HDAC3
HDAC3 (histone deacetylase 3) is a class I histone deacetylase that functions as a central epigenetic regulator of chromatin structure and transcriptional repression through its association with nuclear receptor corepressor complexes containing NCOR and SMRT[1][2]. Mechanistically, HDAC3 forms an enzymatically active complex with NCOR/SMRT and associated cofactors, enabling histone deacetylation and coordinated control of gene expression programs involved in metabolism, circadian regulation, and cellular homeostasis[2][3][4]. HDAC3 also participates in signal-responsive transcriptional regulation, including repression of the JNK pathway and modulation of inflammatory gene expression, linking epigenetic regulation to cellular stress and immune responses[5][6]. In disease models, dysregulation of HDAC3-dependent transcriptional networks has been associated with metabolic disorders, cardiovascular pathology, inflammatory diseases, and cancer-related transcriptional abnormalities[4][6]. HDAC3 is additionally required for normal embryonic development, organ function, and maintenance of metabolic processes, highlighting its broad physiological significance[4]. Compared with related class I HDAC isoforms, HDAC3 is distinguished by its obligate functional interaction with the NCOR/SMRT corepressor complex and its dependence on corepressor-mediated activation for full biological activity[1][2][7]. Structural and genetic studies further demonstrate that disruption of HDAC3-corepressor interactions compromises HDAC3 function in vivo, emphasizing a unique regulatory mechanism not shared to the same extent by other HDAC family members[7][3]. For experimental applications, selective HDAC3 inhibitors are widely used to investigate epigenetic control of inflammation, metabolism, and disease-associated transcriptional programs, while offering greater isoform specificity than pan-HDAC inhibition strategies[6][4].
References:
- [1]. Wen YD, et al. The histone deacetylase-3 complex contains nuclear receptor corepressors. Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7202-7. [Content Brief]
- [2]. Fischle W, et al. Enzymatic activity associated with class II HDACs is dependent on a multiprotein complex containing HDAC3 and SMRT/N-CoR. Mol Cell. 2002 Jan;9(1):45-57. [Content Brief]
- [3]. Watson PJ, et al. Structure of HDAC3 bound to co-repressor and inositol tetraphosphate. Nature. 2012 Jan 9;481(7381):335-40. [Content Brief]
- [4]. He R, et al. The role of HDAC3 and its inhibitors in regulation of oxidative stress and chronic diseases. Cell Death Discov. 2023 Apr 18;9(1):131. [Content Brief]
- [5]. Zhang J, et al. The N-CoR-HDAC3 nuclear receptor corepressor complex inhibits the JNK pathway through the integral subunit GPS2. Mol Cell. 2002 Mar;9(3):611-23. [Content Brief]
- [6]. Watson N, et al. The role of HDAC3 in inflammation: mechanisms and therapeutic implications. Front Immunol. 2024 Jul 10;15:1419685. [Content Brief]
- [7]. Rabezanahary H, et al. Live virus neutralizing antibodies against pre and post Omicron strains in food and retail workers in Québec, Canada. Heliyon. 2024 May 21;10(10):e31026. [Content Brief]
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HDAC3 Related Products (197)
Related Products (197)
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Antibodies (1)
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Vorinostat
0 ImagesSynonyms: SAHA; Suberoylanilide hydroxamic acidVorinostat (SAHA) is a potent and orally active pan-inhibitor of HDAC1, HDAC2 and HDAC3 (Class I), HDAC6 and HDAC7 (Class II) and HDAC11 (Class IV), with ID50 values of 10 nM and 20 nM for HDAC1 and HDAC3, respectively. Vorinostat induces cell apoptosis. Vorinostat is also an effective inhibitor of human papillomaviruse (HPV)-18 DNA amplification.
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Tucidinostat
0 ImagesSynonyms: Chidamide; HBI-8000; CS 055
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HDAC1-IN-13
0 ImagesCat. No.: HY-183150CAS No.: 3053289-22-5HDAC1-IN-13 is an orally active HDAC1 inhibitor with IC50 values of 91, 185, 170, and 280 nM against HDAC1, HDAC2, HDAC3, and HDAC10, respectively, and shows no activity against HDAC4, HDAC5, HDAC6, HDAC7, and HDAC9. HDAC1-IN-13 induces extrinsic apoptosis by activating the caspase-8 pathway and triggers G0/G1 cell cycle arrest. HDAC1-IN-13 can be used for the research of leukemia.
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Syk/HDAC6-IN-1
0 ImagesCat. No.: HY-184415Syk/HDAC6-IN-1 is a dual SYK/HDAC6 selective inhibitor with IC50 values of 0.19 nM (SYK) and 0.66 nM (HDAC6). Syk/HDAC6-IN-1 downregulates p-SYK to block downstream AKT/FOXO1 signaling, elevates acetylated histone H3 and α-tubulin via HDAC suppression, represses SREBF1 -mediated lipid biosynthetic pathways, triggers G0/G1 cell cycle arrest and robust mitochondrial-dependent caspase-3-mediated apoptosis in leukemia cells. Syk/HDAC6-IN-1 can be used for the research of FLT3-mutant acute myeloid leukemia.
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Mocetinostat
0 ImagesSynonyms: MGCD0103
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Quisinostat
0 ImagesSynonyms: JNJ-26481585
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Givinostat
0 ImagesSynonyms: ITF-2357
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Tubacin
0 ImagesTubacin is a potent and selective inhibitor of HDAC6, with an IC50 value of 4 nM and approximately 350-fold selectivity over HDAC1. Tubacin also inhibits metallo-β-lactamase domain-containing protein 2 (MBLAC2).
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Tacedinaline
0 ImagesSynonyms: N-acetyldinaline; CI-994; Goe-5549
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1-Stearoyl-sn-glycero-3-phosphocholine
0 ImagesSynonyms: 18:0 Lyso-PC; LPC(18:0)1-Stearoyl-sn-glycero-3-phosphocholine is a lysophosphatidylcholine that inhibits HDAC3 activity and phosphorylation of STAT3 in K562 cells. 1-Stearoyl-sn-glycero-3-phosphocholine induces apoptosis and exhibits anticancer activity in chronic myelogenous leukemia (CML) K562 cells.
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Pracinostat
0 ImagesSynonyms: SB939Pracinostat is a potent histone deacetylase (HDAC) inhibitor, with IC50s of 40-140 nM, used for cancer research. Pracinostat also inhibits metallo-β-lactamase domain-containing protein 2 (MBLAC2) hydrolase activity with an EC50 below 10 nM.
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Abexinostat
0 ImagesSynonyms: CRA 024781; PCI-24781Abexinostat (CRA 024781) is a novel pan-HDAC inhibitor mostly targeting HDAC1 with Ki of 7 nM. Abexinostat also inhibits metallo-β-lactamase domain-containing protein 2 (MBLAC2) hydrolase activity with an EC50 below 10 nM.
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BRD3308
0 ImagesBRD3308 is a highly selective HDAC3 inhibitor with an IC50 of 54 nM. BRD3308 is 23-fold selectivity for HDAC3 over HDAC1 (IC50 of 1.26 μM) or HDAC2 (IC50 of 1.34 μM). BRD3308 suppresses pancreatic β-cell apoptosis induced by inflammatory cytokines or glucolipotoxic stress, and increases functional insulin release. BRD3308 activates HIV-1 transcription and disrupts HIV-1 latency.
