SN50 is a cell permeable NF-κB translocation inhibitor.

Compared with vehicle-treated groups,pretreatment with SN50 results in a significant reduction in amount of PI-positive cells at 12, 24, and 48 h time-point post TBI [1]. Local SN50 inhibits the activation of nuclear factor-κB in local cells and reduces the occurrence of epithelial defects/ulcers during corneal healing. Myofibroblast generation, macrophage invasion, activity of matrix metalloproteinases, basement membrane destruction, and expression of cytokines are all decreased in treated corneas compared with controls[2]. Treating the human gastric cancer cells SGC7901 with SN50 could significantly enhance the effects of LY294002 on inducing cell death after 24 h[3]. SN50 can inhibit translocation of NF-kB and production of inflammatory cytokines that are implicated in lipopolysaccharide (LPS)-induced lung injury[4].

SN50 enhances motor function recovery from the first to the fourth day and shows a significant reduction in visuospatial learning latencies on the seventh and eighth days post-TBI, compared to the control group. Furthermore, SN50 pretreatment significantly decreases NF-κB p65 and TNF-a protein levels between 6 to 48 hours post-TBI[1].