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 (204)
Related Products (204)
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Antibodies (1)
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HPOB
0 ImagesHPOB is a highly potent and selective inhibitor of HDAC6 with an IC50 of 56 nM. HPOB displays >30 fold less potent against other HDACs. HPOB enhances the effectiveness of DNA-damaging anticancer agents in transformed cells but not normal cells. HPOB does not block the ubiquitin-binding activity of HDAC6.
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SIRT6-IN-3
0 ImagesSIRT6-IN-3 (compound 8a) is a selective inhibitor of SIRT6 (IC50=7.49 μM). SIRT6-IN-3 inhibits pancreatic ductal adenocarcinoma (PDAC) cells proliferation and induces apoptosis. SIRT6-IN-3 increases the sensitivity of cancer cells to gemcitabine (HY-17026) via blocking the DNA damage repair pathway. SIRT6-IN-3 is used in pancreatic cancer research.
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Domatinostat tosylate
0 ImagesSynonyms: 4SC-202
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MC1742
0 ImagesMC1742 is a potent HDAC inhibitor, with IC50s of 0.1 μM, 0.11 μM, 0.02 μM, 0.007 μM, 0.61 μM, 0.04 μM and 0.1 μM for HDAC1, HDAC2, HDAC3, HDAC6, HDAC8, HDAC10 and HDAC11, respectively. MC1742 can increase acetyl-H3 and acetyl-tubulin levels and inhibits cancer stem cells growth. MC1742 can induce growth arrest, apoptosis, and differentiation in sarcoma CSC.
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1-Stearoyl-sn-glycero-3-phosphocholine-d35
0 ImagesSynonyms: 18:0 Lyso-PC-d35; LPC(18:0)-d351-Stearoyl-sn-glycero-3-phosphocholine-d35 is deuterium labeled 1-Stearoyl-sn-glycero-3-phosphocholine (HY-125771). 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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HDAC-IN-27 dihydrochloride
0 ImagesHDAC-IN-27 dihydrochloride (Compound 11h) is a potent, orally active class I HDAC-selective inhibitor with IC50 values ranging from 0.43 to 3.01 nM against HDAC1-3. HDAC-IN-27 dihydrochloride exhibits both in vivo and in vitro antitumor activity. HDAC-IN-27 dihydrochloride demonstrates significant anti-proliferative activity against acute myeloid leukemia (AML) cell lines by inducing apoptosis and histone acetylation (AcHH3 and AcHH4). HDAC-IN-27 dihydrochloride can be used for research in acute myeloid leukemia (AML).
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FNDR-20123
0 ImagesFNDR-20123 is a safe, first-in-class, and orally active anti-malarial HDAC inhibitor with IC50s of 31 nM and 3 nM for Plasmodium and human HDAC, respectively. FNDR-20123 exerts anti-malarial activity against Plasmodium falciparum asexual stage (IC50=41 nM) and sexual blood stage (IC50=190 nM for male gametocytes). FNDR-20123 inhibits HDAC1, HDAC2, HDAC3, HDAC6, and HDAC8 (IC50=25/29/2/11/282 nM, respectively.) and inhibits Class III HDAC isoforms at nanomolar concentrations.
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AES-350
0 ImagesAES-350 is a potent and orally active HDAC6 inhibitor with an IC50 and a Ki of 0.0244 μM and 0.035 μM, respectively. AES-350 is also against HDAC3, HDAC8 in an enzymatic activity assay with IC50 values of 0.187 μM and 0.245 μM, respectively. AES-350 triggers apoptosis in AML cells through HDAC inhibition and can be used for acute myeloid leukemia (AML) research.
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HDAC-IN-53
0 ImagesCat. No.: HY-149208CAS No.: 2921948-27-6HDAC-IN-53 is an orally active, and selective HDAC1-3 inhibitor with IC50 values of 47 nM, 125 nM, and 450 nM, respectively. HDAC-IN-53 does not inhibit class II HDACs (HDAC4, 5, 6, 7, 9; IC50>10 μM). HDAC-IN-53 induces caspase-dependent apoptosis. HDAC-IN-53 significantly inhibits the growth of human tumor xenografts in nude mice and murine tumor growth in immune-competent mice bearing MC38 colon cancer.
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LSD1/HDAC-IN-2
0 ImagesLSD1/HDAC-IN-2 (Compound 20c) is the inhibitor for LSD and HDAC, that inhibits LSD1, HDAC1, HDAC2, HDAC3, HDAC6, and HDAC8, with IC50s of 39.0, 1.4, 1.0, 1.3, 2.9 and 16.0 nM, respectively. LSD1/HDAC-IN-2 inhibits the proliferation of cancer cells, especially the colorectal cancer cells. LSD1/HDAC-IN-2 arrests the cell cycle at G2/M phase, inhibits cell migration, and induces apoptosis in HCT-116 and HT-29 cells. LSD1/HDAC-IN-2 exhibits antitumor efficacy in mouse model without significant toxicity.
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Tucidinostat-d4
0 ImagesSynonyms: Chidamide-d4; HBI-8000-d4; CS 055-d4
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CRA-026440 hydrochloride
0 ImagesCRA-026440 hydrochloride is a potent, broad-spectrum HDAC (HDAC) inhibitor. The Ki values against recombinant HDAC isoenzymes HDAC1, HDAC2, HDAC3, HDAC6, HDAC8, and HDAC10 are 4 nM, 14 nM, 11 nM, 15 nM, 7 nM, and 20 nM respectively. CRA-026440 hydrochloride shows antitumor and antiangiogenic activities. CRA-026440 (hydrochloride) is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
