SN50 acetate is a cell permeable inhibitor of NF-κB translocation.

Pretreatment with SN50 acetate results in a significant reduction in amount of PI-positive cells at 12, 24, and 48 h time-point post TBI compared with vehicle-treated groups[1]. Topical SN50 acetate suppresses nuclear factor-κB activation in local cells and reduces the incidence of epithelial defects/ulceration in healing corneas. 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 acetate 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].

Treatment with SN50 acetate accelerates the recovery of motor functional outcome from 1st to 4th day. Animals subjected to SN50 acetate pretreatment demonstrate a significant decrease in the visuospatial learning latencies relative to the control group at 7 and 8 days post-TBI. Pretreatment with SN50 acetate results in a significant reduction of NF-κB p65 protein levels from 6 to 48 h post-TBI and TNF-a protein levels from 12 to 48 h post-TBI[1].