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Tat-NR2B9c is a 20-aa peptide, which acts as a postsynaptic density-95 (PSD-95) inhibitor, with an EC50 of 6.7 nM for PSD-95d2 (PSD-95 PDZ domain 2), and 670 nM for PSD-95d1; Tat-NR2B9c also reduces NMDA-induced p38 activation, and possesses neuroprotective efficacy.

Tat-NR2B9c is a PSD-95 inhibitor, with an EC50 of 6.7 nM for PSD-95d2, representing a >100-fold higher affinity for this domain than for PSD-95d1 (EC50, 0.67 μM). Tat-NR2B9c inhibits NMDAR2A, NMDAR2B, and NMDAR2C binding to PSD-95, with IC50s of 0.5 μM, ～8 μM, and 0.75 μM, respectively. Tat-NR2B9c also blocks the interaction between PSD-95 and nNOS with an IC50 of ～0.2 μM[1]. Tat-NR2B9c reduces association of PSD-95 with GluN2B by ～50% in the YAC128 striatum, decreases NMDA-induced p38 activation in YAC128 striatal tissue, but shows no effect on the NMDA-induced JNK activation[2].

Tat-NR2B9c (10 nM/g, i.v.) reduces infarction volume of male C57BL/6 mice, but has no effect at 3 nM/g[3].

[1]. Cui H, et al. PDZ protein interactions underlying NMDA receptor-mediated excitotoxicity and neuroprotection by PSD-95 inhibitors. J Neurosci. 2007 Sep 12;27(37):9901-15. [2]. Fan J, et al. P38 MAPK is involved in enhanced NMDA receptor-dependent excitotoxicity in YAC transgenic mouse model of Huntington disease. Neurobiol Dis. 2012 Mar;45(3):999-1009. [3]. Teves LM, et al. Efficacy of the PSD95 inhibitor Tat-NR2B9c in mice requires dose translation between species. J Cereb Blood Flow Metab. 2016 Mar;36(3):555-61. [4]. Huang LE, et al. N-methyl D-aspartate receptor subtype 2B antagonist, Ro 25-6981, attenuates neuropathic pain by inhibiting postsynaptic density 95 expression. Sci Rep. 2018 May 18;8(1):7848.

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