Alpha-Chloralose

[Sphinx (Afterlife)]

Can anyone tell me anything about this stuff??

 

[BilZ0r]

Its used as pest control. It's a GABA-A allosteric modulator, and it binds to a site independent of benzos and barbs. It's got a narrow "therapeutic window" i.e. it's lethal dose and un-noticable dose are very similar.

It might have effects other than this as well.

I wouldn't eat it, if that's what you're thinking.

 

[Ivanhoe]

Chloral Hydrate, Chlorobutanol and Alpha-Chloralose are almost the same thing.
Chlorobutanol and Alpha-Chloralose are metabolites of Chloral Hydrate. (or Cholral Hydrate is the metabolite of Chlorobutanol and A-Chloralose)

Alpha-Chloralose was the drug of choice for anaesthesia in France during XIXth century (maybe the begining of the XXth century too).

I read this on a website:
For those who want to try for recreational use, the "recommended dosage" is between 500mg and 1000mg, and do not exceed 1500mg, it can kill you.
However (eventhough I have tried it one time) I wouldn't recommend it, IMO it is NOT RECREATONAL AT ALL!

The only time I took A-Chloralose, I felt nothing for 2 hours, and then suddenly it knocked me out for 12 hours...

It is sold pure here (in France) in garden shops, in huge doses (10g+), it is used to kill rats.
And I think this substance as nos use beyond this: rat poison...

That was what I culd tell you about this substance from my experience.

 

[Ivanhoe]

Now I will quickly translate you what the biggest site about meds in france tells about it:

ALPHA-CHLORALOSE

PHARMACEUTICAL PROPERTIES:
Hypnotic

HOW IT WORKS
depress the CNS and ??? (I don't understand this, even in french, "reticulous" something..)

EFFECTS
-psycholeptic
-hypnotic

INDICATIONS
-insomnia
-pre-anesthesia

SIDE EFFECTS
nausea, vomitting, epigastric pain, bradycardia, tremors, headache, ataxia, mental confusion

DO NOT USE in case of chronic respiratory depression

ROUTES OF ADMINISTRATION
1. oral
2. rectal

DOSAGE
oral
150mg-300mg daily
rectal
150mg-300mg daily

for kids
37,5mg-150mg daily

 

[BilZ0r]

Chloral Hydrate, Chlorobutanol and Alpha-Chloralose are almost the same thing.
Chlorobutanol and Alpha-Chloralose are metabolites of Chloral Hydrate. (or Cholral Hydrate is the metabolite of Chlorobutanol and A-Chloralose)

I wondered if it was related to Chloral Hydrate... Learn something everyday

 

[Ivanhoe]

I just did a google search, to see if what I said was correct, and I can't find a website that says that two of these compounds are metabolites of the third (*), it seems that they are only very close chemically, and have almost the same effects.
(*)(however I remember I read that somewhere a while ago...)

And an important note: some websites say the toxic dose in humans is 1000mg, some other say it's 1500mg....
I don't know what are the intentions of the poster, but if someone wants to try this substance, do not take more than 1000mg, and it would be a good idea not to take more than the recommended dosage of 150-300mg.

 

[fastandbulbous]

Alpha chloralose is the hemi-acetal formed by heating together equimolar amounts of glucose & chloral hydrate. The chloral is linked to the glucose in the same way that glucose molecule join together to form a starch molecule (alpha linkage). Once your body get ahold of the molecule, it hydrolyses the bond to glucose & chloral hydrate. The glucose part of the molecule might mean that it's subject to active uptake from the gut in the same way glucose (& other sugars) are.

 

[midnight577]

I experimented with alpha d glucochloralose many years ago, the effects at 400mg as I recall were a uncordinated, almost drunken state, but with a much clearer mind, also a strong sedative, most of my experiences only lasted a few hours at most before passing out. Never tried Chloral Hydrate, but the effects are similar, although more physically incordinating than chlorobutanol (500 to 1000mg)

 

[BilZ0r]

Thats odd, because classical pharmacology would tell you that the Choralose was active by itself (according to paper above)... do you think that the Xenopus Oocyte could be metabolising significant quantities of the Parent species?

 

[who mE?]

Chloral Hydrate, Chloretone (aka chlorobutanol), and Alpha-Chloralose all metabolise into a common substance: 2,2,2-trichloroethanol which is responsible for the majority (but not all) of the pharmacological action of the parent drugs.

I think 2,2,2-trichloroethane is also metabolised to 2,2,2-trichloroethanol.

That said, each of these metabolises at different rates, to the extent where chlorobutanol has a 5-20 day half-life in the human body (not exactly recreational if you can't balance, think or drive for a month afterwards).

An analogous relation exists for Bromal, Brometone, Alpha-Bromalose and 2,2,2-tribromoethanol.

 

[BilZ0r]

[paraphrase]Chloral hydrate is active because of metabolism into 222-Cl4-EtOH[/paraphrase]
Although I can see the sense in that arguement, because 222-Cl4-EtOH has a more anaesthetic type profile (NMDA antagonism, GABA-A potentiation, Fucks with Na and K channels), what is your actual proof in saying that? I know that a degree of activity comes from the chloro-ethanol species, but I thought bought of the parent species potentiated GABA-A at quite reasonable concentrations.

 

[who mE?]

First, about the metabolism of Chloral Hydrate:

Chloral hydrate is readily absorbed from the gastrointestinal tract following oral administration; however, significant amounts of chloral hydrate have not been detected in the blood after oral administration. It is generally believed that the central depressant effects are due to the principal pharmacologically active metabolite trichloroethanol, which has a plasma half- life of 8 to 10 hours. A portion of the drug is oxidized to trichloroacetic acid (TCA) in the liver and kidneys; TCA is excreted in the urine and bile along with trichloroethanol in free or conjugated form.

http://www.rxlist.com/cgi/generic3/chloralhyd_cp.htm

The relative bioavailability and pharmacokinetics of chloral hydrate and its metabolites

Two open, randomized cross-over trials were performed in 18 healthy volunteers each to evaluate the relative bioavailability and the pharmacokinetics of chloral hydrate (CAS 302-17-0), the active ingredient of Chloraldurat 500 (immediate release capsules, CH), Chloraldurat rot (immediate release capsules, CR) and Chloraldurat blau (enteric-coated modified release capsules, CB). In the first study the male subjects, aged 21 to 31 years, were randomly given one capsule of CH or 500 mg of chloral hydrate as drinking solution. In the second study the volunteers, aged 20 to 28 years, received either one capsule of CR or one capsule of CB or 250 mg of chloral hydrate as drinking solution. The time of administration was between 6:30 and 7:30 a.m. and the capsules had to be swallowed with 150 ml water. The reference medication consisted of 150 ml drinking solution. The wash out time in both studies was 4 weeks. Prior to the administration and (2, 4, 6, only for CH) 8, 10, 15, 20, 40, 60 min and 1.5, 2, 4, 6, 8, 12, 24, 36, 48, 72, 96, 144, 192, 240 (and 408 only for CR/CB) h afterwards blood samples of 4.5 ml were taken from the antecubital vein. Additional 4.5 ml were drawn before and 10, 20, 40 and 60 min after administration to detect unchanged chloral hydrate. In the second study times of blood sampling were modified up to 4 h after administration due to the estimated later onset of release from CB in comparison to CR. Blood samples were centrifuged within 20 min, the plasma was separated and immediately frozen at -20 degrees C. Due to the extremely short terminal half-life of chloral hydrate its active metabolite trichloroethanol is regarded as the pharmacokinetically relevant parameter for the assessment of the bioavailability of the parent substance. Compared to the reference formulation (drinking solution) the bioavailability of trichloroethanol was 94.8% (CH), 100.7% (CR) and 101.6 (CB), respectively. The maximum plasma concentrations (Cmax) of trichloroethanol were 5176 ng/ml after intake of CH (reference 6131 ng/ml), after intake of CR 3241 ng/ml and CB 3279 ng/ml (reference 2993 ng/ml). Maximum plasma concentrations (tmax) of trichloroethanol were reached after 0.67 h (reference) and after 0.98 (CH), 0.76 (CR) and 2.38 h (CB), respectively. The terminal half-life for trichloroethanol was calculated to be 9.3 to 10.2 h, for the inactive metabolite trichloracetic acid the half-life ranged from 89 to 94 h. Chloral hydrate itself could be detected only 8 to 60 min after application at very low concentrations in some of the plasma samples. It is justified to characterize its bioavailability by the active metabolite trichloroethanol due to the extremely short terminal half-life and high variability of the parent substance.

http://www.ncbi.nlm.nih.gov/entrez/...d&dopt=Abstract&list_uids=9522024&query_hl=19

it led to efforts to establish how chloral hydrate brings about its action. This seems to be through its reduced metabolite, trichloroethanol.

http://www.ncbi.nlm.nih.gov/entrez/...ed&dopt=Abstract&list_uids=1388448&query_hl=9

Binding of the active metabolite of chloral hydrate, 2,2,2-trichloroethanol, to serum albumin demonstrated using tryptophan fluorescence quenching.

http://www.ncbi.nlm.nih.gov/entrez/...d&dopt=Abstract&list_uids=11834892&query_hl=9

However, things are different in neonates:

Sedative/hypnotic effects of chloral hydrate in the neonate: trichloroethanol or parent drug?

Although the metabolism and pharmacokinetics of chloral hydrate (CH) have been reported, there have been no attempts to correlate CH or its metabolite, trichloroethanol (TCE) with the sedative or hypnotic effects. In order to determine whether plasma concentrations of CH or TCE reflect the sedative/hypnotic effects, a sedation/agitation scale was developed. Based on the results of the present study, the sedative/hypnotic effects of TCE cannot be ruled out completely. However, in the neonate, the parent drug CH seems to have a more important role than has been previously suggested from human research.

http://www.ncbi.nlm.nih.gov/entrez/...ed&dopt=Abstract&list_uids=1340434&query_hl=3

And to make matters even stranger:

Trichloroethanol is not a metabolite of alpha chloralose.

Head space capillary gas chromatography was used to detect alpha chloralose and its potent metabolite, trichloroethanol in clinical and forensic cases. Although alpha chloralose was identified in blood and urine in all cases, trichloroethanol was never detected. In a fatal case the alpha chloralose concentration in blood was 151.3 mg/l. It was concluded that trichloroethanol is not a metabolite of alpha chloralose.

http://www.ncbi.nlm.nih.gov/entrez/...d&dopt=Abstract&list_uids=8652423&query_hl=12


Interesting reading:

Chloral hydrate: a hypnotic best forgotten?

Synthesised by Justin Liebig in 1832 chloral hydrate is one of the oldest synthetic agents. Since 1869 it has been in use for hypnotic or sedative purposes. Chloral hydrate was used a lot from the end of the 19th century to the middle of the 20th century. Since then chloral hydrate has been less frequently in use as a hypnotic. In the 1990's, the principal use of chloral hydrate in pediatrics was the sedation of children for minor surgery during dental or diagnostic procedures. In general practice, it is an analgesia found in topical preparations. It was known as safe and easy to use. Now it is shown to be potentially dangerous (risk of death in case of intoxication) and there is doubt about genotoxicity and carcinogenecity. The pharmacological property was known in 1948 when Butler discovered the principal active metabolite, trichloroethanol. The gastro-intestinal tract rapidly absorbs chloral hydrate after oral or rectal use. The sedative and hypnotic effects appear in 20 to 60 minutes. The main metabolites [trichloroethanol (TCE) and trichloroacetic acid (TCA)] are formed by hepatocytes and erythrocytes. The half-life of chloral hydrate is short (a few minutes), the half lives of the metabolics are longer, 8 to 12 hours for TCE and 67 hours for TCA. The affinity for lipids is high. It is eliminated principally by the kidneys. Its mechanism of action is unknown. It is a depressor of the SNC, and the sedation is attributed to chloral hydrate and the hypnotic effect to TCE. The interactions appear with: alcohol, anticoagulants, amitriptyline and furosemide. The use of flumazenil (a gaba antagonist), in case of intoxication, indicates a possible action of GABA. The posology is usually between 0.5 to 2 g per day. Chloral hydrate is taken during meals to prevent gastric irritation. The main side effects are digestive, cardiologic (risk of rhythm disorder), dermatologic, neuropsychiatric (withdrawn, delusions, hallucination, dependence) and ophthalmologic. Death occurs after absorption of doses of around 10 g of hydrate chloral, some cases were reported with 5 g. The use of hydrate chloral is contra-indicated in cases of gastric ulcers, hepatic insufficiency, porphyry, respiratory insufficiency, association with anticoagulants and hyper sensibility. Nowadays should we be using chloral hydrate in cases of insomnia in adult and older people? A recent preclinical working group of the French Agency for evaluation of medicinal products reassessed the benefit/risk ratio of chloral hydrate. Many references are found about genotoxicity and carcinogenicity in recent literature. In France, since the end of 2000, chloral hydrate has been withdrawn from many medications for external use in dermatology and in stomatology. Chloral hydrate can be used as a pediatric sedative only once in a lifetime. The psychiatric indication for insomnia is no longer justified and especially in older people.

http://www.ncbi.nlm.nih.gov/entrez/...d&dopt=Abstract&list_uids=12091779&query_hl=9


Also interesting reading:
Kinetics and metabolism of chloral hydrate in children: identification of dichloroacetate as a metabolite.
http://www.ncbi.nlm.nih.gov/entrez/...ed&dopt=Abstract&list_uids=9207222&query_hl=9

Species- and sex-related differences in metabolism of trichloroethylene to yield chloral and trichloroethanol in mouse, rat, and human liver microsomes.
http://www.ncbi.nlm.nih.gov/entrez/...ed&dopt=Abstract&list_uids=9698293&query_hl=9 (free fulltext!)

Should Chloral Hydrate be banned?
http://www.ncbi.nlm.nih.gov/entrez/...ed&dopt=Abstract&list_uids=8361800&query_hl=9

Enhancement of gamma-aminobutyric acid receptor activity by alpha-chloralose.
http://www.ncbi.nlm.nih.gov/entrez/...d&dopt=Abstract&list_uids=9580613&query_hl=12

By the way Bilz0r, I'm still working on my pharmacology text chapter... personal issues are distracting from my freetime, sorry about the delay. Also, my chapter (pharmacokinetics) needs to be the most accessible to the layman, as it is (in my opinion) the most important to the understanding of safe, practical use of recreational drugs, and fundamental to everything else in the text.

Thanks for bugging me about it, and thanks for your skepticism on this topic, I learned some stuff researching this...

 

[jasoncrest]

This thread made me want to try A-Chloralose again.
If it has pharmaceutical properties and a recommended dosage from a medical website, I think I can try to use it safely for medical purpose only (insomnia).

I bought two brands of Mole Killer:
-the first brand says "alphachloralose 98%" and nothing more. It is a white powder.
-the second brand says "alphachloralose 99%, "sous carbonate de fer*" 1%. It is a pink powder.
*sous carbonate de fer means approx. "iron carbonate"

Is the first brand safe to ingest? Should I worry about the 2% remaining? What can it be?

What about the second brand? Is the Iron Carbonate only a pink colorant? Or is it toxic to prevent abuse?

 

[BilZ0r]

Shit... I don't know... seems like a pretty big risk, even though the 99%:1% sounds reasonable... Iron carbonate is grey I think....

I don't know... makes me nervous as fuck.

 

[jasoncrest]

I found the english translation of "sous carbonate de fer":

So the second brand of "Mole Killer" contains:
-99% Alpha-Chloralose
-1% Iron (III) Oxide Hydrate or Ferric Oxide

Does that mean something to you?
Is the Iron III Oxide Hydrate present only for the pink/red coloring?


[one more thing, I found a study that shows that A-Chloralose "enhance the gamma-aminobutyric acid A receptor activity ", it means it acts on the GHB receptor?]

 

[fastandbulbous]

^ Ferrous (Fe++) salts are generally greenish in colour; ferric (Fe+++) salts are light brownish/reddy in colour. Ferrous salts can cause iron poisoning as that's the form in which the body absorbs it. Ferric salts tend to pass through unabsorbed, but can be irritant to the lining of the gut.

If you want to separate out the ferric carbonate, dissolve it in water then filter; ferric carbonate is insoluble (ferric oxide is better known as rust) so the filtrate should be uncoloured & contain only alphachloralose.

Chloral Hydrate, Chloretone (aka chlorobutanol), and Alpha-Chloralose all metabolise into a common substance: 2,2,2-trichloroethanol which is responsible for the majority (but not all) of the pharmacological action of the parent drugs.

I think 2,2,2-trichloroethane is also metabolised to 2,2,2-trichloroethanol.

As far as I;m aware, chlorbutanol isn't metabolized into trichloroethanol; it's the active compound itself (it's effectively 2,2,2-trichloro-1,1-dimethylethanol & the body isn't good at ripping off those sort of methyl groups).

Trichloroethane isn't metabolized to trichloroethanol; in terms of action it's more like chloroform or other halogenated alkanes that will act like a general anaesthetic. Trichloroethane itself causes fatty degeneration of the liver and is seriously cardiotoxic (especially in the presence of sympathiomimetic compounds like ephedrine, salbutamol, amphetamine etc). Best avoided like the plague

 

[jasoncrest]

If you want to separate out the ferric carbonate, dissolve it in water then filter; ferric carbonate is insoluble (ferric oxide is better known as rust) so the filtrate should be uncoloured & contain only alphachloralose.

I just read that A-Chloralose is also insoluble in water...
Iron III Oxide, or ferric carbonate is insoluble in water, but is Iron III Oxide Hydrate also insoluble in water?

 

[fastandbulbous]

^In that case, wash the stuff with a dilute solution of vinegar (distilled vinegar would be best as it's clear). The acetic acid will react with the ferric carbonate to form ferric acetate (plus carbon dioxide & water); as all acetate salts are soluble, you can simply wash out all of the ferric acetate formed by the reaction leaving behind the alphachloralose.

If you want to be really smart arsed about it, I believe that ferric (iron III) salts exhibit some degree of magnetism (seems to be lacking in ferrous salts). Iron III oxide hydrate (aka hydrated ferric oxide) isn't water soluble - it's better known as rust!

 

[jasoncrest]

Yeah I'll maybe try to wash the stuff with acetic acid.
Thanks for the advice f&b.
Then I'll buy 150mg empty gelatin capsules, put the a-chloralose in them, and put all these pills in a big bottle saying :

"ALPHA-CHLORALOSE
150mg
Hypnotic.
Take 1 or 2 capsules before going to bed."

If it works well, I'll go buy some more. For less than 10 dollars I have 100g a-chloralose powder. Enough to make more than 6 bottles of 100 x 150mg pills.
Maybe some of my friends will be interested.

THANK YOU ALL FOR YOUR ANSWERS.
I now have an unlimited access to a cheap potent hypnotic, that's really cool.

 

[who mE?]

fastandbulbous, after doing some research, you appear to be correct that chlorobutanol is not metabolised into trichloroethanol. There are numerous pieces of disinformation floating around that say otherwise, but there are no papers on pubmed mentioning trichloroethanol as a metabolite of chlorobutanol.

I have found the paper which would lead me to believe that chlorobutanol would be one of the WORST drugs for recreational usage due to its INCREDIBLY LONG half-life, and balance-disturbing properties:

The pharmacokinetics of chlorbutol were studied after oral administration in 4 healthy subjects on two occasions. Following the rapid attainment of peak concentrations, plasma concentrations fell by approximately 50 per cent in 24 h. After the first dose of chlorbutol, the terminal elimination half-life was 10.3 +/-1.3 days (mean +/- S.E.M), the volume of distribution was 233 +/- 141 and the plasma clearance was 11.6 +/- 1.0 ml min-1. The binding to plasma proteins was 57 +/- 3 per cent. In 3 of the 4 subjects, there was a small but significant decrease in the terminal half-life of chlorbutol after the second dose. The mean urinary recovery over 17 days in two of the subjects accounted for only 9.6 per cent of the dose, 7.4 per cent of the total as the glucuronide and sulphate conjugates and 2.2 per cent as unchanged chlorbutol. A significant factor in the elimination of chlorbutol may be its instability under physiological conditions. Its half-life in vitro is 37 days at pH 7.4. The long terminal half-life of chlorbutol makes it unsuitable as a sedative drug because of the considerable accumulation which will occur when the drug is taken in multiple doses.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7159691&dopt=Abstract

This paper is an interesting review of the actions of 13 various drugs of the class described in this thread:
http://www.labanimal.com/bjp/journal/v129/n4/full/0703087a.html
British Journal of Pharmacology (2000) 129, 731−743; doi: 10.1038/sj.bjp.0703087

In it they say:

In addition, alpha-chloralose directly activates GABAA receptors with high potency and efficacy, something not seen with the ether, alkane, and alcohol general anaesthetics analysed in this study. The total pattern of alpha-chloralose activity more closely resembles that of the barbiturates and steroidal anaesthetics

Lastly, jasoncrest, be FREAKING CAREFUL about deciding to take alpha-chloralose regularly, be sure to research potential side-effects thoroughly, and never forget the most notorious side effect: DEATH.
It is extremely easy to die using these drugs, and they have been all but discontinued from medical use for this primary reason, and other side effects.