nNOS - PSD-95 Interaction Inhibitor, ZL006

A cell-permeable and blood-brain barrier-permeant aminosalicylic acid compound that selectively disrupts nNOS and PSD-95 interaction upon NMDAR activation both in primary murine cortical neuron cultures (0.8- and 2.8-fold increase from basal level with or without 30 min 10 uM ZL006 pretreatment before 30 min Glu-Gly stimulation) in vitro and in mice subjected to middle brain artery occlusion (0.4- and 1.9-fold increase from basal level with or without inhibitor pretreatment 15 min before MACO; 1.5 mg/kg i.v.) in vivo without affecting nNOS activity or non-nNOS-mediated NMDAR EPSCs (excitatory postsynaptic currents) in rat hippocampus. Its therapeutic efficacy in limiting ischemia-caused brain tissue damage has been demonstrated in both mice and rats when applied 1 h after blood reperfusion following MACO (60% and 50% reduction of infarction, respectively; 1.5 mg/kg i.v.).

A cell-permeable and blood-brain barrier-permeant aminosalicylic acid compound that selectively disrupts nNOS and PSD-95 interaction upon NMDAR activation both in primary murine cortical neurons (0.8- and 2.8-fold increase from basal level with or without 30 min 10 uM ZL006 pretreatment) in vitro and in mice (0.4- and 1.9-fold increase from basal level with or without inhibitor pretreatment 15 min before ischemia; 1.5 mg/kg i.v.) in vivo without affecting nNOS activity or non-nNOS-mediated NMDAR EPSCs (excitatory postsynaptic currents). Effectively reduce ischemia-caused brain tissue damage in both mice and rats when applied 1 h after blood reperfusion following ishemia (60% and 50% reduction of infarction, respectively; 1.5 mg/kg i.v.).

Packaged under inert gas

Toxicity: Regulatory Review (Z)

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Zhou, L., et al. 2010. Nature Med.16, 1439.

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