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-163090
    HR488B
    		Inhibitor
    HR488B is an efficient HDAC1 inhibitor. HR488B specifically suppressed the growth of CRC cells by inducing cell cycle G0/G1 arrest and apoptosis. HR488B causes mitochondrial dysfunction, reactive oxygen species (ROS) generation, and DNA damage accumulation.
    HR488B
  • HY-162678
    HDAC-IN-75
    		Inhibitor
    HDAC-IN-75 (5d) is a HDAC inhibitor, with IC50 values of 6.32 nM and 1352 nM for HDAC6 and HDAC1, respectively. HDAC-IN-75 (5d) promotes vision rescue in the atp6v0e1–/– zebrafish model of photoreceptor dysfunction.
    HDAC-IN-75
  • HY-151896
    HDAC6-IN-14
    		Inhibitor
    HDAC6-IN-14 is a highly selective HDAC6 (HDAC) inhibitor with an IC50 of 42 nM. HDAC6-IN-14 displays >100-fold selectivity over HDAC1/HDAC2/HDAC3/HDAC4.
    HDAC6-IN-14
  • HY-155397
    PRO-HD2
    		Inhibitor
    PRO-HD2 is a cell-specific, PROTAC-based HDAC6 degrader.
    PRO-HD2
  • HY-W718894
    (R)-Dihydrolipoic acid
    		Inhibitor
    (R)-Dihydrolipoic acid is a compound that inhibits histone deacetylase 6 (HDAC6) activity. The structure of its complex with HDAC6 has been resolved. (R)-Dihydrolipoic acid can inhibit HDAC6 through specific interactions, providing a basis for understanding the relationship between HDAC function and oxidative stress.
    (R)-Dihydrolipoic acid
  • HY-150772
    Tubulin/HDAC-IN-1
    		Inhibitor
    Tubulin/HDAC-IN-1 is a dual tubulin and HDAC-IN-1 inhibitor through CH/π interaction with tubulin and hydrogen bond interaction with HDAC8. Tubulin/HDAC-IN-1 inhibits tubulin polymerization and selectively inhibits HDAC8 (IC50: 150 nM). Tubulin/HDAC-IN-1 has cytotoxicity against various human cancer cells, also arrests cell cycle in the G2/M phase and induces cell apoptosis. Tubulin/HDAC-IN-1 can be used in the research of hematologic and solid tumors such as neuroblastoma, leukemia.
    Tubulin/HDAC-IN-1
  • HY-161778
    ZG-126
    		Inhibitor
    ZG-126 is an agonist for vitamin D receptor (VDR) and an inhibitor for histone deacetylase (HDAC) (IC50=0.63-67.6 μM). ZG-126 exhibits cytotoxicity in cancer cells MDA-MB-231 and 4T1. ZG-126 exhibits antitumor and anti-metastatic efficacy against melanoma and triple-negative breast cancer (TNBC) in mouse models. ZG-126 also exhibits anti-inflammatory activity, through the reduction of macrophage infiltration and immunosuppressive M2-polarization.
    ZG-126
  • HY-B0494R
    Bufexamac (Standard)
    		Inhibitor
    Bufexamac (Standard) is the analytical standard of Bufexamac. This product is intended for research and analytical applications. Bufexamac is a selective Ⅱb HDAC (HDAC6, HDAC10) and LTA4H dual inhibitor, with Kds of 0.53 μM and 0.22 μM for HDAC6 and HDAC10. Bufexamac is a nonsteroida anti-inflammatory drug.
    Bufexamac (Standard)
  • HY-172200
    PD-L1/HDAC6-IN-1
    		Inhibitor
    PD-L1/HDAC6-IN-1 (Compound HP29) is the inhibitor for PD-L1 and HDAC6 that inhibits the PD-L1/PD-1 interaction and HDAC6 with an IC50 of 26.8 nM and 69 nM. PD-L1/HDAC6-IN-1 enhances the killing ability of Jurkat T cells against HepG2 cells with an IC50 of 3.4 μM. PD-L1/HDAC6-IN-1 exhibits good pharmacokinetics characteristics in rats with a drug exposure of 871.62 ng·h/mL, and exhibits antitumor activity in mouse B16-F10 xenograft models.
    PD-L1/HDAC6-IN-1
  • HY-126829
    Coumarin-SAHA
    Coumarin-SAHA is a fluorescent probe for determining the binding affinities (kd) and the dissociation off-rates (koff) of the HDAC8-inhibitor complexes.
    Coumarin-SAHA
  • HY-151569
    SAHA-OH
    		Inhibitor
    SAHA-OH is a selective HDAC6 inhibitor (IC50=23 nM), shows a 10- to 47-fold selectivity for HDAC6 compared to HDAC 1, 2, 3, and 8. SAHA-OH shows anti-inflammatory activity, and attenuates macrophage apoptosis.
    SAHA-OH
  • HY-144292
    HDAC-IN-30
    		Inhibitor
    HDAC-IN-30 is a novel multi-target HDAC inhibitor, including HDAC1 (IC50=13.4 nM),HDAC2 (IC50=28.0 nM), HDAC3 (IC50=9.18 nM), HDAC6 (IC50=42.7 nM), HDAC8 (IC50=131 nM). HDAC-IN-30 exhibits potent antitumor efficacy.
    HDAC-IN-30
  • HY-10585S3
    Valproic acid-d4 sodium
    		Inhibitor
    Valproic acid-d4 (sodium) is the deuterium labeled Valproic acid. Valproic acid (VPA; 2-Propylpentanoic Acid) is an HDAC inhibitor, with IC50 in the range of 0.5 and 2 mM, also inhibits HDAC1 (IC50, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium salt is used in the treatment of epilepsy, bipolar disorder and prevention of migraine headaches.
    Valproic acid-d<sub>4</sub> sodium
  • HY-168493
    FLT3/VEGFR2-IN-1
    		Inhibitor
    FLT3/VEGFR2-IN-1 (Compound 26) is a FLT3/VEGFR2/KDR/Flk-1/HDAC inhibitor with IC50 values of 14.5 nM, 3.9 nM, and 30.8 nM for FLT3, VEGFR2/KDR/Flk-1, and HDAC1, respectively. FLT3/VEGFR2-IN-1 can inhibit the phosphorylation of STAT3 and ERK1/2 and the proliferation of leukemia cells. FLT3/VEGFR2-IN-1 has anti-tumor activity and can be used for the research of acute myeloid leukemia.
    FLT3/VEGFR2-IN-1
  • HY-RS06079
    HDAC6 Human Pre-designed siRNA Set A
    		Inhibitor

    HDAC6 Human Pre-designed siRNA Set A contains three designed siRNAs for HDAC6 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
    HDAC6 Human Pre-designed siRNA Set A
    HDAC6 Human Pre-designed siRNA Set A
  • HY-149630
    VEGFR2/HDAC1-IN-1
    		Inhibitor
    VEGFR2/KDR/Flk-1/HDAC1-IN-1 (compound 13) is a potent VEGFR-2/HDAC dual inhibitor, with IC50s of 57.83 nM and 9.82 nM, respectively. VEGFR2/KDR/Flk-1/HDAC1-IN-1 arrests the cell cycle at the S and G2 phases, and induces apoptosis in HeLa cells. VEGFR2/KDR/Flk-1/HDAC1-IN-1 exhibits anti-angiogenic effect.
    VEGFR2/HDAC1-IN-1
  • HY-149578
    Tubulin/HDAC-IN-3
    		Inhibitor
    Tubulin/HDAC-IN-3 (compound 12a) is a potent tubulin/HDAC dual inhibitor. Tubulin/HDAC-IN-3 effectively disrupts tubulin polymerization (IC50: 5.4 μM). Tubulin/HDAC-IN-3 exhibits potent HDAC1/8 inhibitory activities, with IC50 values of 0.155 and 0.177 μM, respectively. Tubulin/HDAC-IN-3 works through blocking cellular cycle, inducing apoptosis and inhibiting colony formation.
    Tubulin/HDAC-IN-3
  • HY-158371
    HDAC/CK2-IN-1
    		Inhibitor
    HDAC/CK2-IN-1 (compound 38) is a HDAC1 (IC50 = 1.46 μM), HDAC6 (IC50 = 0.66 μM), and CK2 (IC50 = 3.67 μM) inhibitor. HDAC/CK2-IN-1 exhibits promising antproliferative activity against Jurkat, MCF-7, HCT-116, and HL-60 cell lines.
    HDAC/CK2-IN-1
  • HY-139796
    ZYJ-34v
    		Inhibitor
    ZYJ-34v is an orally active histone deacetylase inhibitor. ZYJ-34v has antitumor activity.
    ZYJ-34v
  • HY-155396
    PRO-HD1
    		Degrader
    PRO-HD1 is a PROTAC HDAC6 degrader. PRO-HD1 degrades HDAC6 in A549 cells, and inhibits proliferation of Jurkat cells (IC50: 5.8 μM).
    PRO-HD1
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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