2. Signaling Pathways
  3. Cell Cycle/DNA Damage
    Epigenetics
  4. HDAC

HDAC

Histone deacetylases

HDAC

Related Products

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HDAC (Histone deacetylases) are a class of enzymes that remove acetyl groups (O=C-CH3) from an ε-N-acetyl lysine amino acid on ahistone, allowing the histones to wrap the DNA more tightly. This is important because DNA is wrapped around histones, and DNA expression is regulated by acetylation and de-acetylation. Its action is opposite to that of histone acetyltransferase. HDAC proteins are now also called lysine deacetylases (KDAC), to describe their function rather than their target, which also includes non-histone proteins. Together with the acetylpolyamine amidohydrolases and the acetoin utilization proteins, the histone deacetylases form an ancient protein superfamily known as the histone deacetylase superfamily.

HDAC Isoform Specific Products:

HDAC Isoform Comparison
Cat. No. Product Name Effect Purity Chemical Structure
  • HY-174398
    GSK-3β/HDAC-IN-2
    		Inhibitor
    GSK-3β/HDAC-IN-2 is a potent inhibitor of GSK-3β (IC50 = 0.04 μM), HDAC2 (IC50 = 1.05 μM, Ki = 0.070 μM) and HDAC6 (IC50 = 1.52 μM, Ki = 0.017 μM). GSK-3β/HDAC-IN-2 inhibits HDAC2 and HDAC6 activities and blocks tau hyperphosphorylation. GSK-3β/HDAC-IN-2 exerts neuroprotective effects and shows no significant toxicity. GSK-3β/HDAC-IN-2 can be used in the research of Alzheimer's disease.
    GSK-3β/HDAC-IN-2
  • HY-RS06082
    HDAC7 Human Pre-designed siRNA Set A
    		Inhibitor

    HDAC7 Human Pre-designed siRNA Set A contains three designed siRNAs for HDAC7 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
    HDAC7 Human Pre-designed siRNA Set A
  • HY-144293
    HDAC-IN-31
    		Inhibitor
    HDAC-IN-31 is a potent, selective and orally active HDAC inhibitor with IC50s of 84.90, 168.0, 442.7, >10000 nM for HDAC1, HDAC2, HDAC3, HDAC8, respectively. HDAC-IN-31 induces apoptosis and cell cycle arrests at G2/M phase. HDAC-IN-31 shows good antitumor efficacy. HDAC-IN-31 has the potential for the research of diffuse large B-cell lymphoma.
    HDAC-IN-31
  • HY-115761
    Dihydrochlamydocin
    		Inhibitor
    Dihydrochlamydocin is a histone deacetylases (HDAC) inhibitor. Dihydrochlamydocin shows strong cytostatic activity towards mastocytoma cells.
    Dihydrochlamydocin
  • HY-119690
    T326
    		Inhibitor
    T326 is a potent and selective HDAC3 inhibitor, with an IC50 of 0.26 μM. T326 can be used for the research of cancer and HIV infection.
    T326
  • HY-149529
    HDAC8-IN-5
    		Inhibitor
    HDAC8-IN-5 (Compound 6a) is a HDAC8 inhibitor (IC50: 28 nM). HDAC8-IN-5 can be used for cancer research.
    HDAC8-IN-5
  • HY-176064
    HDAC6-IN-58
    		Inhibitor
    HDAC6-IN-58 (compound 24c) is a selective HDAC6 inhibitor with IC50 values of 9.5 nM and 7374.5 nM for HDAC6 and HDAC1, respectively. HDAC6-IN-58 increases tubulin acetylation, exerts antiproliferative effects, and induces autophagy.
    HDAC6-IN-58
  • HY-155398
    PRO-HD3
    		Inhibitor
    PRO-HD3 is a cell-specific, PROTAC-based HDAC6 degrader.
    PRO-HD3
  • HY-15149G
    Romidepsin (GMP)
    		Inhibitor
    Romidepsin (GMP) (FK 228 (GMP)) is Romidepsin (HY-15149) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Romidepsin (FK 228) is a Histone deacetylase (HDAC) inhibitor with anti-tumor activities. Romidepsin (FK 228) inhibits HDAC1, HDAC2, HDAC4, and HDAC6 with IC50s of 36 nM, 47 nM, 510 nM and 1.4 μM, respectively. Romidepsin (FK 228) is produced by Chromobacterium violaceum, induces cell G2/M phase arrest and apoptosis.
    Romidepsin (GMP)
  • HY-145851
    Top/HDAC-IN-1
    		Inhibitor
    Top/HDAC-IN-1 (Compound 29b) is a topoisomerase/HDAC dual inhibitor with IC50s of 18, 230, 790, 87, and 5250 nM for HDAC1, HDAC2, HDAC3, HDAC6, and HDAC8, respectively. Top/HDAC-IN-1 exhibits potent antitumor activities against the HCT116 cell line with the IC50 of 180 nM. Top/HDAC-IN-1 efficiently induces apoptosis with G2 cell cycle arrest in HCT116 cells.
    Top/HDAC-IN-1
  • HY-168864
    POI ligand 1
    		Inhibitor
    POI ligand 1 is a template for the non-selective HDAC inhibitor Vorinostat (HY-10221). POI ligand 1 can serve as a ligand for target protein (Ligands for Target Protein for PROTAC) for the development of PROTAC HDAC degraders with antitumor activity. POI ligand 1 can be used for the synthesis of FF2049 (HY-168863).
    POI ligand 1
  • HY-143654
    WW437
    WW437 is a histone deacetylase (HDAC) inhibitor with potent anti-breast cancer ability in vitro and in vivo.
    WW437
  • HY-155523
    Tubulin/HDAC-IN-2
    		Inhibitor
    Tubulin/HDAC-IN-2 (Compound II-19k) is a dual inhibitor of Tubulin and HDAC, with an IC50 of 0.403 μM, 0.591μM, 3.552μM, 0.459μM for HDAC1/2/3/6. Tubulin/HDAC-IN-2 blocks cell cycle arrest at G2 phase, induces cell apoptosis. Tubulin/HDAC-IN-2 inhibits the growth of hematoma and solid tumor cells, reduces tumor metastasis, and also inhibits tumor growth in a liver tumor allograft mouse model.
    Tubulin/HDAC-IN-2
  • HY-162630
    HDAC6-IN-44
    		Inhibitor
    HDAC6-IN-44 (compound H10) is a selective HDAC6 inhibitor with an IC50 value of 8.97 nM. HDAC6-IN-44 can inhibit the idiopathic pulmonary fibrosis (IPF) phenotype and exhibits antifibrotic activity. Additionally, HDAC6-IN-44 reduces fibrogenesis in a bleomycin-induced pulmonary fibrosis mouse model and demonstrates good metabolic stability. HDAC6-IN-44 holds promise for research in the field of idiopathic pulmonary fibrosis.
    HDAC6-IN-44
  • HY-162828
    STAT3/HDAC-IN-2
    		Inhibitor
    STAT3/HDAC-IN-2 (compound 18) is a dual inhibitor of STAT3 and HDAC, inducing autophagy and apoptosis. STAT3/HDAC-IN-2 is an amphiphilic hydroxamic acid hybrid based on the natural product isopropanol lactone (IAL) and is a nanoscale anticancer agent. STAT3/HDAC-IN-2 can self-assemble in water to form nanoparticles, which have higher tumor tissue accumulation, cellular uptake and anticancer properties compared to the free state.
    STAT3/HDAC-IN-2
  • HY-163368
    HDAC6-IN-34
    		Inhibitor
    HDAC6-IN-34 (compound 21) is an oral active and selective HDAC6 inhibitor with the IC50 of 18 nM. HDAC6-IN-34 increases the acetylation level of tubulin without affecting histone acetylation in cutaneous T-cell lymphoma cells and inhibits TNF-α secretion in LPS (HY-D1056)-stimulated macrophage cells. HDAC6-IN-34 shows excellent anti-arthritic efficacy in rat.
    HDAC6-IN-34
  • HY-144449
    mTOR/HDAC6-IN-1
    		Inhibitor
    mTOR/HDAC6-IN-1 is a potent mTOR and HDAC6 dual inhibitor (IC50s of 133.7 nM and 56 nM for mTOR and HDAC6, respectively). mTOR/HDAC6-IN-1 can induce significant autophagy, apoptosis and suppress migration. mTOR/HDAC6-IN-1 has potential to research Triple-negative breast cancer (TNBC).
    mTOR/HDAC6-IN-1
  • HY-173076
    HDAC11-IN-1
    		Inhibitor
    HDAC11-IN-1 (Compound 14-NC6OH) is a selective macrocyclic inhibitor of HDAC11 with a Ki of 40 nM. HDAC11-IN-1 exhibits good cell permeability and can inhibit the expression of YAP1 and SOX2.
    HDAC11-IN-1
  • HY-162086A
    HDAC-IN-68 hydrochloride
    		Inhibitor
    HDAC-IN-68 (hydrochloride) (Compound 29) has inhibitory activity against HDACs (IC50=0.04 μM) and fragments microtubules by activating katanin, a microtubule-severing protein. HDAC-IN-68 (hydrochloride) can be used in cancer research.
    HDAC-IN-68 hydrochloride
  • HY-156472
    HDAC6-IN-25
    		Inhibitor
    HDAC6-IN-25 (compound 8) is a selective inhibitor of HDAC6, with the IC50 of 0.6 nM.
    HDAC6-IN-25
Cat. No. Product Name / Synonyms Application Reactivity
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Download HDAC Signaling Pathway Map.

TCR, GPCR and HDAC II interaction: Diverse agonists act through G-protein-coupled receptors (GPCRs) to activate the PKC-PKD axis, CaMK, Rho, or MHC binding to antigens stimulates TCR to activate PKD, leading to phosphorylation of class II HDACs. Phospho-HDACs dissociate from MEF2, bind 14-3-3, and are exported to the cytoplasm through a CRM1-dependent mechanism. CRM1 is inhibited by leptomycin B (LMB). Release of MEF2 from class II HDACs allows p300 to dock on MEF2 and stimulate gene expression. Dephosphorylation of class II HDACs in the cytoplasm enables reentry into the nucleus[1].

 

TLR: TLR signaling is initiated by ligand binding to receptors. The recruitment of TLR domain-containing adaptor protein MyD88 is repressed by HDAC6, whereas NF-κB and MTA-1 can be negatively regulated by HDAC1/2/3 and HDAC2, respectively. Acetylation by HATs enhance MKP-1 which inhibits p38-mediated inflammatory responses, while HDAC1/2/3 inhibits MKP-1 activity. HDAC1 and HDAC8 repress, whereas HDAC6 promotes, IRF function in response to viral challenge. HDAC11 inhibits IL-10 expression and HDAC1 and HDAC2 represses IFNγ-dependent activation of the CIITA transcription factor, thus affecting antigen presentation[2][3].

 

IRNAR: IFN-α/β induce activation of the type I IFN receptor and then bring the receptor-associated JAKs into proximity. JAK adds phosphates to the receptor. STATs bind to the phosphates and then phosphorylated by JAKs to form a dimer, leading to nuclear translocation and gene expression. HDACs positively regulate STATs and PZLF to promote antiviral responses and IFN-induced gene expression[2][3].

 

Cell cycle: In G1 phase, HDAC, Retinoblastoma protein (RB), E2F and polypeptide (DP) form a repressor complex. HDAC acts on surrounding chromatin, causing it to adopt a closed chromatin conformation, and transcription is repressed. Prior to the G1-S transition, phosphorylation of RB by CDKs dissociates the repressor complex. Transcription factors (TFs) gain access to their binding sites and, together with the now unmasked E2F activation domain. E2F is then free to activate transcription by contacting basal factors or by contacting histone acetyltransferases, such as CBP, that can alter chromatin structure[4].

 

The function of non-histone proteins is also regulated by HATs/HDACs. p53: HDAC1 impairs the function of p53. p53 is acetylated under conditions of stress or HDAC inhibition by its cofactor CREB binding protein (CBP) and the transcription of genes involved in differentiation is activated. HSP90: HSP90 is a chaperone that complexes with other chaperones, such as p23, to maintain correct conformational folding of its client proteins. HDAC6 deacetylates HSP90. Inhibition of HDAC6 would result in hyperacetylated HSP90, which would be unable to interact with its co-chaperones and properly lead to misfolded client proteins being targeted for degradation via the ubiquitin-proteasome system[5][6].
 

Reference:

[1]. Vega RB, et al. Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5.Mol Cell Biol. 2004 Oct;24(19):8374-85.
[2]. Shakespear MR, et al. Histone deacetylases as regulators of inflammation and immunity. Trends Immunol. 2011 Jul;32(7):335-43.
[3]. Suliman BA, et al. HDACi: molecular mechanisms and therapeutic implications in the innate immune system.Immunol Cell Biol. 2012 Jan;90(1):23-32. 
[4]. Brehm A, et al. Retinoblastoma protein meets chromatin.Trends Biochem Sci. 1999 Apr;24(4):142-5.
[5]. Butler R, et al. Histone deacetylase inhibitors as therapeutics for polyglutamine disorders.Nat Rev Neurosci. 2006 Oct;7(10):784-96
[6]. Minucci S, et al. Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer.Nat Rev Cancer. 2006 Jan;6(1):38-51.

HDAC Isoform Comparison

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