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-169433
    Naph-Se-TMZ
    		Inhibitor
    Naph-Se-TMZ is a PROTAC-like HDAC1 degrader. Naph-Se-TMZ can reduce the total HDAC activity in glioma cells and enhance the inhibitory effect of Temozolomide (HY-17364). Naph-Se-TMZ consists of the target protein ligand (red part) Temozolomide (HY-17364), the DNA-targeting intercalator (blue part) Nitro-Naphthalimide-C2-acylamide (HY-169437) and the molecular linker (black part). At the same time, the active control of the target protein ligand is: Temozolomide-amino hydrochloride (HY-169439), and the DNA targeting intercalator + linker is: NNISC-2 (HY-169438).
    Naph-Se-TMZ
  • HY-145687
    HDAC-IN-32
    		Inhibitor
    HDAC-IN-32 is a potent HDAC inhibitor with IC50s of 5.2, 11, and 28 nM for HDAC1, HDAC2 and HDAC6, respectively. HDAC-IN-32 possesses potent antiproliferation activities against tumor cells. HDAC-IN-32 shows potent antitumor efficacy in vivo That trigger antitumor immunity.
    HDAC-IN-32
  • HY-162124
    HDAC/NAMPT-IN-1
    		Inhibitor
    HDAC/NAMPT-IN-1 (compound 39h) is a dual inhibitor of HDAC and NAMPT with IC50 values of 0.72-37081 nM and 1618 nM.
    HDAC/NAMPT-IN-1
  • HY-162086
    HDAC-IN-68
    HDAC-IN-68 (Compound 29) is a potent HDAC inhibitor that disrupts microtubule structure and inhibits tumor growth. HDAC-IN-68 significantly inhibits class I HDACs (HDAC1, HDAC2, HDAC3) with IC50 values of 5.1, 11.5 and 8.8 nM, respectively.
    HDAC-IN-68
  • HY-172136
    LSQ-28
    		Inhibitor
    LSQ-28 is an orally active HDAC3 inhibitor with an IC50 of 42 nM, and exhibits potent anticancer, antiproliferative, antimigratory, anti-invasive, and antiwound healing activities. LSQ-28 can be utilized in cancer research.
    LSQ-28
  • HY-169014
    HDAC-IN-77
    		Inhibitor
    HDAC-IN-77 (HL-5s) is an HDAC inhibitor. HDAC-IN-77 can induce ferroptosis and inhibit the Nrf2/HO-1 signaling pathway. HDAC-IN-77 can be used in cancer research.
    HDAC-IN-77
  • HY-170907
    HDAC-IN-85
    		Inhibitor
    HDAC-IN-85 (Compound 1) is a BBB-permeable HDAC inhibitor. HDAC-IN-85 has an inhibitory effect on brain tumor cell lines. HDAC-IN-85 can induce acetylation, leading to DNA double-strand breaks, and induce the ubiquitination of RAD51, disrupting the DNA repair process. HDAC-IN-85 can be used in the research of glioblastoma.
    HDAC-IN-85
  • HY-149497
    HDAC6-IN-19
    		Inhibitor
    HDAC6-IN-19 (Compound 14g) is a HDAC6 inhibitor (IC50: 2.68 nM). HDAC6-IN-19 also inhibits HDAC1, HDAC2 and HDAC3 with IC50s of 61.6 nM, 98.7 nM and 103 nM. HDAC6-IN-19 potently inhibits multiple cancer cell proliferation, including leukemia, colon cancer, melanoma, and breast cancer cell lines.
    HDAC6-IN-19
  • HY-168962
    HDAC-IN-88
    		Inhibitor
    HDAC-IN-88 (Compound HJ-9) is the inhibitor for HDAC that inhibits HDAC6, HDAC1, HDAC2, HDAC8 and HDAC3 with IC50s of 0.226, 1.103, 2.308, 3.255 and 3.864 μM, respectively. HDAC-IN-88 inhibits the proliferation of cancer cell HepG2, HCT116 and MV4-11 with IC50 of 5.47, 9.78 and 0.38 μM, inhibits the migration of HCT116, arrests the cell cycle at G0/G1 phase, and induces apoptosis and autophagy in MV4-11. HDAC-IN-88 reduces ROS level and mitochondrial membrane potential. HDAC-IN-88 exhibits antimalarial activity that inhibits P. falciparum 3D7 with EC50 of 165 nM. HDAC-IN-88 also exhibits anti-angiogenic activity.
    HDAC-IN-88
  • HY-173558
    PD-L1/HDAC3-IN-1
    		Inhibitor
    PD-L1/HDAC3-IN-1 (PH3) is a dual PD-L1/HDAC3 Inhibitor with IC50 values of 89.4 nM and 107 nM for PD-1/PD-L1 and HDAC3, respectively. PD-L1/HDAC3-IN-1 induces cell apoptosis and arrests cell cycle at G0/G1 phase. PD-L1/HDAC3-IN-1 shows anticancer activity both in vivo and in vitro.
    PD-L1/HDAC3-IN-1
  • HY-150595
    HDAC6-IN-10
    		Inhibitor
    HDAC6-IN-10 is a highly selective HDAC6 inhibitor with the IC50 of 0.73 nM. HDAC6-IN-10 has 144~10941-fold selectivity over other HDAC isoforms. HDAC6-IN-10 shows anti-proliferative activities against multiple myeloma cells.
    HDAC6-IN-10
  • HY-107550
    HDAC6-IN-7
    		Inhibitor
    TCS HDAC6 20b is a HDAC6-selective inhibitor. TCS HDAC6 20b blocks the growth of estrogen receptor α-positive breast cancer MCF-7 cells.
    HDAC6-IN-7
  • HY-157490
    PARP/HDAC-IN-1
    		Inhibitor
    PARP/HDAC-IN-1 (compound B102) is a potent dual inhibitor of PARP and HDAC. PARP/HDAC-IN-1 inhibits PARP1, PARP2 and HDAC1 with IC50s of 19.01, 2.13, 1690 nM, respectively.
    PARP/HDAC-IN-1
  • HY-149238
    Topo II/HDAC-IN-1
    		Inhibitor
    Topo II/HDAC-IN-1 (7d) exhibits excellent dual inhibitory activities against Topo II and HDAC. Topo II/HDAC-IN-1 (8d) induces apoptosis.
    Topo II/HDAC-IN-1
  • HY-146539
    HDAC-IN-35
    		Inhibitor
    HDAC-IN-35 (Compound 14) is a potent, selective HDAC and VEGFR-2 inhibitor, with IC50 values of 0.166 and 13.2 µM for HDAC6 and VEGFR-2, respectively.
    HDAC-IN-35
  • HY-147991
    PDE5/HDAC-IN-1
    		Inhibitor
    PDE5/HDAC-IN-1 (Compound 26) is a potent phosphodiesterase 5 (PDE5) and HDAC inhibitor with IC50 values of 46.3 nM and 14.5 nM, respectively. PDE5/HDAC-IN-1 induces cell apoptosis and shows anticancer activities.
    PDE5/HDAC-IN-1
  • HY-123971
    HDAC6 degrader-4
    		Degrader
    HDAC6 degrader-4 is a PROTAC and a selective HDAC6 degrader consists of a non-selective HDAC inhibitor and thalidomide-type E3 ligase ligand. HDAC6 degrader-4 can be used for cancer research.
    HDAC6 degrader-4
  • HY-172133
    HDAC3-IN-6
    		Inhibitor
    HDAC3-IN-6 (Compound SC26) is a selective HDAC3 inhibitor with an IC50 of 53 nM. HDAC3-IN-6 dose-dependently induces the expression of PD-L1. HDAC3-IN-6 induces more pronounced Apoptosis and production of ROS. HDAC3-IN-6 exhibits high antitumor efficacy against colorectal cancer.
    HDAC3-IN-6
  • HY-173520
    EGFR/HDAC-IN-1
    		Inhibitor
    EGFR/HDAC-IN-1 (Compound 22c2) is a potent dual inhibitor of epidermal growth factor receptor (EGFR) and histone deacetylase (HDAC) with IC50 values of 4.81 nM, 119.4 nM and 354.8 nM for EGFR, HDAC1 and HDAC3, respectively. EGFR/HDAC-IN-1 blocks the EGFR signaling pathway and affects the histone acetylation status, thereby inhibiting tumor cell proliferation. EGFR/HDAC-IN-1 is promising for research of non-small cell lung cancer (NSCLC).
    EGFR/HDAC-IN-1
  • HY-146351
    HDAC-IN-38
    		Inhibitor
    HDAC-IN-38 (compound 13) is a potent HDAC inhibitor. HDAC-IN-38 shows similar micro-molar inhibitory activity toward HDAC1, 2, 3, 5, 6, and 8. HDAC-IN-38 increases cerebral blood flow (CBF), attenuates cognitive impairment, and improves hippocampal atrophy. HDAC-IN-38 also increases the level of histone acetylation (H3K14 or H4K5).
    HDAC-IN-38
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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