Blocking specific NF-κB-DNA binding can also be accomplished with decoy oligodeoxynucleotides (ODNs). These ODNs have κB sites and competes for NF-κB dimer binding to specific genomic promoters [123–125]. These oligonucleotides have modifications to increase their stability and their affinity for NF-κB in vivo [126–128]. Decoy ODNs have been reported to have therapeutic potential in a number of animal models of inflammation and cancer; for example, directly injecting NF-κB decoy ODNs into implanted adenocarcinoma colon 26 tumors in mice inhibited cachexia without affecting tumor growth [129].
