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

HDAC

Histone deacetylases

HDAC

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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-10990
    Abexinostat
    		Inhibitor 98.61%
    Abexinostat (CRA 024781) is a novel pan-HDAC inhibitor mostly targeting HDAC1 with Ki of 7 nM. Abexinostat also inhibits metallo-β-lactamase domain-containing protein 2 (MBLAC2) hydrolase activity with an EC50 below 10 nM.
    Abexinostat
  • HY-128918
    SIS17
    		Inhibitor 99.65%
    SIS17 is a mammalian histone deacetylase 11 (HDAC 11) inhibitor with an IC50 value of 0.83 μM, inhibits the demyristoylation HDAC11 substrate, serine hydroxymethyl transferase 2, without inhibiting other HDACs.
    SIS17
  • HY-13606
    Dacinostat
    		Inhibitor 98.45%
    Dacinostat is a potent HDAC inhibitor, with an IC50 of 32 nM; Dacinostat also inhibits HDAC1 with an IC50 of 9 nM, and used in cancer research.
    Dacinostat
  • HY-145757
    Elevenostat
    		Inhibitor
    Elevenostat (JB3-22) is a selective HDAC11 inhibitor (IC50=0.235 µM). Anti-multiple myeloma (MM) activity.
    Elevenostat
  • HY-16699
    Nexturastat A
    		Inhibitor 99.03%
    Nexturastat A is a potent, selective HDAC6 inhibitor. Nexturastat A has inhibitory for HDAC6 with an IC50 of 5 nM. Nexturastat A can be used for the research of multiple myeloma (MM).
    Nexturastat A
  • HY-W009732
    Sinapinic acid
    		Inhibitor 99.95%
    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
  • HY-111791
    ACY-1083
    		Inhibitor 99.80%
    ACY-1083 is a selective and brain-penetrating HDAC6 inhibitor with an IC50 of 3 nM and is 260-fold more selective for HDAC6 than all other classes of HDAC isoforms. ACY-1083 effectively reverses chemotherapy-induced peripheral neuropathy.
    ACY-1083
  • HY-19327
    ACY-738
    		Inhibitor 99.92%
    ACY-738 is a potent, selective and orally-bioavailable HDAC6 inhibitor, with an IC50 of 1.7 nM; ACY-738 also inhibits HDAC1, HDAC2, and HDAC3, with IC50s of 94, 128, and 218 nM.
    ACY-738
  • HY-100719
    BRD-6929
    		Inhibitor 99.04%
    BRD-6929 is a potent, selective brain-penetrant inhibitor of class I histone deacetylase HDAC1 and HDAC2 inhibitor with IC50 of 1 nM and 8 nM, respectively. BRD-6929 shows high-affinity to HDAC1 and HDAC2 with Ki of 0.2 and 1.5 nM, respectively. BRD-6929 can be used for mood-related behavioral model research.
    BRD-6929
  • HY-14842B
    Givinostat hydrochloride monohydrate
    		Inhibitor ≥98.0%
    Givinostat hydrochloride monohydrate (ITF-2357 hydrochloride monohydrate) is a HDAC inhibitor with an IC50 of 198 and 157 nM for HDAC1 and HDAC3, respectively.
    Givinostat hydrochloride monohydrate
  • HY-16425
    RG2833
    		Inhibitor 99.86%
    RG2833 is a brain-penetrant HDAC inhibitor with IC50s of 60 nM and 50 nM for HDAC1 and HDAC3, respectively. The Ki values for HDAC1 and HDAC3 are 32 and 5 nM, respectively.
    RG2833
  • HY-15433A
    Quisinostat dihydrochloride
    		Inhibitor 98.28%
    Quisinostat dihydrochloride (JNJ-26481585 dihydrochloride) is an orally available, potent pan-HDAC inhibitor with IC50s of 0.11 nM, 0.33 nM, 0.64 nM, 0.46 nM, and 0.37 nM for HDAC1, HDAC2, HDAC4, HDAC10 and HDAC11, respectively. Quisinostat dihydrochloride has a broad spectrum antitumoral activity.
    Quisinostat dihydrochloride
  • HY-100748
    Zabadinostat
    		Inhibitor 99.81%
    Zabadinostat (CXD101) is a potent, selective and orally active class I HDAC inhibitor with IC50s of 63 nM, 570 nM and 550 nM for HDAC1, HDAC2 and HDAC3, respectively. Zabadinostat has no activity against HDAC class II. Zabadinostat has antitumor activity.
    Zabadinostat
  • HY-16012A
    Domatinostat
    		Inhibitor 99.43%
    Domatinostat (4SC-202 free base) is a selective class I HDAC inhibitor with IC50 of 1.20 μM, 1.12 μM, and 0.57 μM for HDAC1, HDAC2, and HDAC3, respectively. It also displays inhibitory activity against Lysine specific demethylase 1 (LSD1).
    Domatinostat
  • HY-19618
    BRD3308
    		Inhibitor 98.82%
    BRD3308 is a highly selective HDAC3 inhibitor with an IC50 of 54 nM. BRD3308 is 23-fold selectivity for HDAC3 over HDAC1 (IC50 of 1.26 μM) or HDAC2 (IC50 of 1.34 μM). BRD3308 suppresses pancreatic β-cell apoptosis induced by inflammatory cytokines or glucolipotoxic stress, and increases functional insulin release. BRD3308 activates HIV-1 transcription and disrupts HIV-1 latency.
    BRD3308
  • HY-16914
    MC1568
    		Inhibitor
    MC1568 is a selective class II (IIa) histone deacetylas (HDAC II) inhibitor, used for cancer research.
    MC1568
  • HY-104008
    ACY-957
    		Inhibitor 99.87%
    ACY-957 is an orally active and selective inhibitor of HDAC1 and HDAC2, with IC50s of 7 nM, 18 nM, and 1300 nM against HDAC1/2/3, respectively, and shows no inhibition on HDAC4/5/6/7/8/9.
    ACY-957
  • HY-15489
    Scriptaid
    		Inhibitor 98.59%
    Scriptaid is a potent histone deacetylase (HDAC) inhibitor, used in cancer research. Scriptaid is also a sensitizer to antivirals and has potential for epstein-barr virus (EBV)-associated lymphomas treatment.
    Scriptaid
  • HY-112719
    BRD 4354
    		Inhibitor 99.66%
    BRD 4354 is a moderately potent inhibitor of HDAC5 and HDAC9, with IC50s of 0.85 and 1.88 μM, respectively.
    BRD 4354
  • HY-14842
    Givinostat
    		Inhibitor 98.05%
    Givinostat (ITF-2357) is a HDAC inhibitor with an IC50 of 198 and 157 nM for HDAC1 and HDAC3, respectively.
    Givinostat
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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