ArticleFrontiers in pharmacology2024
Repurposed drugs as histone deacetylase 8 inhibitors: Implications in cancer and neuropathological conditions.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Research Progress of Histone Deacetylase and Its Inhibitors in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Chemical Epigenetics: Small Molecules Targeting Chromatin Modifiers in Disease Modulation.Cell biochemistry and biophysics · 2026Review
- Epigenetic Dysregulation in Neurodegeneration: The Role of Histone Deacetylases and Emerging Inhibitor Strategies.Biomolecules · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase 8 (HDAC8) is a member of class I histone deacetylases (HDACs) that catalyzes the deacetylation of both histone and non-histone proteins. Dysregulation and overexpression of HDAC8 are implicated in the development of various complex diseases, including cancer and neurodegenerative disorders. HDAC8 plays a significant role in cancer progression, contributing to cancer cell proliferation, metastasis, immune evasion, and drug resistance. The available HDAC8-targeting inhibitors suffer from poor target engagement and low tolerability, and demonstrate off-target toxicity due to limited selectivity, leading to adverse effects in patients, and thus urging for the identification and development of new molecules. Drug repurposing is a useful strategy for identifying useful drugs for predefined targets which can be exploited here for identifying promising drug molecules against HDAC8. This study involved an integrated virtual screening against HDAC8 using the DrugBank database to identify repurposed drugs capable of inhibiting HDAC8 activity. The process started by selecting the top 10 drug molecules based on their binding affinity. The drug profiling and biological function of selected molecules were then evaluated, showing anti-cancer and anti-neurological properties with a high probability of being active. Interaction analysis revealed crucial binding of radotinib and sertindole molecules with the HDAC8 protein. Both molecules showed higher binding affinity than reference inhibitor droxinostat. The elucidated molecules were further evaluated for 500 ns long-run molecular dynamics (MD) simulation with HDAC8. Structural deviation, compactness, folding behavior, hydrogen bonds analysis, and secondary structure content profiling revealed complex stability formed by HDAC8 and the selected compounds. Principal component analysis and Gibbs free energy calculations strongly recommend that both complexes were highly stable during the simulation. Overall, the results indicate that radotinib and sertindole can be promising candidates as HDAC8-targeting repurposed drugs against cancer and neuropathological conditions.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.