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    GENE:

    HDAC3 (Histone Deacetylase 3)

    i
    Other names: HDAC3, Histone Deacetylase 3, RPD3-2, HD3, KDAC3, RPD3, SMAP45
    Associations

    News

    Trials
    3d
    Structural diversification and selective inhibition of HDAC3: A comprehensive review of inhibitors and degraders. (PubMed, Eur J Med Chem)
    These emerging therapeutic agents not only reduce adverse effects by minimizing off-target activity but also enable novel treatment strategies for complex diseases through precise modulation of disease-associated signaling pathways. This review summarizes recent advances in the development of HDAC3 inhibitors and degraders, with particular emphasis on their structural features and biological functions, aiming to provide up-to-date insights for rational inhibitor design and to guide future optimization of their therapeutic applications.
    Review • Journal
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    HDAC3 (Histone Deacetylase 3)
    4d
    HDAC3 inhibition as a therapeutic strategy in T-cell acute lymphoblastic leukemia via the TYK2-STAT1-BCL2 signaling pathway. (PubMed, Front Immunol)
    HDAC3 was found to associate with TYK2 and contributed to activation of the TYK2-STAT1-BCL2 signaling pathway in T-ALL cells. Our results highlight the effectiveness of the combination of chidamide and chemotherapy in the treatment of T-ALL patients and suggest that HDAC3 can act as a potential novel therapeutic target to inhibit the TYK2-STAT1-BCL2 signaling pathway in T-ALL.
    Journal • IO biomarker
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    BCL2 (B-cell CLL/lymphoma 2) • HDAC2 (Histone deacetylase 2) • TYK2 (Tyrosine Kinase 2) • HDAC10 (Histone Deacetylase 10) • HDAC3 (Histone Deacetylase 3)
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    Epidaza (chidamide)
    4d
    Reversible acetylation of Hpo regulates the Hippo pathway. (PubMed, Proc Natl Acad Sci U S A)
    Additionally, knockdown of the acetyltransferase Nej decreases the expression of Hippo target genes, a phenotype that can be reversed by simultaneously silencing Hdac3. Taken together, these findings shed light on the role of reversible acetylation in controlling the Hippo pathway and provide insights into growth regulation and potential therapeutic approaches for related diseases.
    Journal
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    HDAC3 (Histone Deacetylase 3)
    13d
    Preoperative exercise induces anti-tumor Kupffer cells to prevent surgical stress-promoted colorectal cancer liver metastasis. (PubMed, Cell Rep Med)
    Furthermore, exercise-induced butyrate accumulation in Kupffer cells inhibits histone deacetylase 3 activity, promoting CXCL9 expression. These findings suggest that PEx may serve as a non-invasive strategy to reduce recurrence and provide potential targets for exercise-mimetic therapies.
    Journal
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    CD8 (cluster of differentiation 8) • CXCL9 (Chemokine (C-X-C motif) ligand 9) • CXCR3 (C-X-C Motif Chemokine Receptor 3) • HDAC3 (Histone Deacetylase 3)
    14d
    Phytic acid (InsP6) activates HDAC3 epigenetic axis to maintain intestinal barrier function. (PubMed, Nat Commun)
    InsP6 treatment is sufficient to rescue these effects. In inflammatory bowel disease, diminished IPMK levels exacerbate intestinal permeability, while oral InsP6 treatment mitigates leaky gut effects by restoring the HDAC3 epigenetic axis, highlighting the clinical significance of the IPMK-HDAC3 pathway and the therapeutic potential of phytic acid.
    Journal
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    HDAC3 (Histone Deacetylase 3)
    25d
    Design, synthesis, and biological evaluation of novel HDAC3 PROTACs for combined therapy with Venetoclax in acute myeloid leukemia. (PubMed, Bioorg Chem)
    Mechanistically, the combination of B22 and Venetoclax synergistically induces DNA damage and downregulates the anti-apoptotic proteins Mcl-1 and Bcl-xL. In conclusion, this study provided insights into novel HDAC3-directed PROTACs development and proposed their therapeutic potential against AML.
    Journal
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    MCL1 (Myeloid cell leukemia 1) • BCL2L1 (BCL2-like 1) • HDAC3 (Histone Deacetylase 3)
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    Venclexta (venetoclax)
    28d
    Dual epigenetic and nuclear export inhibition by chidamide and selinexor in high grade B-cell lymphomas via survivin and PI3K/AKT inhibition. (PubMed, Clin Epigenetics)
    Our preclinical data highlighted the potential synergistic efficacy of chidamide and selinexor in targeting HGBL-DHL, providing a rationale for further clinical investigation of this therapeutic combination for the treatment of this refractory disease.
    Journal
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    MYC (V-myc avian myelocytomatosis viral oncogene homolog) • BCL2 (B-cell CLL/lymphoma 2) • BCL6 (B-cell CLL/lymphoma 6) • BCL2L1 (BCL2-like 1) • BIRC5 (Baculoviral IAP repeat containing 5) • CCNA2 (Cyclin A2) • ANXA5 (Annexin A5) • HDAC3 (Histone Deacetylase 3)
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    Xpovio (selinexor) • Epidaza (chidamide)
    1m
    USP18 promotes cell proliferation and inhibits ferroptosis by stabilizing HDAC3 in endometrial carcinoma. (PubMed, Exp Cell Res)
    Moreover, USP18 silencing promoted the accumulation of lipid reactive oxygen species (ROS), malondialdehyde (MDA), and Fe2+, thereby enhancing erastin-induced ferroptosis...Subsequent rescue experiments confirmed that the tumor-promoting effects of USP18 were abrogated upon HDAC3 knockdown. Taken together, our results identify the USP18/HDAC3 axis as a key regulator of EC cell proliferation and ferroptosis suppression, underscoring the potential of USP18 as a therapeutic target in EC.
    Journal
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    USP18 (Ubiquitin Specific Peptidase 18) • HDAC3 (Histone Deacetylase 3) • USP1 (Ubiquitin Specific Peptidase 1)
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    erastin
    2ms
    Targeting Class I Histone Deacetylases Triggers Antitumor Responses in Colorectal Cancer In Vitro and In Vivo. (PubMed, J Med Chem)
    The short-term in vitro effects of 5d were modulated by a compensatory upregulation of autophagy. However, in long-term, this protective mechanism becomes insufficient to sustain tumor survival, resulting in strong antitumor efficacy in vivo in the CAM assay for both compounds even outperforming entinostat.
    Preclinical • Journal
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    HDAC2 (Histone deacetylase 2) • HDAC1 (Histone Deacetylase 1) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • HDAC3 (Histone Deacetylase 3)
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    Jingzhuda (entinostat)
    2ms
    A2 astrocyte polarization mediates ketogenic diet protection of blood-central nervous system barriers in experimental autoimmune encephalomyelitis. (PubMed, Neural Regen Res)
    Ketogenic diet suppressed astrocytic NOD-, LRR- and pyrin domain-containing protein 3 inflammasome activation, as evidenced by reduced NOD-, LRR- and pyrin domain-containing protein 3/glial fibrillary acidic protein co-localization. In summary, the ketogenic diet promotes neuroprotection in the experimental autoimmune encephalomyelitis model by inhibiting A1 astrogliogenesis and protecting the integrity of the blood-brain barrier/blood-spinal cord barrier.
    Journal
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    IL6 (Interleukin 6) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • TNFA (Tumor Necrosis Factor-Alpha) • CXCL10 (Chemokine (C-X-C motif) ligand 10) • STAT3 (Signal Transducer And Activator Of Transcription 3) • CXCL12 (C-X-C Motif Chemokine Ligand 12) • CCL2 (Chemokine (C-C motif) ligand 2) • CLDN1 (Claudin 1) • CCR2 (C-C Motif Chemokine Receptor 2) • IL1B (Interleukin 1, beta) • IL4 (Interleukin 4) • TJP1 (Tight Junction Protein 1) • CDH5 (Cadherin 5) • GFAP (Glial Fibrillary Acidic Protein) • HDAC3 (Histone Deacetylase 3) • OCLN (Occludin)
    2ms
    Peptide‑based therapeutics targeting the SLC39A14‑PIWIL2 fusion in hepatocellular carcinoma. (PubMed, Genomics Inform)
    Among the tested candidates, NEP1 markedly suppressed PIWIL2-driven oncogenic activity, and its co-administration with 5-fluorouracil (5-FU) significantly reduced PIWIL2-induced chemoresistance, thereby enhancing therapeutic efficacy. Collectively, these findings establish SLC39A14-PIWIL2 as a novel oncogenic fusion in HCC and highlight fusion protein-targeted peptide therapeutics as a promising avenue for precision treatment in HCC.
    Journal
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    HDAC3 (Histone Deacetylase 3)
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    5-fluorouracil
    2ms
    Proteolysis Targeting Chimera Loaded Extracellular Vesicles for Developing Triple Negative Breast Cancer Treatment. (PubMed, J Extracell Vesicles)
    Intraperitoneal injections of YX968 loaded EVs led to significantly enhanced intratumoral degradation of HDAC3 and HDAC8 than YX986 alone, which resulted in advanced TNBC tumour inhibition without noticeable tissue toxicity. Such EV-based delivery strategy, with a scalable EV loading approach, enhanced the in vivo PROTAC drug stability and bioavailability and improved tissue penetration and targeting, filling an important gap in the clinical translation of PROTAC-based cancer therapy.
    Journal
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    HDAC3 (Histone Deacetylase 3)