Tat-NR2Baa TFA 

Tat-NR2BAA TFA is the control peptide of Tat-NR2B9c (HY-P0117), inactive. The sequence of Tat-NR2BAA TFA is similar to Tat-NR2B9c, but it has a double-point mutation in the COOH terminal tSXV motif, making it incapable of binding PSD-95. Tat-NR2B9c is a membrane-permeant peptide and disrupts PSD-95/NMDAR binding, correlate with uncoupling NR2B- and/or NR2A-type NMDARs from PSD-95^[1].

Tat-NR2BAA TFA (125 ng; 20 mins) does not effects interactions between PSD-95 and NR2B subunits. In contrast, coimmunoprecipitation of PSD-95 with NR2B subunits is markedly decreased in rats pretreated with the disrupting peptide Tat-NR2B9c in lumbar dorsal horn tissue^[1].
Tat-NR2BAA TFA (125 ng or 1.25 μg; 20 minutes before collection of lumbar dorsal horn tissue) is the control group of Tat-NR2B9c. Tat-NR2B9c produces a significant and robust reduction of postdischarge, indicating the hyperexcitability of the cell.But Tat-NR2BAA TFA has no effects, even at a dose 100× greater than the active peptide Tat-NR2B9c (HY-P0117)^[1].
Tat-NR2BAA TFA (1 μM; pre-treatment 1 hour) is the control group in the Co-IP assay. Tat-NR2B9c (1 μM) disrupts NR2B/PSD95 interaction, and the coupling of NR2B to PSD-95 is more sensitive than NR2A/PSD95 to disruption in hippocampal neurons^[2].

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

2588.85

C₁₀₅H₁₈₅F₃N₄₂O₃₁

Tyr-Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Lys-Leu-Ser-Ser-Ile-Glu-Ala-Asp-Ala

YGRKKRRQRRRKLSSIEADA

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• [1]. Michelle Aarts, et al. Treatment of Ischemic Brain Damage by Perturbing NMDA Receptor- PSD-95 Protein Interactions. Science  [Content Brief]

  [2]. Jing Fan, et al. N-methyl-D-aspartate Receptor Subunit- And Neuronal-Type Dependence of Excitotoxic Signaling Through Post-Synaptic Density 9. J Neurochem. 2010 Nov;115(4):1045-56.  [Content Brief]