Evidence map›Paper›PMID 39758147›Full record

ArticleIn silico pharmacology2025

Structure similarity based screening coupled to integrated structural biochemistry approach for exploring the high affinity inhibitors against histone deacetylase (HDAC)-6.

Shabir Ahmad Ganai, Suma Mohan

Abstract read
In one paragraph

Article in In silico pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Shabir Ahmad GanaiDivision of Basic Sciences & Humanities, FoH, SKUAST-Kashmir, Shalimar, Srinagar, 190025 Jammu and Kashmir India.
Suma MohanSchool of Chemical and Biotechnology, SASTRA University, Thanjavur, 613401 Tamil Nadu India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase (HDAC)-6 has overwhelming implications in multiple cancers and neurodegenerative disorders. Unusual HDAC6 expression modulates various signalling mechanisms which in turn forms the aetiology of the above-mentioned disorders. Thus, restoring the typical activity of HDAC6 through small molecules may prove as a promising approach to beat these disorders. Herein, we employed an integrated approach for exploring the high binding affinity manifesting molecules against HDAC6. We screened the entire PubChem database using Tubastatin A as the reference (query) molecule following which we carried out 110 molecular docking (XP-mode) and 110 MM-GBSA experiments. Thirty-three molecules demonstrated raised binding affinity than query in the HDAC6 active site. Further, the top 3 binders selected on logical grounds were subjected to interaction study, two hit molecules and tubastatin-A were subjected to convoluted molecular dynamics and three-dimensional e-Pharmacophores mapping was done to delineate the rationale behind the high binding tendency of hit molecules over control molecule. This work provides a solid foundation for additional research towards the development of lead molecules from the said hits for therapeutic intervention against HDAC6 overexpression-driven disorders.

Indexed as

CancerHDAC6MM-GBSA, 3D-E-pharamacophore hypothesisNeurodegenerative disordersTubastatin AXP-molecular docking

Identifiers

PMID39758147
PMCPMC11695532

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.