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-149646
    HDAC6-IN-24
    		Inhibitor
    HDAC6-IN-24 (compound N1) is a inhibitor of HDAC6.
    HDAC6-IN-24
  • HY-173184
    HDAC6-IN-53
    		Inhibitor
    HDAC6-IN-53 (Compound W28) is an inhibitor targeting histone deacetylase 6 (HDAC6) with an IC50 of 19.65 nM. HDAC6-IN-53 exerts the activity of inhibiting the phenotype of idiopathic pulmonary fibrosis (IPF) by suppressing the collagen expression induced by TGF-β1, and it has demonstrated a good therapeutic effect in a mouse model of pulmonary fibrosis induced by bleomycin (HY-108345). HDAC6-IN-53 can be used in the research of idiopathic pulmonary fibrosis and other related pulmonary fibrosis diseases.
    HDAC6-IN-53
  • HY-145816
    JPS016
    JPS016 is a benzamide-based Von Hippel-Lindau (VHL) E3-ligase proteolysis targeting chimeras (PROTAC). JPS016 degrades class I histone deacetylase (HDAC). JPS016 is potent HDAC1/2 degrader correlated with greater total differentially expressed genes and enhanced apoptosis in HCT116 cells.
    JPS016
  • HY-161412
    STR-V-53
    		Inhibitor
    STR-V-53 is an HDAC inhibitor (IC50 in nM).STR-V-53 increases histone acetylation in tumor cells by inhibiting the activity of these enzymes, which in turn regulates gene expression.STR-V-53 inhibits tumor growth, and induces apoptosis.
    STR-V-53
  • HY-154855
    HDAC-IN-56
    		Inhibitor
    HDAC-IN-56 ((S)-17b) is an orally active class I histone deacetylase (HDAC) inhibitor with IC50 values of 56.0 ± 6.0, 90.0 ± 5.9, 422.2 ± 105.1, >10000 nM for HDAC1, HDAC2, HDAC3, and HDAC4-11, respectively. HDAC-IN-56 has potent inhibitory activity while strongly increasing intracellular levels of acetylhistone H3 and P21 and effectively inducing G1 cell cycle arrest and apoptosis.HDAC-IN-56 has antitumor activity .
    HDAC-IN-56
  • HY-162910
    HDAC-IN-79
    		Inhibitor
    HDAC-IN-79 (compound 4) is an orally active dual xanthine oxidase-HDAC inhibitor (Xanthine oxidase: IC50=6.6 nM; HDAC1: IC50=134 nM; HDAC2: IC50=284 nM; HDAC3: IC50=173 nM; HDAC6: IC50=1.32 nM;), with significant in vivo anti-hyperuricemia and anti-tumor activities. HDAC-IN-79 is the most potent cell growth inhibitor (IC50=0.706 μM) of leukemia HL60 cells, induces apoptosis and autophagy, and can regulate the expression levels of signature biomarkers associated with intracellular HDAC inhibition.
    HDAC-IN-79
  • HY-161688
    HDAC-IN-73
    		Inhibitor
    HDAC-IN-73 (compound P-503) is a histone deacetylase (HDAC) inhibitor. HDAC-IN-73 shows IC50s values of 0.17, 0.49 µM for HDAC1 and HDAC6, respectively. Notably, HDAC-IN-73's inhibitory potency against HDAC6 is heightened, exhibiting a 9-fold greater efficacy than PsA (HY-N2150) (IC50=3.9 μM). HDAC-IN-73 shows potent antiproliferative activity, induces apoptosis, and causes cell cycle arrest at G2 / M phase. HDAC-IN-73 has the potential to be used for the research of cancer such as colon cancer .
    HDAC-IN-73
  • HY-163894
    HDAC6-IN-48
    		Inhibitor
    HDAC6-IN-48 (compound 5i) is a potent and selective HDAC6 inhibitor with IC50 values of 5.16, 396.72, 638.08 nM for HDAC6, HDAC3, HDAC1, respectively. HDAC6-IN-48 induces apoptosis and cell cycle arrest at G0/G1 phase. HDAC6-IN-48 increases the protein expression of acetylated α-tubulin.
    HDAC6-IN-48
  • HY-168863
    FF2049
    		Degrader
    FF2049 is a selective HDAC PROTAC degrader (DC50 = 257 nM for HDAC1). FF2049 promotes ubiquitination and degradation of HDAC. FF2049 promotes Apoptosis. FF2049 can be used for the research of hematological and solid cancer (Pink: POI ligand 1 (HY-168864); Blue: E3 ligase FEM1B ligand (HY-168865)).
    FF2049
  • HY-161287
    HDAC6-IN-32
    		Inhibitor
    HDAC6-IN-32 (compound 25202) is a selective and potent inhibitor of HDAC6. HDAC6-IN-32 blocks HDAC6 activity and interferes with microtubule dynamics, leading to SAC activation and prolonged mitotic arrest, ultimately leading to apoptosis in CRPC cells.
    HDAC6-IN-32
  • HY-145406
    IHCH-3064
    		Inhibitor
    IHCH-3064 is a dual-acting compounds targeting Adenosine A2A Receptor and HDAC. IHCH-3064 exhibits potent binding to A2AR (Ki=2.2 nM) and selective inhibition of HDAC1 (IC50=80.2 nM), with good antiproliferative activity against tumor cell lines in vitro. IHCH-3064 is a tumor immunotherapeutic agent.
    IHCH-3064
  • HY-169157
    HDAC6-IN-50
    		Inhibitor
    HDAC6-IN-50 (Compound 4) is a potent HDAC6 inhibitor with an IC50 of 35 nM. HDAC6-IN-50 can be used for the study of Parkinson's disease (PD) and Alzheimer's disease (AD) research.
    HDAC6-IN-50
  • HY-161306
    ITF5924
    		Inhibitor
    ITF5924 (compound 1) is a potent and highly selective HDAC6 inhibitor with an IC50 of 7.7 nM. ITF5924 shows greater than 104-fold selectivity for HDAC6 over all other HDAC subtypes. ITF5924 containing a difluoromethyl-1,3,4-oxadiazole (DFMO) moiety is slow-binding substrate analog of HDAC6 that undergo an enzyme-catalyzed ring opening reaction, forming a tight and long-lived enzyme-inhibitor complex.
    ITF5924
  • HY-168477
    HDAC1-IN-8
    		Inhibitor
    HDAC1-IN-8 (compound 5c) is a potent and selective HDAC1 inhibitor with IC50 values of 11.94, 22.95, >500 µM for HDAC1, HDAC6, HDAC8, respectively. HDAC1-IN-8 shows antiproliferative activity. HDAC1-IN-8 induces cell cycle arrest at G1 and G2/M. HDAC1-IN-8 induces autophagy. HDAC1-IN-8 shows anticancer activity and has the potential for the research of lung cancer.
    HDAC1-IN-8
  • HY-168508
    PB200
    		Inhibitor
    PB200 is an HDAC6 inhibitor with an IC50 value of 1.97 nM. PB200 demonstrates significant antidepressant effects by restoring abnormal HDAC6 expression levels and alleviating neuroinflammation.
    PB200
  • HY-163920
    PROTAC HDAC8 Degrader-1
    		Degrader
    Degrader-1 (compound Z16) is a potent and selective HDAC8 PROTAC degrader with an DC50 of 0.27 nM in A549 cells.
    PROTAC HDAC8 Degrader-1
  • HY-175671
    LSD1/HDAC-IN-3
    		Inhibitor
    LSD1/HDAC-IN-3 is a inhibitor targeting class I HDAC and LSD1 enzymes. LSD1/HDAC-IN-3 inhibits HDAC1, HDAC2, HDAC3, and LSD1 with IC50 values of 1702 nM, 842 nM, 358 nM, and 1074 nM, respectively. LSD1/HDAC-IN-3 exhibits antioxidant effects in H2O2-stressed ARPE-19 and 661W retinal cells, increasing levels of acetylated and methylated histone H3. LSD1/HDAC-IN-3 enhances photoreceptor survival in the rd10 mouse model of retinitis pigmentosa. LSD1/HDAC-IN-3 can be used for the study of inherited retinal diseases such as retinitis pigmentosa (RP).
    LSD1/HDAC-IN-3
  • HY-117374
    HDAC3-IN-1
    		Inhibitor
    HDAC3-IN-1 (compound 5) is a potent and selective HDAC3 inhibitor, with an IC50 of 5.96 nM.
    HDAC3-IN-1
  • HY-178948
    HDAC10-IN-3
    		Inhibitor
    HDAC10-IN-3 (Compound 2a) is a potent HDAC10 inhibitor with an IC50s of 0.41, 37, 350 and 4500 nM against HDAC10, HDAC6, HDAC8 and HDAC1. HDAC10-IN-3 exhibits moderate cytotoxicity in KB and SK-OV-3 cells, but does not show significant cytotoxicity against most cancer cell lines. HDAC10-IN-3 can be used for the study of cancers.
    HDAC10-IN-3
  • HY-163806
    NT376
    		Inhibitor
    NT376 is a high potency and selectivity inhibitor of class-IIa Histone deacetylases (HDAC) with an IC50 value of 32 nM, similar to NT160 (HY-149285) (IC50= 46 nM) in HT-29 cells. NT376 is proming for research of various cancers and in the diseases of the central nervous system (CNS) such as Alzheimer’s and Huntington’s diseases.
    NT376
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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