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-172200
    PD-L1/HDAC6-IN-1
    		Inhibitor
    PD-L1/HDAC6-IN-1 is an orally active dual inhibitor of PD-L1 and HDAC6, with IC50 values of 26.8 nM and 78 nM, respectively. PD-L1/HDAC6-IN-1 binds to human and murine PD-L1 proteins with high affinity, while it reduces STAT3 phosphorylation and downregulates PD-L1 expression by inhibiting HDAC6, thus blocking the PD-1/PD-L1 interaction. PD-L1/HDAC6-IN-1 exhibits potent anti-tumor activity in a mouse melanoma model. PD-L1/HDAC6-IN-1 is suitable for research on tumor immune regulation related to melanoma.
    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-178023
    HDAC6-IN-64
    		Inhibitor
    HDAC6-IN-64 (Compound 8) is a HDAC6 inhibitor with an IC50 of 11.9  nM. HDAC6-IN-64 has poor cell permeability. HDAC6-IN-64 can be used for chemotherapy of cancers like NSCLC research.
    HDAC6-IN-64
  • 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/HDAC inhibitor with IC50 values of 14.5 nM, 3.9 nM, and 30.8 nM for FLT3, VEGFR2, 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-181678
    DNA-PK/HDAC6-IN-1
    		Inhibitor
    DNA-PK/HDAC6-IN-1 is a selcetive and orally active dual DNA-PK and HDAC6 inhibitor with IC50 values of 84.2 and 64.8 nM. DNA-PK/HDAC6-IN-1 suppresses cancer cells proliferation, induces cancer cell cycle G2/M arrest, apoptosis, and decreases the mitochondrial membrane potential. DNA-PK/HDAC6-IN-1 induces DNA damage and elevates γ-H2AX levels. DNA-PK/HDAC6-IN-1 exhibits antitumor efficacy in AML animal mouse model. DNA-PK/HDAC6-IN-1 can be used for the research of acute myeloid leukemia.
    DNA-PK/HDAC6-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
  • HY-149630
    VEGFR2/HDAC1-IN-1
    		Inhibitor
    VEGFR2/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/HDAC1-IN-1 arrests the cell cycle at the S and G2 phases, and induces apoptosis in HeLa cells. VEGFR2/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-153514
    HDAC-IN-54
    		Inhibitor
    HDAC-IN-54 is a HDAC inhibitor with an IC50 of 25 nM against human HDAC1, 66 nM against HDAC2, 6.5 nM against HDAC3, and 281 nM against HDAC6. HDAC-IN-54 induces acetylation of α-tubulin and histone H3. HDAC-IN-54 acts synergistically with cisplatin to induce cancer cell apoptosis. HDAC-IN-54 can be used in research related to head and neck cancer, ovarian cancer, and tongue squamous cell carcinoma.
    HDAC-IN-54
  • 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
  • HY-143241
    HDAC-IN-34
    		Inhibitor
    HDAC-IN-34 (compound 27) is a potent HDAC inhibitor, with IC50 values of 0.022 and 0.45 μM for HDAC1 and HDAC6, respectively. HDAC-IN-34 can bind to DNA and cause DNA damage. HDAC-IN-34 causes cells apoptosis through p53 signaling pathway. HDAC-IN-34 exhibits significant anti-proliferation effect against HCT-116 cells, with an IC50 of 1.41 μM.
    HDAC-IN-34
  • HY-10221G
    Vorinostat (GMP)
    		Inhibitor
    Vorinostat (GMP) is a GMP grade Vorinosta (HY-10221). GMP-grade small molecules can be used as auxiliary agents in cell therapy. Vorinostat is a potent, orally available HDAC1, HDAC2, HDAC3 (Class I), HDAC6 and Inhibitors of HDAC7 (Class II) and Class IV (HDAC11).
    Vorinostat (GMP)
  • HY-181805
    HDAC6-IN-76
    		Inhibitor
    HDAC6-IN-76 (Compound G25) is a selective HDAC6 inhibitor with an IC50 of 12 nM. HDAC6-IN-76 induces Autophagy in a p53-dependent manner. HDAC6-IN-76 induces Apoptosis in a p53-dependent manner. HDAC6-IN-76 exhibits anticancer activity against hematologic malignancies, including acute myeloid leukemia.
    HDAC6-IN-76
  • HY-W769286
    Valproic acid β-D-glucuronide-d15
    Valproic acid β-D-glucuronide-d15 is the deuterium labeled Valproic acid β-D-glucuronide (HY-W400496). Valproic acid β-D-glucuronide is the major urinary metabolite of Valproic acid (HY-10585).
    Valproic acid β-D-glucuronide-d<sub>15</sub>
  • HY-143325
    A2AAR/HDAC-IN-2
    		Inhibitor
    A2AAR/HDAC-IN-2 is a potent A2AAR/HDAC dual inhibitor, with good binding affinity for A2AAR (Ki=10.3 nM) and good inhibitory activity against HDAC1 (IC50=18.5 nM). A2AAR/HDAC-IN-2 can be used in study of antitumor.
    A2AAR/HDAC-IN-2
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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