ReviewJournal of child neurology2012
Rationale for the development of 2-aminobenzamide histone deacetylase inhibitors as therapeutics for Friedreich ataxia.
Review in Journal of child neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 36 citations in OpenAlex.
- Epigenetic therapy for Friedreich ataxia.Annals of neurology · 2014Trial
- Role of Protein Lysine Acetylation in the Pathogenesis and Treatment of Obesity and Metabolic Syndrome.Current obesity reports · 2025Review
- A non-synonymous single nucleotide polymorphism inFrontiers in molecular biosciences · 2022Article
- HDAC4 Inhibitors as Antivascular Senescence Therapeutics.Oxidative medicine and cellular longevity · 2022Review
- The application of histone deacetylases inhibitors in glioblastoma.Journal of experimental & clinical cancer research : CR · 2020Review
- Lysine acetyltransferases and lysine deacetylases as targets for cardiovascular disease.Nature reviews. Cardiology · 2020Review
- The Process and Strategy for Developing Selective Histone Deacetylase 3 Inhibitors.Molecules (Basel, Switzerland) · 2018Review
- Translating HDAC inhibitors in Friedreich's ataxia.Expert opinion on orphan drugs · 2016Article
- TORC1 Inhibition by Rapamycin Promotes Antioxidant Defences in a Drosophila Model of Friedreich's Ataxia.PloS one · 2015Article
- Class I and IIa histone deacetylases have opposite effects on sclerostin gene regulation.The Journal of biological chemistry · 2014Article
- Histone deacetylases and their inhibitors in cancer, neurological diseases and immune disorders.Nature reviews. Drug discovery · 2014Review
- Nicotinamide in Friedreich's ataxia: useful or not?Lancet (London, England) · 2014Article
- Therapies for ataxias.Current treatment options in neurology · 2014Article
- Involvement of HDAC1 and HDAC3 in the Pathology of Polyglutamine Disorders: Therapeutic Implications for Selective HDAC1/HDAC3 Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2014Article
- Epigenetic-based therapies for Friedreich ataxia.Frontiers in genetics · 2014Review
- New and emerging HDAC inhibitors for cancer treatment.The Journal of clinical investigation · 2014Review
- A GAA repeat expansion reporter model of Friedreich's ataxia recapitulates the genomic context and allows rapid screening of therapeutic compounds.Human molecular genetics · 2013Article
- Increasing frataxin gene expression with histone deacetylase inhibitors as a therapeutic approach for Friedreich's ataxia.Journal of neurochemistry · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Numerous studies have pointed to histone deacetylase inhibitors as potential therapeutics for various neurodegenerative diseases, and clinical trials with several histone deacetylase inhibitors have been performed or are under way. However, histone deacetylase inhibitors tested to date either are highly cytotoxic or have very low specificities for different histone deacetylase enzymes. The authors' laboratories have identified a novel class of histone deacetylase inhibitors (2-aminobenzamides) that reverses heterochromatin-mediated silencing of the frataxin (FXN) gene in Friedreich ataxia. The authors have identified the histone deacetylase enzyme isotype target of these compounds and present evidence that compounds that target this enzyme selectively increase FXN expression from pathogenic alleles. Studies with model compounds show that these histone deacetylase inhibitors increase FXN messenger RNA levels in the brain in mouse models for Friedreich ataxia and relieve neurological symptoms observed in mouse models and support the notion that this class of molecules may serve as therapeutics for the human disease.
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What OpenQuestion 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 OpenQuestion graph.