Table 1. . List of epigenetic modifying tool compounds.

Epigenetic mark	Target	Tool compound	Affected process
Histone acetylation	Pan histone deacetylase inhibitors	Trichostatin A	Cancer treatment reduced IL-17 and T helper cell number, reduced TGF-β in mouse BAL [62,63]
		Vorinostat	Cancer treatment and graft vs host disease [63]
	BET domain mimics – block readers of acetylation	JQ1	Prevent cell cycle progression and investigated as an anticancer treatment [64,65]
Histone methylation:
– Histone 3 lysine 4 (H3K4)	SETD7	PFI-2	H3K4 is linked to activation of inflammatory responses [26,66]
– Histone 3 lysine 9 (H3K9)	G9a (H3K9 methyltransferase)	UNC0642	Macrophages and dendritic cells of asthmatics undergoing allergen exposure may benefit from the inhibition of H3K9 methyltransferases, to prevent activation of the inflammation
	JMJD2 H3K9 demethylase	ML324	Decrease the effects of Herpes virus in mice [67]
– Histone 3 lysine 27 (H3K27)	JMJ3D (H3K27 demethylase)	GSK-J1 + GSK-J4	Inhibits LPS-induced macrophage inflammation [68]
	Lysine-specific demethylases	Compound 12d	Additive effects with HDAC inhibitors on inhibiting cell proliferation and may inhibit inflammatory cytokines [69]
DNA methylation	DNMT1 complexes		DNMT inhibitors may return T cells to a Th1 phenotype in asthma [70]
	DNMT1/PCNA	Peptide inhibitor - 163–174	Target DNA methylation at specific regions [71]
	DNMT1/USP7	Peptide inhibitor - 561–567	Target DNA methylation at specific regions [71]
	DNMT1/STAT3	Peptide inhibitor - 683–174	Target DNA methylation at specific regions [71]
	DNMT1/CFP1	Peptide inhibitor - 1081–1097	Target DNA methylation at specific regions [71]
miRNAs	miR-34 mimic	MRX34	Inhibits tumor growth [72]
	miR-122		Hepatitis C is supressed by the inhibition of miR-122 [73]
	miR-150	Nanovesicles containing miR-150	Enter effector T cells and suppressing allergic contact dermatitis and promoting antigen-specific tolerance in mice [74]
	miR-9	miR-9 antagamirs	Inhibition of miR-9 increased PP2A activity and GR nuclear translocation in macrophages and restored steroid sensitivity in multiple mouse models of steroid-resistant AHR [75]
	miR-145	miR-145 antagamir	miR-145 antagamir inhibited eosinophilic inflammation, mucus hypersecretion, Th2 cytokine production and AHR in murine model of asthma [76]
	miR-126	miR-126 antagamir	Blockade of miR-126 suppressed Th2 responses, inflammation, AHR, eosinophil recruitment and mucus hypersecretion in mouse model of asthma via suppression of GATA3 expression [77]

AHR: Airways hyper-responsiveness; BET: Bromo and extraterminal domain; GR: Glucocorticoid receptor; LPS: Lipopolysaccharide.