Nuclear factor kappa B (NF-κB) is an ubiquitous rapid response transcription factor in cells involved in immune and inflammatory reactions, and exerts its effect by expressing cytokines, chemokines, cell adhesion molecules, growth factors, and immunoreceptors. In this manner, NF-κB contributes to immunologically medicated diseases such as allograft rejection, rheumatoid arthritis, and bronchial asthma. The prototypic inducible form of NF-κB is a heterodimer composed of NF-κB1 and RelA, which both belong to the NF-κB/Rel family of proteins. Inactive NF-κB is present in the cytoplasm complexed with an inhibitory protein, IκB. NF-κB is activated by a number of incoming signals from the cell surface. Released from IκB inhibition, NF-κB translocates into the nucleus and binds to the κB motif of the target gene. The NF-κB activation process can be inhibited by pharmacologic agents at each activation step. Glucocorticoids inhibit NF-κB by directly associating with NF-κB or by upregulating IκB expression. Cyclosporine and tacrolimus prevent NF-κB activation by inhibiting the action of calcineurin, a phosphatase that indirectly induces IκB degradation. Deoxyspergualin inhibits NF-κB by blocking its nuclear translocation. Aspirin and salicylates inhibit upstream events inducing IκB phosphorylation. Tepoxalin and antioxidants inhibit NF-κB activation by influencing the redox state of the cell. Further research is required to develop more specific inhibitors to treat diseases mediated by NF-κB.