These cytokines such as IFN-γ and TNF-α induce the release of inducible NO synthase (iNOS) via nuclear factor-κB (NF-κB) pathway which results in increased production of NO.[41] NO overproduction via iNOS upregulation by intestinal epithelium has been consistently associated with IBD.[42] The effects of compounds, PH46 (2) and the indane dimers (6-10) on NO inhibition were evaluated in this study, to elucidate if such activity may be a contributing factor to the observed beneficial in vivo effects of the novel scaffold in murine colitis models. The gene discussed is TNF; the disease is inflammatory bowel disease.