Atopic dermatitis (AD), a pro-inflammatory skin disorder, is characterized by recurrent severe episodes of scaling and uncontrolled pruritis that are exacerbated by genetic and environmental factors.

Two recent key findings in AD have been the recent identification of miR-335 as a driver of keratinocyte differentiation and cornification and that miR-335 expression is lost in AD, leading to barrier defect.

Belinostat, a histone deacetylase (HDAC) inhibitor, can restore miR-335 expression and repair the defective barrier.

The toxicity issue with HDAC inhibitors which can be addressed using analogues of belinostat with chemical modifications; thiese may be less toxic and could serve as a therapeutic alternatives for the alleviation of AD.