As A Drug Target
Aberrant activation of NF-κB is frequently observed in many cancers. Moreover, suppression of NF-κB limits the proliferation of cancer cells. In addition, NF-κB is a key player in the inflammatory response. Hence methods of inhibiting NF-κB signaling has potential therapeutic application in cancer and inflammatory diseases.
The discovery that activation of NF-κB nuclear translocation can be separated from the elevation of oxidant stress gives an important hint to the development of strategies for NF-κB inhibition.
A new drug called denosumab acts to raise bone mineral density and reduce fracture rates in many patient sub-groups by inhibiting RANKL. RANKL acts through its receptor RANK, which in turn promotes NF-κB, RANKL normally works by enabling the differentiation of osteoclasts from monocytes.
Disulfiram, olmesartan and dithiocarbamates can inhibit the nuclear factor-κB (NF-κB) signaling cascade.
Anatabine alleged antiinflammatory effects are claimed to result from modulation of NF-κB activity.
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