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Review
. 2016;4(1):73-89.
doi: 10.1007/s40487-016-0023-1. Epub 2016 Jun 10.

Panobinostat as Pan-deacetylase Inhibitor for the Treatment of Pancreatic Cancer: Recent Progress and Future Prospects

Avineesh Singh  1 , Vijay K Patel  1 , Deepak K Jain  1 , Preeti Patel  1 , Harish Rajak  1
Affiliations
Review

Panobinostat as Pan-deacetylase Inhibitor for the Treatment of Pancreatic Cancer: Recent Progress and Future Prospects

Avineesh Singh et al. Oncol Ther. 2016.

Abstract

The histone deacetylase (HDAC) inhibitors have been demonstrated as an emerging class of anticancer drugs. HDACs are involved in regulation of gene expression and in chromatin remodeling, thus indicating valid targets for different types of cancer therapeutics. The pan-deacetylase inhibitor panobinostat (Farydac®, LBH589) was developed by Novartis Pharmaceuticals and has been recently approved by the US Food and Drug Administraion (FDA) as a drug to treat multiple myeloma. It is under clinical investigation for a range of haematological and solid tumors worldwide in both oral and intravenous formulations. Panobinostat inhibits tumor cell growth by interacting with acetylation of histones and non-histone proteins as well as various apoptotic, autophagy-mediated targets and various tumorogenesis pathways involved in development of tumors. The optimal combination regimen for pancreatic cancer remains to be fully elucidated with various combination regimens, and should be investigated in clinical trials. This article summarizes the current preclinical and clinical status of panobinostat in pancreatic cancer. Preclinical data suggests that panobinostat has potential inhibitory activity in pancreatic cancer cells by targeting various pathways and factors involved in the development of cancer. Herein, we reviewed the status of mono and combination therapy and the rationale behind the combination therapy undergoing trials, as well as possible future prospective use in the treatment of pancreatic cancer.

Keywords: HDAC inhibitors; Histone deacetylase inhibitors; Pan-deacetylase inhibitor; Pancreatic cancer; Panobinostat.

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Figures

Fig. 1
Fig. 1
Role and effects of HDACi in pancreatic cancer with their corresponding targets. HIF-1α hypoxia-inducible factor-1 alpha, TRAIL tumor necrosis factor-related apoptosis-inducing ligand, VEGF vascular endothelial growth factor, HSP90 heat shock protein 90, CDK cyclin-dependent kinase, up arrow symbol upregulation, down arrow symbol downregulation
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