1. Membrane Transporter/Ion Channel Neuronal Signaling
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  3. 5,7-Dichlorokynurenic acid sodium

5,7-Dichlorokynurenic acid sodium  (Synonyms: 5,7-DCKA sodium)

Cat. No.: HY-100834A
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5,7-Dichlorokynurenic acid (5,7-DCKA) sodium is a selective and competitive antagonist of the glycine site on NMDA receptor with a KB of 65 nM. 5,7-Dichlorokynurenic acid sodium reduces NMDA-induced neuron injury. 5,7-Dichlorokynurenic acid sodium increases social interaction time, increases open arm exploration time, disinhibits suppressed conflict responding in rodent models. 5,7-Dichlorokynurenic acid sodium exhibits anxiolytic-like activity in rodent models and supports exploration of glycine’s role in NMDA receptor-mediated synaptic transmission.

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5,7-Dichlorokynurenic acid sodium

5,7-Dichlorokynurenic acid sodium Chemical Structure

CAS No. : 1184986-70-6

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Description

5,7-Dichlorokynurenic acid (5,7-DCKA) sodium is a selective and competitive antagonist of the glycine site on NMDA receptor with a KB of 65 nM. 5,7-Dichlorokynurenic acid sodium reduces NMDA-induced neuron injury. 5,7-Dichlorokynurenic acid sodium increases social interaction time, increases open arm exploration time, disinhibits suppressed conflict responding in rodent models. 5,7-Dichlorokynurenic acid sodium exhibits anxiolytic-like activity in rodent models and supports exploration of glycine’s role in NMDA receptor-mediated synaptic transmission[1][2].

In Vitro

5,7-dichlorokynurenic acid (0.2-400 μM) sodium is a potent, competitive antagonist of the glycine site on NMDA receptors expressed in rat brain mRNA-injected Xenopus oocytes, with a KB of 65 nM, and is 509-fold more selective for this site than for kainate receptors[1].
5,7-dichlorokynurenic acid (40 nM-10 μM; 60 min on ice) sodium potently displaces [3H]glycine from strychnine-insensitive glycine sites on rat brain cortex membranes with a Ki of 40 nM, and does not bind to the NMDA recognition site at 10 μM[1].
5,7-dichlorokynurenic acid (1-10 μM) sodium reduces NMDA-induced neuronal injury in primary rat cortical cell cultures, with 1 μM yielding 55-79% protection and 10 μM yielding 62-90% protection[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

5,7-Dichlorokynurenic acid (30.0-100.0 mg/kg; i.p.; single dose) sodium produces anxiolytic-like effects in the social interaction model, increasing social interaction time by +37% at 30.0 mg/kg and +32% at 100.0 mg/kg, with reduced motor activity at the highest dose[2].
5,7-Dichlorokynurenic acid (100.0 mg/kg; i.p.; single dose) sodium produces anxiolytic-like effects in the elevated plus maze model, increasing open arm exploration time by +41% at 100.0 mg/kg, with reduced motor activity[2].
5,7-Dichlorokynurenic acid (100.0-173.0 mg/kg; i.p.; single dose) sodium disinhibits suppressed conflict responding in the Cook and Davidson conditioned anxiety model at 100.0 mg/kg and 173.0 mg/kg without altering non-punished responding[2].
5,7-Dichlorokynurenic acid (10.0-100.0 mg/kg; i.p.; single dose) sodium does not generalize to the MK-801 discriminative cue at 10.0 mg/kg, and shows minimal partial generalization in 1 of 4 rats at 100.0 mg/kg[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Wistar rats (male, 200-300 g)[2]
Dosage: 30.0 mg/kg; 100.0 mg/kg
Administration: i.p.; single dose
Result: Increased social interaction time significantly by +37% with no significant change in motor activity at 30.0 mg/kg.
Increased social interaction time significantly by +32%, and decreased motor activity significantly by -34% at 100.0 mg/kg.
Molecular Weight

280.04

Formula

C10H4Cl2NNaO3

CAS No.
SMILES

O=C(C1=NC2=CC(Cl)=CC(Cl)=C2C(O)=C1)O[Na]

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Please store the product under the recommended conditions in the Certificate of Analysis.

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5,7-Dichlorokynurenic acid sodium
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