nr2b

Tat-NR2B9c acetate (NA-1 acetate) is a postsynaptic density-95 (PSD-95) inhibitor, with EC50 values of 6.7 nM and 670 nM for PSD-95d2 (PSD-95 PDZ domain 2) and PSD-95d1, respectively. Tat-NR2B9c acetate disrupts the PSD-95 NMDAR interaction, inhibiting NR2A and NR2B binding to PSD-95 with IC50 values of 0.5 μM and 8 μM, respectively. Tat-NR2B9c acetate also inhibits neuronal nitric oxide synthase (nNOS) PSD-95 interaction, and possesses neuroprotective efficacy.

Tat-NR2BAA TFA serves as the inactive control peptide for Tat-NR2B9c, featuring a comparable sequence with a crucial distinction: a double-point mutation in its COOH-terminal tSXV motif. This alteration renders Tat-NR2BAA TFA unable to bind to PSD-95, in contrast to Tat-NR2B9c. The latter is a membrane-permeant peptide that impedes PSD-95 NMDAR interaction, specifically detaching NR2B- and or NR2A-type NMDARs from PSD-95 [1].

Tat-HA-NR2B9, comprising an HIV-1 Tat transduction domain fragment, an influenza virus hemagglutinin (HA) epitope-tag, and the C-terminal 9 amino acids of NR2B (NR2B9c), has demonstrated efficacy in reducing infarct size and enhancing neurological function following ischemia-induced cerebral injury in rats [1].

Tat-NR2BAA is an inactive control peptide of Tat-NR2B9c. It shares a similar sequence with Tat-NR2B9c, but possesses a double-point mutation in the COOH terminal tSXV motif. This mutation renders Tat-NR2BAA unable to bind PSD-95. Tat-NR2B9c, on the other hand, is a membrane-permeable peptide that interferes with PSD-95 NMDAR binding. This interference leads to the decoupling of NR2B- and or NR2A-type NMDARs from PSD-95[1][2].

Tat-NR2B9c (NA-1) is a postsynaptic density-95 (PSD-95) inhibitor with neuroprotective and antiepileptic effects.Tat-NR2B9c inhibits PSD-95d2, PSD-95d1, and PSD-95, which prevents the activation of NMDA-induced NADPH oxidase in neurons, thereby blocking the production of superoxide, which reduces ischemic injury in the acute phase after stroke.

Tat-NR2B9c TFA is a 20-aa peptide, and acts as an inhibitor of postsynaptic density-95 (PSD-95)(EC50 of 6.7 nM for PSD-95d2), and possesses neuroprotective efficacy.

Tat-CBD3 is a chemical compound inhibiting the interaction between the N-type voltage-gated calcium channel Cav2.2 and collapsin response mediator protein 2 (CRMP2), as well as the interaction between CRMP2 and the NMDA receptor NR2B subunit. At a concentration of 10 µM, Tat-CBD3 reduces the Cav2.2-CRMP2 interaction by 43% in cell-free assays and impedes the NMDA receptor NR2B subunit-CRMP2 interaction in immunoprecipitation assays. It lowers voltage-induced calcium currents by about 60% in primary rat dorsal root ganglion (DRG) neurons and decreases glutamate-induced cytosolic calcium level rises in primary rat hippocampal neurons. When administered at 20 mg/kg, Tat-CBD3 lessens infarct volume in a rat model of cerebral ischemia following middle cerebral artery occlusion (MCAO). Additionally, intrathecal delivery of Tat-CBD3 at a dose of 20 µg/5 µl mitigates carrageenan-induced thermal hypersensitivity in rats.

GluN2B (formally NR2B) selective, competitive antagonist of the NMDA receptor. Blocks NMDA-evoked current in mouse cortical neurons (IC50 = 480 nM); also inhibits NMDA-evoked responses in oocytes expressing GluN2B (formally NR2B), but not GluN2A (formally