Role of histone deacetylases in pancreas: Implications for pathogenesis and therapy

Table 1 Overview of histone deacetylase inhibitors based on their structure, class specificity; current clinical trials and suggested therapeutic effects[63,77,84-88]

Structureclass	HDAC class specificity	HDAC inhibitor	Clinical trials	Effects
Hydroxamic acid	I, II, IV	Trichostatin A	-	-
		Quisinostat	Phase I	-
		Vorinostat	FDA approved (2006), phase II, III	Vorinostat significantly sensitized pancreatic cancer cells for radiotherapy
		Panobinostat	Phase II, III	Panobinostat induced the death of pancreatic tumor cell by apoptosis
		Resminostat	Phase I, II	-
		Abexinostat		-
		Belinostat		-
	I, II	Givinostat		The orally active HDAC inhibitor ITF2357 (givinostat) favors β-cell survival during inflammatory conditions
Cyclic peptide	I	Depsipeptide	FDA approved (2009), phase I, II	-
Benzamides	I	Entinostat	Phase II	-
	HDAC1	Mocetinostat	Phase I, II	Mocetinostat + gemcitabine might be an effective treatment for gemcitabine-refractory pancreatic cancer
Fatty acid	I, II	Valporic acid	Phase I, II, III	Valporic acid may protect β-cells from palmitate-induced apoptosis and ER stress via GSK-3β inhibition, independent of ATF4/CHOP pathway
	I, II	Butyrate	Phase II	Butyrate regulates both the survival and replication of human β-cells

HDAC: Histone deacetlyase; FDA: Food and Drug Administration.