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5,7-Dichlorokynurenic acid sodium salt

CAS# 1184986-70-6

5,7-Dichlorokynurenic acid sodium salt

Catalog No. BCC7758----Order now to get a substantial discount!

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5,7-Dichlorokynurenic acid sodium salt: 5mg $58 In Stock
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Chemical structure

5,7-Dichlorokynurenic acid sodium salt

3D structure

Chemical Properties of 5,7-Dichlorokynurenic acid sodium salt

Cas No. 1184986-70-6 SDF Download SDF
PubChem ID 44134672 Appearance Powder
Formula C10H4Cl2NNaO3 M.Wt 280.04
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in 1eq. NaOH
Chemical Name sodium;5,7-dichloro-4-oxo-1H-quinoline-2-carboxylate
SMILES C1=C(C=C2C(=C1Cl)C(=O)C=C(N2)C(=O)[O-])Cl.[Na+]
Standard InChIKey VPRPMJHKWHCUFW-UHFFFAOYSA-M
Standard InChI InChI=1S/C10H5Cl2NO3.Na/c11-4-1-5(12)9-6(2-4)13-7(10(15)16)3-8(9)14;/h1-3H,(H,13,14)(H,15,16);/q;+1/p-1
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 5,7-Dichlorokynurenic acid sodium salt

DescriptionSodium salt of 5,7-Dichlorokynurenic acid, a potent antagonist at the glycine site of the NMDA receptor (Ki = 79 nM vs. [3H]-glycine).

5,7-Dichlorokynurenic acid sodium salt Dilution Calculator

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5,7-Dichlorokynurenic acid sodium salt Molarity Calculator

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Preparing Stock Solutions of 5,7-Dichlorokynurenic acid sodium salt

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.5709 mL 17.8546 mL 35.7092 mL 71.4184 mL 89.273 mL
5 mM 0.7142 mL 3.5709 mL 7.1418 mL 14.2837 mL 17.8546 mL
10 mM 0.3571 mL 1.7855 mL 3.5709 mL 7.1418 mL 8.9273 mL
50 mM 0.0714 mL 0.3571 mL 0.7142 mL 1.4284 mL 1.7855 mL
100 mM 0.0357 mL 0.1785 mL 0.3571 mL 0.7142 mL 0.8927 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 5,7-Dichlorokynurenic acid sodium salt

Activity of 5,7-dichlorokynurenic acid, a potent antagonist at the N-methyl-D-aspartate receptor-associated glycine binding site.[Pubmed:2172769]

Mol Pharmacol. 1990 Oct;38(4):554-61.

5,7-Dichlorokynurenic acid (5,7-DCKA), one of the most potent excitatory amino acid receptor antagonists yet described, binds to a strychnine-insensitive glycine binding site located on the N-methyl-D-aspartate (NMDA) receptor complex (Ki = 79 nM versus [3H]glycine). 5,7-DCKA (10 microM) antagonized the ability of NMDA to stimulate the binding of the radiolabeled ion channel blocker N-[3H][1-(2-thienyl)cyclohexyl]-piperidine ([3]TCP). Glycine was able to overcome this effect and in the presence of 5,7-DCKA enhanced [3H]TCP binding to antagonist-free levels. 5,7-DCKA completely and noncompetitively antagonized several NMDA receptor-mediated biochemical and electrophysiological responses. Thus, micromolar concentrations of 5,7-DCKA inhibited NMDA-stimulated elevation of cytosolic calcium in cultured hippocampal neurons, cGMP accumulation in cerebellar slices, and norepinephrine release from hippocampal slices. The glycine antagonist could also block the action of synaptically released agonist, as shown by its ability to inhibit the increase in the magnitude of the population spike that follows tetanic stimulation of the hippocampus in vitro (long term potentiation). Inclusion of glycine or D-serine prevented all these effects of the antagonist. 5,7-DCKA was a potent anticonvulsant when administered intracerebroventricularly to mice. As in the in vitro experiments, the dose-response curve for the antagonist was shifted rightward in a parallel fashion when D-serine was coinjected. This spectrum of activity displayed by a compound acting at the glycine binding site suggests that the therapeutic utility of glycine antagonists will be similar to those proposed for other types of glutamate receptor antagonists.

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