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-RS06061
    HDAC10 Human Pre-designed siRNA Set A
    		Inhibitor

    HDAC10 Human Pre-designed siRNA Set A contains three designed siRNAs for HDAC10 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
    HDAC10 Human Pre-designed siRNA Set A
  • HY-153358A
    (S)-TNG260
    		98.84%
    (S)-TNG260 is an isomer of TNG260 (HY-153358). TNG260 is a CoREST selective deacetylase (CoreDAC) inhibitor. TNG260 inhibits HDAC1 with 10-fold selectivity over HDAC3. TNG260 causes HDAC1 inhibition and reverses anti-PD1 resistance driven by STK11 deletion. TNG260 reduces intratumoral infiltration of neutrophils. TNG260 exhibits immune-mediated cell killing.
    (S)-TNG260
  • HY-W009732R
    Sinapinic acid (Standard)
    		Inhibitor
    Sinapinic acid (Sinapic acid) is a phenolic compound isolated from Hydnophytum formicarum Jack. Rhizome, acts as an inhibitor of HDAC, with an IC50 of 2.27 mM, and also inhibits ACE-I activity. Sinapinic acid posssess potent anti-tumor activity, induces apoptosis of tumor cells. Sinapinic acid shows antioxidant and antidiabetic activities. Sinapinic acid reduces total cholesterol, triglyceride, and HOMA-IR index, and also normalizes some serum parameters of antioxidative abilities and oxidative damage in ovariectomized rats.
    Sinapinic acid (Standard)
  • HY-N8707
    Homobutein
    		Inhibitor 98.35%
    Homobutein a natural chalcones (can be found in many medicinal plants, fruits, vegetables, spices and nuts), is a potent HDACs/NF-κB dual inhibitor with IC50s of 190 and 38 μM, respectively. Homobutein also a chelator of iron (II and III) cations, shows various activities, including anticancer, anti-inflammatory, antiparasite and antioxidation.
    Homobutein
  • HY-139701
    NI-Pano
    		Inhibitor
    NI-Pano (CH-03) is a novel hypoxia-activated KDAC inhibitor. NI-Pano (CH-03) is reduced in an O2-dependent manner to release panobinostat.
    NI-Pano
  • HY-A0281S3
    4-Phenylbutyric acid-d2
    		99.70%
    4-Phenylbutyric acid-d2 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>2</sub>
  • HY-123976A
    MPT0G211 mesylate
    		Inhibitor
    MPT0G211 mesylate is a potent, orally active and selective HDAC6 inhibitor (IC50=0.291 nM). MPT0G211 mesylate displays >1000-fold selective for HDAC6 over other HDAC isoforms. MPT0G211 mesylate can penetrate the blood-brain barrier. MPT0G211 mesylate ameliorates tau phosphorylation and cognitive deficits in an Alzheimer’s disease model. MPT0G211 mesylate has anti-metastatic and neuroprotective effects. Anticancer activities.
    MPT0G211 mesylate
  • HY-146678
    HDAC6-IN-5
    		Inhibitor
    HDAC6-IN-5 (compound 11b) is a potent and BBB-penetrated HDAC6 inhibitor, with an IC50 of 0.025 μM. HDAC6-IN-5 exhibits strong inhibitory activity against Aβ1-42 self-aggregation and AChE, with IC50 values of 3.0 and 0.72 μM. HDAC6-IN-5 can enhance neurite outgrowth without significant neurotoxicity.
    HDAC6-IN-5
  • HY-112147
    IDO1 and HDAC1 Inhibitor
    		Inhibitor
    IDO1 and HDAC1 Inhibitor (Compound 10) is a dual IDO1 and HDAC1 inhibitor with IC50s of 69.0 nM and 66.5 nM, respectively.
    IDO1 and HDAC1 Inhibitor
  • HY-151464
    SHP2/HDAC-IN-1
    		Inhibitor
    SHP2/HDAC-IN-1 is a dual allosteric SHP2/HDAC inhibitor with IC50 values of 20.4 nM (SHP2) and 25.3 nM (HDAC1) respectively. SHP2/HDAC-IN-1 triggers efficient antitumor immunity by activating T cells, enhancing the antigen presentation function and promoting cytokine secretion. SHP2/HDAC-IN-1 can be used in the research of cancer immunoresearch.
    SHP2/HDAC-IN-1
  • HY-112908
    RTS-V5
    		Inhibitor
    RTS-V5 is a dual HDAC/proteasome inhibitor with IC50s of 6.9, 18, 15, 0.27, 0.53 μM for HDAC1, HDAC2, HDAC3, HDAC6, HDAC8, respectively.
    RTS-V5
  • HY-143497
    HDAC1/2 and CDK2-IN-1
    		Inhibitor
    HDAC1/2 and CDK2-IN-1 (compound 14d) is a potent HDAC1, HDAC2 and CDK2 dual inhibitor, with IC50 values of 70.7, 23.1 and 0.80 μM, respectively. HDAC1/2 and CDK2-IN-1 can block the cell cycle and induce apoptosis. HDAC1/2 and CDK2-IN-1 exhibits desirable in vivo antitumor activity.
    HDAC1/2 and CDK2-IN-1
  • HY-105246
    Pracinostat dihydrochloride
    		Inhibitor
    Pracinostat dihydrochloride is a potent histone deacetylase (HDAC) inhibitor, with IC50s of 40-140 nM, used for cancer research. Pracinostat dihydrochloride also inhibits metallo-β-lactamase domain-containing protein 2 (MBLAC2) hydrolase activity with an EC50 below 10 nM.
    Pracinostat dihydrochloride
  • HY-128582
    PI3K/HDAC-IN-1
    		Inhibitor
    PI3K/HDAC-IN-1 is a potent dual inhibitor of PI3K/HDAC, potently inhibits PI3Kδ and HDAC1 with IC50s of 8.1 nM and 1.4 nM, respectively.
    PI3K/HDAC-IN-1
  • HY-138799A
    KA2507 monohydrochloride
    		Inhibitor 99.43%
    KA2507 hydrochloride is a potent and highly selective inhibitor of HDAC6 (IC50=2.5 nM) with no significant toxicities. KA2507 hydrochloride shows antitumor efficacy and immune modulatory effects.
    KA2507 monohydrochloride
  • HY-131970
    LSD1/HDAC6-IN-1
    		Inhibitor
    LSD1/HDAC6-IN-1 is an orally active dual inhibitor of lysine specific demethylase 1(LSD1)/Histone deacetylase 6 (HDAC6), with anti-tumor activity. LSD1/HDAC6-IN-1 can be used for the research of multiple myeloma (MM).
    LSD1/HDAC6-IN-1
  • HY-151872
    HDAC-IN-48
    		Inhibitor
    HDAC-IN-48 is a potent HDAC inhibitor. HDAC-IN-48 is a hybrid molecule with great cytotoxic profile (GI50~20 nM). HDAC-IN-48 consists of harmacophores of SAHA and CETZOLE molecules. HDAC-IN-48 induces ferroptosis and inhibits HDAC proteins. HDAC-IN-48 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    HDAC-IN-48
  • HY-131708
    FNDR-20123 free base
    		Inhibitor
    FNDR-20123 free base 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 free base exerts anti-malarial activity against Plasmodium falciparum asexual stage (IC50=41 nM) and sexual blood stage (IC50=190 nM for male gametocytes). FNDR-20123 free base inhibits HDAC1, HDAC2, HDAC3, HDAC6, and HDAC8 (IC50=25, 29, 2, 11, and 282 nM, respectively) and inhibits Class III HDAC isoforms at nanomolar concentrations.
    FNDR-20123 free base
  • HY-172177
    ROCK/HDAC-IN-2
    		Inhibitor
    ROCK/HDAC-IN-2 (Compound C-9) is a ROCK/HDAC inhibitor, with IC50 values of 0.185 µM, 0.8 µM, and 0.7 µM for HDAC6, ROCK1, and ROCK2, respectively. ROCK/HDAC-IN-2 can induce apoptosis and changes in mitochondrial membrane potential in cancer cells, demonstrating significant antitumor activity. ROCK/HDAC-IN-2 can be used in the research of pancreatic ductal adenocarcinoma (PDAC) and triple-negative breast cancer (TNBC).
    ROCK/HDAC-IN-2
  • HY-107909
    Theophylline sodium glycinate
    		Activator
    Theophylline (1,3-Dimethylxanthine) sodium glycinate is a potent phosphodiesterase (PDE) inhibitor, adenosine receptor antagonist, and histone deacetylase (HDAC) activator. Theophylline sodium glycinate inhibits PDE3 activity to relax airway smooth muscle. Theophylline sodium glycinate has anti-inflammatory activity by increase IL-10 and inhibit NF-κB into the nucleus. Theophylline sodium glycinate induces apoptosis. Theophylline sodium glycinate can be used for asthma and chronic obstructive pulmonary disease (COPD) research.
    Theophylline sodium glycinate
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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