QNZ46

QNZ46 is a highly selective noncompetitive NMDA receptor antagonist targeting GluN2C/D (IC50=3.9 μM), GluN1/GluN2C (IC50=7.1 μM), and GluN1/GluN2D (IC50=182 μM) subunits. QNZ46 inhibits glutamate-mediated calcium influx, thereby blocking excitotoxicity. QNZ46 is membrane permeable and can cross the blood-brain barrier, where it inhibits myelin damage and axonal degeneration[1][2][3].

Product Specifications

CAS Number

[1237744-13-6]

UNSPSC

12352005

Hazard Statement

H302, H315, H319, H335

Target

IGluR

Type

Reference compound

Related Pathways

Membrane Transporter/Ion Channel; Neuronal Signaling

Applications

Neuroscience-Neurodegeneration

Field of Research

Neurological Disease

Assay Protocol

https://www.medchemexpress.com/QNZ46.html

Purity

99.46

Solubility

DMSO : 4 mg/mL (ultrasonic; warming; heat to 60°C)

Smiles

O=C(O)C1=CC=C(N2C(/C=C/C3=CC=CC([N+]([O-])=O)=C3)=NC4=C(C=C(OC)C=C4)C2=O)C=C1

Molecular Formula

C24H17N3O6

Molecular Weight

443.41

Precautions

H302, H315, H319, H335

References & Citations

[1]Hansen KB, et al. Structural and mechanistic determinants of a novel site for noncompetitive inhibition of GluN2D-containing NMDA receptors. J Neurosci. 2011 Mar 9;31 (10) :3650-3661.|[2]Doyle S, et al. Vesicular glutamate release from central axons contributes to myelin damage. Nat Commun. 2018 Mar 12;9 (1) :1032.|[3]Guo F, et al. Sevoflurane acts as an antidepressant by suppression of GluN2D-containing NMDA receptors on interneurons. Br J Pharmacol. 2024 Sep;181 (18) :3483-3502.