CNQX disodium salt

AMPA/Kainate Receptor Antagonist
Cat #: C-141
  • Lyophilized Powder
  • Bioassay Tested
  • Source Synthetic
    MW: 276.1
    Purity: >98%
    Effective concentration 300 nM - 500 µM.
    Chemical name 6-Cyano-7-nitroquinoxaline-2,3-dione disodium.
    Molecular formula C9H2N4O4Na2.
    CAS No.: 479347-85-8.
    Activity AMPA/Kainate receptor antagonist. The concentrations that inhibit 50% of AMPA binding (IC50) for CNQX in dorsal horn neurons and motoneurons are 300 nM - 1.3 µM, It was about one-fifth as effective at kainate binding sites1,2. The association of AMPA receptors with TARPs converts CNQX from an antagonist to a weak partial agonist. CNQX binds with high affinity to both high and low affinity AMPA binding sites in rat brain. CNQX is a potent antagonist in electrophysiological responses mediated by non-NMDA receptors. Effects at NMDA receptors are much weaker.
    Shipping and storage Shipped at room temperature. Product as supplied can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C. Desiccation is recommended.
    Solubility Up to 20 mM in water. Centrifuge all product preparations before use (10000 x g 5 min).
    Storage of solutions It is recommended to prepare stock solutions afresh whenever possible, and avoid long term storage. Otherwise, store in single use aliquots up to four weeks at 4°C or three months at -20°C.
      • Alomone Labs CNQX disodium salt inhibits GluA1 channels expressed in Xenopus oocytes.
        Time course of current reversible inhibition by 20, 2 and 10 μM CNQX disodium salt (#C-141) (at -80 mV) in the presence of 100 μM glutamate. Amplitude change as a result of the application of different  concentrations of CNQX disodium salt (perfusion duration indicated by the horizontal bar, concentration as indicated).
      • The first widely used competitive AMPA receptor antagonists were quinoxalinediones (CNQX, DNQX, NBQX), which were highly selective over NMDA receptors but antagonized kainate receptors. CNQX is a potent, competitive AMPA/kainate receptor antagonist. It also acts as an antagonist at the NMDA receptor glycine site.

        This non-NMDA receptor antagonist inhibits [3H]AMPA binding to quisqualate receptors at submicromolar concentrations. CNQX also selectively blocks the excitatory action of quisqualate and kainate on spinal neurons with little or no effect on that of NMDA.

        The concentrations that inhibit 50% of [3H]AMPA binding (IC50) for CNQX in dorsal horn neurons is 300 nM1.

        The association of AMPA receptors with TARP auxiliary subunits converts CNQX from an antagonist to a weak partial agonist. CNQX induces partial domain closure, consistent with the activity of a partial agonist. CNQX blocks both fast AMPA-mediated and slow kainate receptor-mediated mEPSCs2.

        EC50 values for depression of the monosynaptic ventral root reflex is 1.0 ± 0.3 µM3.

        Direct binding studies using CNQX as a radioligand show that CNQX binds with high affinity (40 nM) to both high (14 nM) and low (235 nM) affinity AMPA binding sites in rat brain4.

    Target AMPA/Kainate receptors
    Image & Title

    CNQX disodium salt
    Alomone Labs CNQX disodium salt abolishes glutamatergic synaptic currents in rat dorsal horn.Whole-cell patch-clamp recordings on spinal cord neurons. Monosynaptic evoked EPSCs (eEPSCs) of C- and Aδ-fibers of the dorsal root were sensitive to 1 µM CNQX disodium salt (#C-141), (left) indicating that glutamatergic synaptic transmission is likely associated with nociceptive signaling. In the absence of stimulation (right), spontaneous glutamatergic synaptic currents were also observed and were sensitive to CNQX disodium salt.Adapted from Muqeem, T. et al. (2018) J. Neurosci. 38, 3729. with permission of the Society for Neuroscience.

    Last update: 27/06/2019

    CNQX disodium salt (#C-141) is a highly pure, synthetic, and biologically active compound.

    For research purposes only, not for human use
    Citations
      • Muqeem, T. et al. (2018) J. Neurosci. 38, 3729.
      • Tang, Y. et al. (2018) Eur. J. Neurosci. 47, 866.
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