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-150577
    HDAC-IN-45
    		Inhibitor
    HDAC-IN-45 (Compound 14) is a small molecule HDAC inhibitor and has anticancer activity, also can forms a hydrogen bond with residue Y303. HDAC-IN-45 (Compound 14) has substantial inhibitory effects towards HDAC1, 2 and 3 isoforms with IC50 values of 0.108, 0.585 and 0.563 μM respectively.
    HDAC-IN-45
  • HY-124007
    4-Iodo-SAHA
    		Inhibitor
    4-Iodo-SAHA (1k) is an orally active class I and class II histone deacetylase (HDAC) inhibitor with EC50s of 1.1, 0.95, 0.12, 0.24, 0.85 and 1.3 μM for Skbr3, HT29, U937, JA16 and HL60 cell lines, respectively. 4-Iodo-SAHA (1k) can be used for the research of cancer.
    4-Iodo-SAHA
  • HY-145350
    HDAC-IN-26
    		Inhibitor
    HDAC-IN-26 is a highly selective class I HDAC inhibitor with an EC50 value of 4.7 nM.
    HDAC-IN-26
  • HY-149417
    BChE/HDAC6-IN-1
    		Inhibitor
    BChE/HDAC6-IN-1 is a potent and selective dual BChE/HDAC6 inhibitor with IC50 values of 4 and 8.9 nM, respectively. BChE/HDAC6-IN-1 ameliorates the cognitive impairment in an Aβ1–42-induced mouse model and has the potental for AD research.
    BChE/HDAC6-IN-1
  • HY-168650
    ROCK/HDAC-IN-1
    		Inhibitor
    ROCK/HDAC-IN-1 (Compound 10h) is an orally active ROCK/HDAC inhibitor. ROCK/HDAC-IN-1 inhibits ROCK1/2 (IC50: 254.9 nM, 58.18 nM) and HDAC1/2/3/6/8 (IC50: 9.09, 8.03, 6.26, 0.41, 7.69 nM). ROCK/HDAC-IN-1 stimulates the activation of DAMPs, specifically Calreticulin (CRT) exposure and HMGB1 release, indicating that it is a potential ICD inducer.. ROCK/HDAC-IN-1 has antiproliferative activity against breast cancer cells (IC50: 0.37 μM for MDA-MB-231 cell), and inhibits tumor growth and activates T cells without apparent toxicity.
    ROCK/HDAC-IN-1
  • HY-118672
    HNHA
    		Inhibitor 99.76%
    HNHA is a potent HDAC inhibitor with an IC50 of 100 nM. HNHA arrests the cell cycle at the G1/S phase via p21 induction. HNHA inhibits tumor growth and tumor neovascularization. HNHA may be a potent anti-cancer agent against breast cancer.
    HNHA
  • HY-145819
    JPS036
    JPS036 is a benzamide-based Von Hippel-Lindau (VHL) E3-ligase proteolysis targeting chimeras (PROTAC). JPS036 degrades class I histone deacetylase (HDAC). JPS036 is potent HDAC1/2 degrader correlated with greater total differentially expressed genes and enhanced apoptosis in HCT116 cells.
    JPS036
  • HY-151248
    HDAC2-IN-1
    		Inhibitor
    HDAC2-IN-1 (Compound 17) is a brain penetrant, orally active, competitive HDAC2 inhibitor with an IC50 of 0.5 μM. HDAC2-IN-1 also inhibits HDAC1 and HDAC8 with IC50s of 1.61 μM and 0.98 μM, respectively.
    HDAC2-IN-1
  • HY-172129
    HDAC6-IN-52
    		Inhibitor
    HDAC6-IN-52 (EX.1) is a potent inhibitor of HDAC6, with the inhibitory rate of 100% at 10 μM. HDAC6-IN-52 plays an important role in central nervous system diseases including neurodegenerative diseases such as Alzheimer’s disease andprogressive supranuclear palsy.
    HDAC6-IN-52
  • HY-146684
    HDAC-IN-36
    		Inhibitor
    HDAC-IN-36 (compound 23 g) is an orally active and potent HDAC (histone deacetylase) inhibitor, with an IC50 of 11.68 nM (HDAC6). HDAC-IN-36 promotes apoptosis, autophagy and suppresses migration. HDAC-IN-36 shows anti-tumor and anti-metastatic activity, and can be used for breast cancer research.
    HDAC-IN-36
  • HY-149631
    HFY-4A
    		Inhibitor 99.34%
    HFY-4A is a HDAC inhibitor. HFY-4A inhibits breast cancer cell proliferation, migration, and invasion, and induces cell apoptosis. HFY-4A induces immunogenic cell death (ICD). HFY-4A inhibits tumor growth in breast cancer xenograft mouse models.
    HFY-4A
  • HY-173555
    HDAC6-IN-54
    		Inhibitor
    HDAC6-IN-54 (Compound 9m) is a highly selective HDAC6 (histone deacetylase 6) inhibitor with an IC50 value of 0.021 μM. HDAC6-IN-54 blocks the activation of the NLRP3 inflammasome, which alleviates symptoms of NLRP3 inflammasome-related diseases such as acute peritonitis, inflammatory bowel disease, and psoriasis.
    HDAC6-IN-54
  • HY-126566
    Trichostatin C
    		Inhibitor
    Trichostatin C is an inhibitor for histone deacetylase (HDAC), induces apoptosis and arrests cell cycle at G2/M phase, and exhibits anticancer activity against lung cancer and urothelial bladder cancer. Trichostatin C induces differentation of Friend leukemic cells. Trichostatin C exhibits antifungal activity.
    Trichostatin C
  • HY-152235
    HDAC6-IN-15
    		Inhibitor
    HDAC6-IN-15 is a selective histone deacetylase 6 (HDAC6) inhibitor. HDAC6-IN-15 has potent inhibitory activity for HDAC6 with IC50 value of 38.2 nM. HDAC6-IN-15 can be used for the research of cancer and neurodegenerative diseases.
    HDAC6-IN-15
  • HY-174877
    PROTAC HDAC6 degrader 6
    		Degrader
    PROTAC HDAC6 degrader 6 (Compound 12) is a selective HDAC6-targeting photochemically targeting chimeras (PHOTACs) (subset of PROTAC) degrader with a ∼50% Dmax only upon activation to its cis-state with 390 nm light irradiation. Pink: HDAC6 ligand; Blue: CRBN ligase ligand (HY-A0003); Black: linker
    PROTAC HDAC6 degrader 6
  • HY-156094
    JMJD3/HDAC-IN-1
    		Inhibitor
    JMJD3/HDAC-IN-1 (compound A5b) is a dual inhibitor targeting Jumonji domain-containing protein demethylase 3 (JMJD3) and histone deacetylase (HDAC1, IC50=16 nM). JMJD3/HDAC-IN-1 promotes hypermethylation of histone H3K27 and hyperacetylation of H3K9, and also cleaves caspase-7 and PARP to induce apoptosis. JMJD3/HDAC-IN-1 effectively inhibits cancer cell cloning, migration, and invasion.
    JMJD3/HDAC-IN-1
  • HY-146392
    HDAC-IN-39
    		Inhibitor
    HDAC-IN-39 (compound 16c) is a potent HDAC inhibitor, with IC50 values of 1.07 μM (HDAC1), 1.47 μM (HDAC2), and 2.27 μM (HDAC3), respectively. HDAC-IN-39 also significantly inhibits microtubule polymerization. HDAC-IN-39 induces cell cycle arrest at the G2/M phase. HDAC-IN-39 displays promising anticancer activity against resistant cancer cells.
    HDAC-IN-39
  • HY-147873
    NMDAR/HDAC-IN-1
    		Inhibitor
    NMDAR/HDAC-IN-1 (Compound 9d) is a dual NMDAR and HDAC inhibitor with a Ki of 0.59 μM for NMDAR and IC50 values of 2.67, 8.00, 2.21, 0.18 and 0.62 μM for HDAC1, HDAC2, HDAC3, HDAC6 and HDAC8, respectively. NMDAR/HDAC-IN-1 efficiently penetrates the blood brain barrier.
    NMDAR/HDAC-IN-1
  • HY-173064
    DS-103
    		Inhibitor
    DS-103 is an inhibitor for HDAC that inhibits HDAC1, HDAC2, HDAC3, HDAC6 and HDAC8 with IC50s of 0.029, 0.123, 0.022, 0.367 and 9.26 μM, respectively. DS-103 inhibits Plasmodium falciparum 3D7 with IC50 of 5.08 μM. DS-103 exhibits cytotoxicity in cells A2780 and Cal27 with IC50 of 1.48 μM and 1.47 μM, reverses Cisplatin (HY-17394) resistance in A2780 and Cal27 with IC50 of 4.62 μM and 2.23 μM. DS-103 exhibits synergistic effect with Cisplatin (HY-17394), enhances Cisplatin-induced apoptosis.
    DS-103
  • HY-159966
    Top/HDAC-IN-3
    		Inhibitor
    Top/HDAC-IN-3 (Compound 31) is an orally active dual inhibitor of Topoisomerase and HDAC. Top/HDAC-IN-3 increases reactive oxygen species (ROS) levels, leading to DNA damage, thereby inhibiting cancer cell colony formation and migration, inducing cancer cell Apoptosis, and causing cell cycle arrest. In the NSCLC model, Top/HDAC-IN-3 exhibited significant antitumor effects, with a tumor growth inhibition (TGI) of 77.5% at 100 mg/kg, surpassing the efficacy of the HDAC inhibitor SAHA (HY-10221) and the combination of SAHA (HY-10221) with the topoisomerase inhibitor Irinotecan (HY-16562).
    Top/HDAC-IN-3
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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