2. Signaling Pathways
  3. Cell Cycle/DNA Damage
    Epigenetics
  4. HDAC

HDAC

Histone deacetylases

HDAC

Related Products

PDF 2.58 MB

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-N6017
    Bakkenolide A
    		Inhibitor 99.99%
    Bakkenolide A is a natural product extracted from Petasites tricholobus. Bakkenolide A inhibits leukemia by regulation of HDAC3 and PI3K/Akt-related signaling pathways.
    Bakkenolide A
  • HY-116818
    Crebinostat
    		Inhibitor 99.79%
    Crebinostat is a potent histone deacetylase (HDAC) inhibitor with IC50 values of 0.7 nM, 1.0 nM, 2.0 nM and 9.3 nM for HDAC1, HDAC2, HDAC3 and HDAC6, respectively. Crebinostat potently induces acetylation of both histone H3 and histone H4 as well as enhances the expression of the cAMP response element-binding protein (CREB) target gene Egr1. Crebinostat increases the density of synapsin-1 punctae along dendrites in cultured neurons. Crebinostat can modulate chromatin-mediated neuroplasticity and exhibits enhanced memory in mice.
    Crebinostat
  • HY-B0896
    Triacetin
    		Inhibitor 99.58%
    Triacetin (Glyceryl triacetate) is a synthetic compound that is a triester of glycerol and acetic acid, orally active. Triacetin increases acetate bioavailability in glioma cells. Triacetin induces glioma cell growth arrest and Apoptosis. Triacetin freely crosses the blood brain barrier/plasma membrane. Triacetin increases histone acetylation and enhances Temozolomide (HY-17364) (TMZ) chemotherapeutic efficacy .
    Triacetin
  • HY-100871
    WT-161
    		Inhibitor 98.36%
    WT-161 is a potent and selective HDAC6 inhibitor with an IC50 of 0.40 nM. WT-161 also inhibits metallo-β-lactamase domain-containing protein 2 (MBLAC2).
    WT-161
  • HY-19747
    HPOB
    		Inhibitor 99.80%
    HPOB is a highly potent and selective inhibitor of HDAC6 with an IC50 of 56 nM. HPOB displays >30 fold less potent against other HDACs. HPOB enhances the effectiveness of DNA-damaging anticancer agents in transformed cells but not normal cells. HPOB does not block the ubiquitin-binding activity of HDAC6.
    HPOB
  • HY-B0809R
    Theophylline (Standard)
    		Activator
    Theophylline (Standard) is the analytical standard of Theophylline. This product is intended for research and analytical applications. Theophylline (1,3-Dimethylxanthine) is a potent phosphodiesterase (PDE) inhibitor, adenosine receptor antagonist, and histone deacetylase (HDAC) activator. Theophylline (1,3-Dimethylxanthine) inhibits PDE3 activity to relax airway smooth muscle. Theophylline (1,3-Dimethylxanthine) has anti-inflammatory activity by increase IL-10 and inhibit NF-κB into the nucleus. Theophylline (1,3-Dimethylxanthine) induces apoptosis. Theophylline (1,3-Dimethylxanthine) can be used for asthma and chronic obstructive pulmonary disease (COPD) research.
    Theophylline (Standard)
  • HY-132242
    DL-Sulforaphane N-acetyl-L-cysteine
    		Inhibitor 99.90%
    DL-Sulforaphane N-acetyl-L-cysteine (SFN-NAC) is an orally active HDAC inhibitor and metabolite of sulforaphane (HY-13755) with longer half-life and better blood-brain barrier permeability. DL-Sulforaphane N-acetyl-L-cysteine activates autophagy-mediated downregulation of α-tubulin expression through the ERK pathway and can be used in cancer research.
    DL-Sulforaphane N-acetyl-L-cysteine
  • HY-118052
    BPKDi
    		99.60%
    BPKDi is an inhibitor of PKD. BPKDi inhibits three members of the PKD family, PKD1, PKD2, and PKD3, with IC50 values of 1 nM, 9 nM, and 1 nM, respectively. BPKDi blocks signal-dependent phosphorylation and nuclear export of class IIa HDACs in cardiomyocytes and concomitantly suppresses hypertrophy of these cells.
    BPKDi
  • HY-W009776
    Suberoyl bis-hydroxamic acid
    		Inhibitor ≥98.0%
    Suberoyl bis-hydroxamic acid (Suberohydroxamic acid; SBHA) is a competitive and cell-permeable HDAC1 and HDAC3 inhibitor with ID50 values of 0.25 μM and 0.30 μM, respectively.Suberoyl bis-hydroxamic acid renders MM cells susceptible to apoptosis and facilitates the mitochondrial apoptotic pathways.Suberoyl bis-hydroxamic acid can be used for the study of medullary thyroid carcinoma (MTC).
    Suberoyl bis-hydroxamic acid
  • HY-100365
    Remetinostat
    		Inhibitor ≥98.0%
    Remetinostat (SHP-141) is a hydroxamic acid-based histone deacetylase (HDAC) inhibitor. Remetinostat alleviates Imiquimod (HY-B0180)-induced psoriatic dermatitis. Remetinostat can be used for study of cutaneous T-cell lymphoma.
    Remetinostat
  • HY-144782A
    HDAC10-IN-2 hydrochloride
    		Inhibitor
    HDAC10-IN-2 hydrochloride (compound 10c) is a potent and highly selective HDAC10 inhibitor, with an IC50 of 20 nM. HDAC10-IN-2 hydrochloride modulates autophagy in aggressive FLT3-ITD positive acute myeloid leukemia cells.
    HDAC10-IN-2 hydrochloride
  • HY-N7676
    Marein
    		Inhibitor 99.71%
    Marein has the neuroprotective effect due to a reduction of damage to mitochondria function and activation of the AMPK signal pathway. Marein improves insulin resistance induced by high glucose in HepG2 cells through CaMKK/AMPK/GLUT1 to promote glucose uptake, through IRS/Akt/GSK-3β to increase glycogen synthesis, and through Akt/FoxO1 to decrease gluconeogenesis. Marein is a HDAC inhibitor with an IC50 of 100 μM. Marein has beneficial antioxidative, antihypertensive, antihyperlipidemic and antidiabetic effects.
    Marein
  • HY-149285
    NT160
    		Inhibitor 99.58%
    NT160 is a highly potent class-IIa HDAC inhibitor with an IC50 value of 0.046 μM. NT160 can be used for the research of central nervous system diseases.
    NT160
  • HY-N2150
    Psammaplin A
    		Inhibitor
    Psammaplin A is a marine metabolite. Psammaplin A is a selective HDAC1 (IC50: 45 nM), DNA methyltransferases (IC50: 18.6 nM) and aminopeptidase N (APN) (IC50: 18 μM) inhibitor. Psammaplin A also inhibits DNA topoisomerase and farnesyl protein transferase. Psammaplin A is a PPARγ activator and induces apoptosis. Psammaplin A has antitumor and anti-inflammatory activities. Psammaplin A has antibacterial activity against Gram-positive bacteria and inhibits DNA synthesis and DNA gyrase activity. Psammaplin A inhibits angiogenesis.
    Psammaplin A
  • HY-102033
    Oxamflatin
    		Inhibitor 98.13%
    Oxamflatin (Metacept-3) is a potent HDAC inhibitor with an IC50 of 15.7 nM. Oxamflatin is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    Oxamflatin
  • HY-10585R
    Valproic acid (Standard)
    		Inhibitor
    Valproic acid (Dipropylacetic Acid) (Standard) is an analytical standard for valproic acid. This product is intended for research and analytical applications. Valproic acid is an orally active HDAC inhibitor (IC50=0.5-2 mM), inhibits the activity of HDAC1 (IC50=400 μM), and induces the degradation of HDAC2. Valproic acid activates Notch1 signaling and inhibits the proliferation of small cell lung cancer (SCLC) cells. Valproic acid is used in the study of epilepsy, bipolar disorder, metabolic diseases, HIV infection, and migraine.
    Valproic acid (Standard)
  • HY-164050
    HDAC2-IN-2
    		Inhibitor 99.74%
    HDAC2-IN-2 (compound 124) is an inhibitor of HDAC2 with Kd value of 0.1-1 μM.
    HDAC2-IN-2
  • HY-149766
    PB94
    		Inhibitor
    PB94 is a selective HDAC11 inhibitor (IC50=108 nM). PB94 can be radiolabeled as [11C]-PB94 for use in positron emission tomography (PET), as well as brain uptake and metabolic properties in administered live animals. PB94 improves neuropathic pain in mice and could be used to study neurological indications.
    PB94
  • HY-18712
    BG45
    		Inhibitor 99.95%
    BG45 is a potent HDAC3 inhibitor with IC50 values of 0.289, 2, 2.2 and ﹥20 μM for HDAC3, HDAC1, HDAC2 and HDAC6, respectively. BG45 selectively targets multiple myeloma (MM) cells and induces caspase-dependent apoptosis.
    BG45
  • HY-19772
    GSK3117391
    		Inhibitor 99.40%
    GSK3117391 (ESM-HDAC391) is a histone deacetylase (HDAC) inhibitor, extracted from patent WO/2008040934 A1.
    GSK3117391
Cat. No. Product Name / Synonyms Application Reactivity
All Rights Reserved.
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

Your Search Returned No Results.

Sorry. There is currently no product that acts on isoform together.

Please try each isoform separately.