Table 2. Small molecule inhibitors of HDACs and their effects on (NF-κB-mediated) inflammation.

HDAC inhibitor	Selectivity	Effects in disease models	Refs
Trichostatin A (TSA)	pan-HDAC	Suppression of TNFα in vitro	[60]
SAHA (Vorinostat)	pan-HDAC	Reduces LPS-induced cytokine release in vitro and in vivo Suppresses LPS-stimulated NF-κB nuclear accumulation	[50,68]
LBH589 (Panabinostat)	pan-HDAC	Promotes NF-κB activation	[57]
ITF2357 (Givinostat)	pan-HDAC	Inhibition TNFα expression in peripheral blood mononuclear cells Therapeutic benefit in patients suffering from juvenile idiopathic arthritis	[58,62]
LAQ824 (Dacinostat)	pan-HDAC	Inhibition of IL-10 expression	[63]
MS-275 (Entinostat)	HDAC 1-3	Promotes NF-κB activation Suppresses LPS-stimulated NF-κB nuclear accumulation	[64,68]
MGCD0103 (Mocetinostat)	HDAC 1-3, 11	-	[61,65]
MI192	HDAC 2-3	Suppresses IL-6 production in primary PBMCs	[69]
KBH-A42	HDAC 1-2	Suppression of TNFβ production in vitro and in vivo	[70]
RGFP966	HDAC 3	Supresses TNFα-induced CCL2 expression	[71]
		Inhibition of pro-inflammatory genes in vitro and ex vivo; ↑ IL-10	[72]