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Chlormethiazole hydrochloride

Potentiates GABAA receptor function CAS# 6001-74-7

Chlormethiazole hydrochloride

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Quality Control of Chlormethiazole hydrochloride

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Chemical structure

Chlormethiazole hydrochloride

3D structure

Chemical Properties of Chlormethiazole hydrochloride

Cas No. 6001-74-7 SDF Download SDF
PubChem ID 19035073 Appearance Powder
Formula C6H9Cl2NS M.Wt 198.11
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in water
Chemical Name 5-(2-chloroethyl)-4-methyl-1,3-thiazole;hydrochloride
SMILES CC1=C(SC=N1)CCCl.Cl
Standard InChIKey OFXYKSLKNMTBHK-UHFFFAOYSA-N
Standard InChI InChI=1S/C6H8ClNS.ClH/c1-5-6(2-3-7)9-4-8-5;/h4H,2-3H2,1H3;1H
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Chlormethiazole hydrochloride

DescriptionSedative and anticonvulsant which is neuroprotective in a number of animal models. Prevents the degeneration of serotonergic nerve terminals induced by MDMA ('Ecstasy').

Chlormethiazole hydrochloride Dilution Calculator

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Chlormethiazole hydrochloride Molarity Calculator

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Preparing Stock Solutions of Chlormethiazole hydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 5.0477 mL 25.2385 mL 50.477 mL 100.954 mL 126.1925 mL
5 mM 1.0095 mL 5.0477 mL 10.0954 mL 20.1908 mL 25.2385 mL
10 mM 0.5048 mL 2.5239 mL 5.0477 mL 10.0954 mL 12.6193 mL
50 mM 0.101 mL 0.5048 mL 1.0095 mL 2.0191 mL 2.5239 mL
100 mM 0.0505 mL 0.2524 mL 0.5048 mL 1.0095 mL 1.2619 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Chlormethiazole hydrochloride

The protective action of chlormethiazole against ischaemia-induced neurodegeneration in gerbils when infused at doses having little sedative or anticonvulsant activity.[Pubmed:7599932]

Br J Pharmacol. 1995 Apr;114(8):1625-30.

1. The effect of chlormethiazole administration on delayed neuronal death in gerbil hippocampus following transient global ischaemia has been examined. Chlormethiazole was administered either intraperitoneally or by intravenous infusion with either the dose or the time of infusion varied. 2. Chlormethiazole (600 mumol kg-1, i.p.) given 60 min after ischaemia produced substantial (> 60%) neuroprotection when damage was assessed 5, 14 or 21 days later, indicating the drug does not merely delay cell death. 3. Infusion protocols were developed which would result in sustained and defined plasma concentrations. Chlormethiazole (930 mumol kg-1) was then infused intravenously for 30 min, 76.5 min or 110 min in ways resulting in sustained plasma concentrations of 200, 100 and 50 nmol ml-1 respectively. When treatment was initiated 30 min after the ischaemic episode all protocols provided effective neuroprotection. There was a dose-dependent decline in protection when plasma chlormethiazole concentrations of 50, 30 and 10 nmol ml-1 were sustained for 110 min with no protection observed at 10 nmol ml-1. 4. In contrast, when a plasma concentration of 10 nmol ml-1 was sustained by infusion for 24 h, almost total neuroprotection against the ischaemic damage was achieved. This plasma concentration produced no sedative or anticonvulsant activity. 5. These data suggest that neuroprotection depends on both dose and duration of chlormethiazole administration and that excellent neuroprotection is possible in the absence of the sedative and anticonvulsant effects of the drug.

Chlormethiazole, dizocilpine and haloperidol prevent the degeneration of serotonergic nerve terminals induced by administration of MDMA ('Ecstasy') to rats.[Pubmed:7539115]

Neuropharmacology. 1994 Dec;33(12):1589-95.

An investigation has been made into the effect of 3,4-methylenedioxymethamphetamine (MDMA or 'Ecstasy') administration on the concentration of 5-hydroxytryptamine (5-HT), uptake of [3H]5-HT and [3H]paroxetine binding in rat cerebral cortex tissue. Four days after 2 injections of MDMA (20 mg/kg i.p., 6 hr apart) the concentrations of 5-HT and its metabolite 5-HIAA were reduced by 60%. The binding of [3H]paroxetine to the presynaptic 5-HT transporter was decreased and high affinity uptake of [3H]5-HT was reduced by a similar amount, indicating neurodegeneration of 5-HT terminals. Pretreatment with chlormethiazole (100 mg/kg i.p.), 10 min before each MDMA injection prevented the decrease in both [3H]parotextine binding and uptake of [3H]5-HT. The loss in 5-HT and 5-HIAA content was also attenuated. Pretreatment with dizocilpine (1 mg/kg i.p.) or haloperidol (2 mg/kg i.p.) also prevented the MDMA-induced loss of [3H]paroxetine binding and attenuated the loss of 5-HT and 5-HIAA content. All three compounds also decreased the degree of hyperthermia that follows MDMA administration, although previous studies suggest that the long term neurodegeneration is not associated with the acute hyperthermic response. These data support the findings of others that MDMA injection produces degeneration of 5-HT nerve terminals in the cortex, confirm that chlormethiazole, dizocilpine and haloperidol attenuate MDMA-induced neurotoxic loss of 5-HT and demonstrate for the first time that these compounds prevent the neurodegeneration of 5-HT nerve terminals that follows MDMA administration.

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