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-173053
    HDAC-IN-87
    		Inhibitor 99.89%
    HDAC-IN-87 (Compound XII6) is a nonselective HDAC inhibitor, with pIC50 of 6.9 (HDAC4) and 5.8 (HDAC6) respectively. HDAC-IN-87 has fungicidal activity against P. sorghi and P. pachyrhizi. HDAC-IN-87 shows an acute oral LD50 of greater than 500 mg/kg in male and female rats.
    HDAC-IN-87
  • HY-RS06060
    Hdac1 Rat Pre-designed siRNA Set A
    		Inhibitor

    Hdac1 Rat Pre-designed siRNA Set A contains three designed siRNAs for Hdac1 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
    Hdac1 Rat Pre-designed siRNA Set A
  • HY-16138
    Ivaltinostat
    		Inhibitor
    Ivaltinostat (CG-200745) is an orally active, potent pan-HDAC inhibitor which has the hydroxamic acid moiety to bind zinc at the bottom of catalytic pocket. Ivaltinostat inhibits deacetylation of histone H3 and tubulin. Ivaltinostat induces the accumulation of p53, promotes p53-dependent transactivation, and enhances the expression of MDM2 and p21 (Waf1/Cip1) proteins. Ivaltinostat enhances the sensitivity of Gemcitabine-resistant cells to Gemcitabine (HY-16138) and 5-Fluorouracil (5-FU; HY-90006). Ivaltinostat induces apoptosis and has anti-tumour effects.
    Ivaltinostat
  • HY-12163S
    Entinostat-d4
    Entinostat-d4 is the deuterium labeled Entinostat. Entinostat is an oral and selective class I HDAC inhibitor, with IC50s of 243 nM, 453 nM, and 248 nM for HDAC1, HDAC2, and HDAC3, respectively.
    Entinostat-d<sub>4</sub>
  • HY-A0281S2
    4-Phenylbutyric acid-d5
    4-Phenylbutyric acid-d5 is the deuterium labeled 4-Phenylbutyric acid. 4-Phenylbutyric acid (4-PBA) is an inhibitor of HDAC and endoplasmic reticulum (ER) stress, used in cancer and infection research.
    4-Phenylbutyric acid-d<sub>5</sub>
  • HY-150109
    Purinostat mesylate
    		Inhibitor 99.45%
    Purinostat mesylate is a selective inhibitor of HDAC. Purinostat mesylate inhibits class I and class IIb HDACs with IC50s from 0.81 to 11.5 nM. Purinostat mesylate induces apoptosis and affects cell cycle of LAMA84 and 188 BL-2 cells, and shows potently anti-leukemia effects in vivo. Purinostat mesylate can be used for the research of lymphoblastic leukemia.
    Purinostat mesylate
  • HY-131708A
    FNDR-20123
    		Inhibitor 98.08%
    FNDR-20123 is a safe, first-in-class, and orally active anti-malarial HDAC inhibitor with IC50s of 31 nM and 3 nM for Plasmodium and human HDAC, respectively. FNDR-20123 exerts anti-malarial activity against Plasmodium falciparum asexual stage (IC50=41 nM) and sexual blood stage (IC50=190 nM for male gametocytes). FNDR-20123 inhibits HDAC1, HDAC2, HDAC3, HDAC6, and HDAC8 (IC50=25/29/2/11/282 nM, respectively.) and inhibits Class III HDAC isoforms at nanomolar concentrations.
    FNDR-20123
  • HY-138831
    AES-350
    		Inhibitor 99.30%
    AES-350 is a potent and orally active HDAC6 inhibitor with an IC50 and a Ki of 0.0244 μM and 0.035 μM, respectively. AES-350 is also against HDAC3, HDAC8 in an enzymatic activity assay with IC50 values of 0.187 μM and 0.245 μM, respectively. AES-350 triggers apoptosis in AML cells through HDAC inhibition and can be used for acute myeloid leukemia (AML) research.
    AES-350
  • HY-145613
    5-Phenylpentan-2-one
    		Inhibitor 99.81%
    5-Phenylpentan-2-one is a potent histone deacetylases (HDACs) inhibitor. 5-Phenylpentan-2-one can be used for urea cycle disorder research.
    5-Phenylpentan-2-one
  • HY-115412
    Vorinostat-d5
    		Inhibitor ≥99.0%
    Vorinostat-d5 (SAHA-d5) is the deuterium labeled Vorinostat. Vorinostat (SAHA) is a potent and orally active pan-inhibitor of HDAC1, HDAC2 and HDAC3 (Class I), HDAC7 (Class II) and HDAC11 (Class IV), with ID50 values of 10 nM and 20 nM for HDAC1 and HDAC3, respectively. Vorinostat induces cell apoptosis. Vorinostat is also an effective inhibitor of human papillomaviruse (HPV)-18 DNA amplification.
    Vorinostat-d5
  • HY-10585S
    Valproic acid-d4
    		Inhibitor ≥98.0%
    Valproic acid-d4 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[1][2].
    Valproic acid-d<sub>4</sub>
  • HY-W014004
    m-Carboxycinnamic acid bishydroxamide
    		Inhibitor ≥98.0%
    m-Carboxycinnamic acid bishydroxamide is a potent HDAC inhibitor, exhibiting ID50 values of 10 and 70 nM in vitro for HDAC1 and HDAC3, respectively. m-Carboxycinnamic acid bishydroxamide also induces apoptosis and suppresses tumor growth.
    m-Carboxycinnamic acid bishydroxamide
  • HY-130493
    HPB
    		Inhibitor 99.11%
    HPB (HDAC6 inhibitor HPB) is a selective HDAC6 inhibitor with an IC50 of 31 nM. HPB exhibits >30-flod selectivity for HDAC6 over HDAC1.
    HPB
  • HY-173266
    TO-1187
    		Degrader
    TO-1187 is a selective HDAC6 PROTAC degrader (DC50: 5.81 nM). TO-1187 promotes the ubiquitination and degradation of HDAC6 and can be used in the study of hematological malignancies and solid tumors (Pink: HDAC6 ligand (HY-173386); Blue: CRBN ligand (HY-41547); Black: linker (HY-140212)).
    TO-1187
  • HY-155840
    KH16
    		Inhibitor 98.62%
    KH16 is a potent and low nanomolar HDAC inhibitor. KH16 is against class I HDACs HDAC1, HDAC2, and HDAC3, with IC50 values ranging from 6 to 34 nM. KH16 induces cell apoptosis and is against tumor cells with various gene expression patterns.
    KH16
  • HY-117554
    BRD9757
    		Inhibitor 99.75%
    BRD9757 is a potent, capless and selective HDAC6 inhibitor with an IC50 of 30 nM. BRD9757 shows excellent selectivity toward HDAC6 versus the class I (>20-fold) and class II (>400-fold) HDACs.
    BRD9757
  • HY-173076A
    HDAC11-IN-1 TFA
    		Inhibitor 99.25%
    HDAC11-IN-1 (Compound 14-NC6OH) TFA is a selective macrocyclic inhibitor of HDAC11 with a Ki of 40 nM. HDAC11-IN-1 TFA exhibits good cell permeability and can inhibit the expression of YAP1 and SOX2.
    HDAC11-IN-1 TFA
  • HY-113957
    MPI_5a
    		Inhibitor ≥99.0%
    MPI_5a is a potent and selective HDAC6 inhibitor (IC50=36 nM). MPI_5a weakly inhibits other HDAC isoforms. MPI_5a inhibits acyl-tubulin accumulation in cells with an IC50 value of 210 nM.
    MPI_5a
  • HY-10226
    JNJ-16241199
    		Inhibitor 99.05%
    JNJ-16241199 (R306465) is an orally active, selectivehydroxamate-based histone deacetylase (HDAC) inhibitor, with theIC50of 3.3 nM and 23 nM for HDAC1and HDAC8, respectively.JNJ-16241199induces histone 3 acetylation and strongly increases the expression of p21waf1, cip1 in A2780 ovarian carcinoma cells.JNJ-16241199 inducescell apoptosisand shows anticancer activityin a broad spectrum of human malignancies. JNJ-16241199 can be used for cancer study.
    JNJ-16241199
  • HY-RS06088
    HDAC9 Human Pre-designed siRNA Set A
    		Inhibitor

    HDAC9 Human Pre-designed siRNA Set A contains three designed siRNAs for HDAC9 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
    HDAC9 Human Pre-designed siRNA Set A
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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