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Development of Putative Isospecific Inhibitors for HDAC6 using Random Forest, QM-Polarized docking, Induced-fit docking, and Quantum mechanics

Joel, I. y.; ADIGUN, T. O.; BANKOLE, O. O.; AJIBOLA, A. O.; OFENIFORO, E. B.; AUTA, F. B.; OZOJIOFOR, U. O.; REMI-ESAN, I. A.; AKANDE, A. I.

2020-08-10 bioinformatics
10.1101/2020.08.10.243824 bioRxiv
Show abstract

Histone deacetylases have been recognized as a potential target for epigenetic aberrance reversal in the various strategies for cancer therapy, with HDAC6 implicated in various forms of tumor growth and cancers. Diverse inhibitors of HDAC6 has been developed, however, there is still the challenge of iso-specificity and toxicity. In this study, we trained a Random forest model on all HDAC6 inhibitors curated in the ChEMBL database (3,742). Upon rigorous validations the model had an 85% balanced accuracy and was used to screen the SCUBIDOO database; 7785 hit compounds resulted and were docked into HDAC6 CD2 active-site. The top two compounds having a benzimidazole moiety as its zinc-binding group had a binding affinity of -78.56kcal/mol and -78.21kcal/mol respectively. The compounds were subjected to exhaustive docking protocols (Qm-polarized docking and Induced-Fit docking) in other to elucidate a binding hypothesis and accurate binding affinity. Upon optimization, the compounds showed improved binding affinity (-81.42kcal/mol), putative specificity for HDAC6, and good ADMET properties. We have therefore developed a reliable model to screen for HDAC6 inhibitors and suggested a series of benzimidazole based inhibitors showing high binding affinity and putative specificity for HDAC6.

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