the patient self-stimulated throughout the day, neglecting personal hygiene and family commitments. A chronic ulceration developed at the tip of the finger used to adjust the amplitude dial and she frequently tampered with the device in an effort to increase the stimulation amplitude. At times, she implored her family to limit her access to the stimulator, each time demanding its return after a short hiatus. During the past 2 years, compulsive use has become associated with frequent attacks of anxiety, depersonalization, periods of psychogenic polydipsia, and virtually complete inactivity.

---

sekio's comment: Holy shit, her brain lights up like a christmas tree... and it's interesting to note she had prior instances of alcohol and opioid misuse. Skinner box anyone?

Rectify · May 6, 2020

1-(2-chloroindole-3-yl)-2-dimethylaminoethane.png

ALAN
1-(2-chloroindole-3-yl)-2-dimethylaminoethane

atara · May 7, 2020

I've always used http://py-chemist.com/mol_2_chemfig

Rectify · May 7, 2020

1-(4-methoxyphenyl)-1-oxo-2-methylaminopropane.png

METHEDRONE
1-(4-methoxyphenyl)-1-oxo-2-methylaminopropane

1-(6-iodoindole-3-yl)-2-dimethylaminoethane.png

PALLAS ATHENA (Scarlett)
1-(6-iodoindole-3-yl)-2-dimethylaminoethane

2-carbomethoxy-3-(2-(1-oxopropoxy)phenyl)tropane.png

AXL ROSE
2-carbomethoxy-3-(2-(1-oxopropoxy)phenyl)tropane

Welcome To The Jungle. We've Got Fun And Games. We've Got Everything You Want. Honey, We Know The Names.

1-(7-bromoindole-3-yl)-2-dimethylaminoethane.png

BARBARO / BARBARA
1-(7-bromoindole-3-yl)-2-dimethylaminoethane

Rectify · May 8, 2020

1-(4-cyclopropylmethylthio-2,5-dimethoxyphenyl)-2-aminopropane.png

T4
1-(4-cyclopropylmethylthio-2,5-dimethoxyphenyl)-2-aminopropane

1-(3,4,5-tribromophenyl)-1-carbomethoxy-1-(piperidine-2-yl)methane.png

MORGAN
1-(3,4,5-tribromophenyl)-1-carbomethoxy-1-(piperidine-2-yl)methane

1-(4-nitrophenyl)-2-propylaminopropane.png

SAMUEL
1-(4-nitrophenyl)-2-propylaminopropane

STEVE(N)
1-(4-bromophenyl)-2-aminopropane

clubcard · May 9, 2020

atara said:
I've always used http://py-chemist.com/mol_2_chemfig

Nice one.

Now, some 8 years ago I talked to a couple of programmers who had written an IMAGE<->SMILES<->IUPAC converter in Java (I think). They were prepared to let any IP to use it for about £3000 which isn't cheap BUT did have a 5 year QC on it so any problems, they fixed. I reckon they were too nice to do well but I loved their work.

If WE stored everything as IUPAC and the board brought up images and allowed people to copy as SMILES, it would end us having to hose images and I HOPE it would allow people to exchange ideas more readily.

roi · May 9, 2020

https://cactus.nci.nih.gov/chemical/structure is nice to convert just about any identifier.

And https://chemaxon.com/products/marvin is a free alternative to chemdraw.

Rectify · May 11, 2020

2-(1-carbomethoxy-1-phenylmethyl)-4-phenyloxy-5-carbomethoxypiperidine.png

PABLO_HONEY
2-(1-carbomethoxy-1-phenylmethyl)-4-phenyloxy-5-carbomethoxypiperidine

N-(1-oxo-dichloroethyl)-1-oxo-1-(4-nitrophenyl)-2-aminopropane3-ol.png

OXO-CHLORAMPHENICOL
N-(1-oxo-dichloroethyl)-1-oxo-1-(4-nitrophenyl)-2-aminopropane3-ol

(1S,2S,5R,6R)-2-carbomethoxy-3,3-dimethyl-7-oxo-6-%5B(2-phenyl)-1-methyl-ethylamino%5D-4-thia-1-azabicyclo%5B3.2.0%5Dheptane.png

ULYSSEYS
COVID19 treatment

2-%5B(diethylaminocarbonyl)oxy%5D-N,N-dimethyl-1-propanamine.png

SAMMY
nootropic

Skorpio · May 16, 2020

Here's a recent one that made a pretty big splash. This paper is pretty big because it was a collaboration between multiple labs including the lab that made the claim that respiratory depression is due to beta arrestin functional selectivity. This really kills the boners (non gender specific) of all the people pouring money and time into looking into mu opioid biased signalling.

The error was in the mouse strain, knockout mice are usually backcrossed (inbred) enough times to produce a true knockout.

Morphine-induced Respiratory Depression Is Independent of β-arrestin2 Signalling
Andrea Kliewer et al. Br J Pharmacol. 2020.

Morphine-induced respiratory depression is independent of β-arrestin2 signalling - PubMed

Our findings do not support the original suggestion that β-arrestin2 signalling plays a key role in opioid-induced respiratory depression and call into question the concept of developing G protein-biased μ-opioid receptor agonists as a strategy for the development of safer opioid analgesic drugs.

pubmed.ncbi.nlm.nih.gov

Abstract
Background and purpose: GPCRs can signal through both G proteins and β-arrestin2. For the μ-opioid receptor, early experimental evidence from a single study suggested that G protein signalling mediates analgesia, whereas β-arrestin2 signalling mediates respiratory depression and constipation. Consequently, for more than a decade, much research effort has been focused on developing biased μ-opioid agonists that preferentially target G protein signalling over β-arrestin signalling, as it was believed that such drugs would be analgesics devoid of respiratory depressant activity. However, the prototypical compounds that have been developed based on this concept have so far failed in clinical and preclinical development.
Experimental approach: The present study was set up to re-examine opioid-induced respiratory depression in β-arrestin2 knockout mice. To this end, a consortium was formed consisting of three different laboratories located in different countries to evaluate independently opioid-induced respiratory depression.
Key results: Our consensus results unequivocally demonstrate that the prototypical μ-opioid agonist morphine (3.75-100 mg·kg-1 s.c. or 3-30 mg·kg-1 i.p.) as well as the potent opioid fentanyl (0.05-0.35 mg·kg-1 s.c.) do indeed induce respiratory depression and constipation in β-arrestin2 knockout mice in a dose-dependent manner indistinguishable from that observed in wild-type mice.
Conclusion and implications: Our findings do not support the original suggestion that β-arrestin2 signalling plays a key role in opioid-induced respiratory depression and call into question the concept of developing G protein-biased μ-opioid receptor agonists as a strategy for the development of safer opioid analgesic drugs.