Table 3.

NF-κB pharmacological models that interfere with muscular pathology

Pharmacological components	Way of action	Reported muscle effect	Animal	References
NBD peptide	NEMO-specific inhibitor dystrophic	Improving pathology	Mice	[83]
Salicylate	IKKβ inhibitor but also has a range of other targets	Severe reduction of muscle atrophy	Mice	[4]
Remicade	Silencing TNF-α activity	Reduced breakdown of dystrophic muscle	Mice	[90, 91]
Enbrel	Silencing TNF-α activity	Reduced inflammation	Mice	[91]
Curcumin	NF-κB inhibitor also induces AP-1 and Nrf2	Stimulates muscle regeneration	Mice	[102]
Synthetic antioxidant also induces Nrf2 pyrrolidine dithiocarbamate (PDTC)	NF-κB inhibitor	Ameliorates the dystrophic phenotype	Mice	[93]
mTNFα gene transfer	Induce TNF activity	Induces cachexia, inhibits muscle regeneration	Mice	[92]
Thalidomide	Inhibitor of TNF-α synthesis	Attenuation of loss weight and lean body mass in patients with pancreatic cancer	Humans	[100]
Pentoxifylline	TNF-α inhibitor, also a PDE4 inhibitor (increasing cAMP and stimulating PKA activity)	No benefits	Humans	[99]
		On-going clinical trial in DMD, phase II	Humans	[104]

AP-1 Activating protein 1, Nrf2 nuclear respiratory factor 2, PDE4 phosphodiesterase 4