Abstract
The transcription factor NF-κB has been implicated in the pathogenesis of a variety of both acute and chronic inflammatory diseases. Many agents have shown promise and potential to abrogate NF-κB activity in both in vitro and in vivo systems. These include antioxidants, corticosteroids, proteasome inhibitors, arachadonic acid pathway metabolites, salicylates, molecular interventions and cell-permeable peptides. Unfortunately, therapies aimed at blocking its activation have not proven clinically feasible at this time. As the complex signal transduction pathways leading to NF-κB activation are further elucidated, more specific inhibitors of NF-κB are likely to be identified.