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-159172
    HDAC3-IN-4
    		Inhibitor
    HDAC3-IN-4 is a selective and orally active HDAC3 inhibitor with an IC50 of 89 nM. HDAC3-IN-4 induces the degradation of PD-L1 by regulating cathepsin B (CTSB) in the lysosomes, with a DC50 of 5.7 μM. HDAC3-IN-4 shows better selectivity for HDAC3 over HDAC1, HDAC6, HDAC7, and HDAC8.
    HDAC3-IN-4
  • HY-164816
    FITC-SAHA
    		Inhibitor
    FITC-SAHA is SAHA (HY-10221) conjugated with fluorescein. SAHA is an inhibitor of histone deacetylase (HDAC). FITC-SAHA can be used in cancer and Alzheimer's disease related research.
    FITC-SAHA
  • HY-121512
    SK-7041
    		Inhibitor
    SK-7041 is a HDAC inhibitor with the IC50 of 172 nM. SK-7041 induces the hyperacetylation of histones H3 and H4 .SK-7041 inhibits tumor cell growth in vivo and in vitro, induces cell apoptosis, and arrests cell cycle at the G1 phase.
    SK-7041
  • HY-144298
    HDAC1-IN-4
    		Inhibitor
    HDAC1-IN-4 (JX34) is a potent Plasmodium falciparum HDAC1 inhibitor shows antimalarial activity (IC50 < 5 nM) and lower cytotoxicity.
    HDAC1-IN-4
  • HY-RS06062
    Hdac10 Mouse Pre-designed siRNA Set A
    		Inhibitor

    Hdac10 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Hdac10 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
    Hdac10 Mouse Pre-designed siRNA Set A
  • HY-161667
    GSK-3β/HDAC-IN-1
    		Inhibitor
    GSK-3β/HDAC-IN-1 (Compd 4) is a brain-penetrant and first in class dual non-ATP-competitive Glycogen Synthase Kinase 3β/Histone Deacetylases (GSK-3β/HDACs) Inhibitor with IC50s of 0.142, 0.03 and 0.045 μM against GSK-3β, HDAC2 and HDAC6, respectively. GSK-3β/HDAC-IN-1 can be used for Alzheimer’s disease research.
    GSK-3β/HDAC-IN-1
  • HY-147934
    HDAC8-IN-3
    		Inhibitor
    HDAC8-IN-3 (compound P19) is a potent HDAC8 inhibitor with IC50 value of 9.3 μM and produces thermal stabilization. HDAC8-IN-3 has cytotoxicity and induces apoptosis in leukemic cell lines.
    HDAC8-IN-3
  • HY-146159
    PI3K/HDAC-IN-2
    		Inhibitor
    PI3K/HDAC-IN-2 is a potent dual PI3K/HDAC inhibitor with IC50s of 226 nM, 279 nM, 467 nM, 29 nM for PI3Kα, PI3Kβ, PI3Kγ, PI3Kδ, respectively, and IC50s of 1.3 nM, 3.4 nM, 972 nM, 17 nM, 12 nM for HDAC1, HDAC2, HDC4, HDAC6, HDAC8, respectively. PI3K/HDAC-IN-2 exhibits PI3Kδ and class I and IIb HDAC selectivity. PI3K/HDAC-IN-2 has remarkable anticancer effects.
    PI3K/HDAC-IN-2
  • HY-169400
    HDACs/EZH2-IN-1
    		Inhibitor
    HDACs/EZH2-IN-1 (Compound 22a) is a HDACs/EZH2 inhibitor (EZH2 Y641N inhibition rate at 50 nM: 98%), with selective inhibition against HDAC1 and HDAC6 (IC50: 0.23 μM and 0.07 μM, respectively). HDACs/EZH2-IN-1 exerts a antiproliferative effect on diffuse large B-cell lymphoma cells harboring an EZH2 mutation and on various acute myeloid leukemia cells. HDACs/EZH2-IN-1 has the ability to induce cell differentiation and Apoptosis.
    HDACs/EZH2-IN-1
  • HY-170841
    HDAC3/BRD4-IN-1
    		Inhibitor
    HDAC3/BRD4-IN-1 (compound 26n) is an inhibitor of HDAC3/BRD4 with an IC50 of 8 nM for HDAC3 (IC50s are 220 nM and 120 nM for HDAC1 and HDAC2, respectively). HDAC3/BRD4-IN-1 has anti-tumor and anti-proliferative effects by upregulating Ac-H3 and downregulating c-Myc. The half-life of HDAC3/BRD4-IN-1 in human liver microsomes is 29.36 min.
    HDAC3/BRD4-IN-1
  • HY-D2280
    Estrogen receptor β/HDAC probe 1
    Estrogen receptor β/HDAC probe 1 (compound P1) is a near-infrared fluorescent probe that dual-targets the estrogen receptor (Estrogen Receptor/ERR) β/histone deacetylase HDAC.
    Estrogen receptor β/HDAC probe 1
  • HY-141701
    mTOR/HDAC-IN-1
    		Inhibitor
    mTOR/HDAC-IN-1 (Compound 50) is a selective mTOR and HDAC dual inhibitor with IC50 values of 0.49 and 0.91 nM against mTOR and HDAC1, respectively. mTOR/HDAC-IN-1 can be studied as an anti-cancer agent.
    mTOR/HDAC-IN-1
  • HY-144297
    HDAC1-IN-3
    		Inhibitor
    HDAC1-IN-3 is a potent Pf HDAC1 inhibitor. HDAC1-IN-3 shows antimalarial activity in wild-type and multidrug-resistant parasite strains. HDAC1-IN-3 shows a significant in vivo killing effect against all life cycles of parasites.
    HDAC1-IN-3
  • HY-150774
    HDAC6/HSP90-IN-2
    		Inhibitor
    HDAC6/HSP90-IN-2 (compound 6e) is a dual inhibitor of HDAC6 and Hsp90, with IC50s of 105.7 and 61 nM, respectively. HDAC6/HSP90-IN-2 can be used for the research of cancer.
    HDAC6/HSP90-IN-2
  • HY-174854
    PySAHA
    		Inhibitor
    PySAHA is a multifunctional HDAC inhibitor. PySAHA can degrade intracellular HDAC via a hydrophobic tagging mechanism. PySAHA also possesses photodynamic therapeutic activity and can generate reactive oxygen species under light irradiation. PySAHA can inhibit the proliferation, migration and induce cell apoptosis of breast cancer cells. PySAHA has antitumor activity and can be used in breast cancer research.
    PySAHA
  • HY-157436
    HDAC6-IN-30
    		Inhibitor
    HDAC6-IN-30 (compound 8g) is a selective HDAC6 inhibitor with the IC50 21 nM, and increase cell protein acetylation levels.
    HDAC6-IN-30
  • HY-163535
    J208
    		Inhibitor
    J208 is a dual inhibitor for histone deacetylase (HDAC) and DNA methyltransferase (DNMT). J208 inhibits proliferation of cancer cells, as well as the migration/invasion of triple-negative breast cancer (TNBC) cells. J208 induces apoptosis, arrests the cell cycle at G0/G1 phase. J2008 activates the innate immune signalling pathway in TNBC, by inducing the expression of endogenous retroviruses (ERVs).
    J208
  • HY-161868
    DLC-50
    		Inhibitor
    DLC-50 is a dual inhibitor for PARP-1 and HDAC-1 with IC50 of 1.2 nM and 31 nM. DLC-50 inhibits the proliferation of cancer cells MDA-MB-436, MDA-MB-231, and MCF-7 with IC50 of 0.3, 2.7 and 2.41 μM. DLC-50 induces apoptosis in MDA-MB-231, arrests the cell cycle at G2 phase.
    DLC-50
  • HY-172891
    CDK9/HDAC1/HDAC3-IN-1
    		Inhibitor
    CDK9/HDAC1/HDAC3-IN-1 is dual-functional inhibitor of CDK9 and HDAC. CDK9/HDAC1/HDAC3-IN-1 inhibits the protein activity of CDK9/HDAC/HDAC3 with IC50 s of 0.17  μM, 1.73  μM and 1.11 μM for CDK9, HDAC1, and HDAC3, respectively. CDK9/HDAC1/HDAC3-IN-1 inhibits cancer cells by inducing cell apoptosis and cell cycle arrest in the G2/M phase, as well as tumor growth in a murine TNBC MDA-MB-231 xenograft model. CDK9/HDAC1/HDAC3-IN-1 has a broad-spectrum anti-cancer activity, such as breast cancer, cervical cancer, and liver cancer.
    CDK9/HDAC1/HDAC3-IN-1
  • HY-174409
    HDAC6 ligand-Linker Conjugate 1
    		Degrader
    HDAC6 ligand-linker conjugate 1 is a conjugate of HDAC6 ligand and linker, which can be used to synthesize PROTACs such as PROTAC HDAC6 degrader 5 (HY-174401).
    HDAC6 ligand-Linker Conjugate 1
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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