HDAC

Histone deacetylases

HDAC

HDAC Isoform Specific Products:

HDAC Isoform Comparison

HDAC Related Products (626)
Antibodies (16)
HDAC Signaling Pathway
HDAC Isoform Comparison

By Effects:	Controls (2) Ligands (2) Inhibitors (561) Degraders (13) Antagonists (2) Activators (9) Modulators (2)

Cat. No.	Product Name	Effect	Purity	Chemical Structure

HY-128918

SIS17	Inhibitor	99.65%
SIS17 is a mammalian histone deacetylase 11 (HDAC 11) inhibitor with an IC50 value of 0.83 μM. SIS17 inhibits the demyristoylation of serine hydroxymethyltransferase 2, a substrate of HDAC 11, but does not inhibit other HDACs.

HY-111048

Corin	Inhibitor	98.16%
Corin is a dual inhibitor of histone lysine specific demethylase (LSD1) and histone deacetylase (HDAC), with a K_i(inact) of 110 nM for LSD1 and an IC₅₀ of 147 nM for HDAC1.

HY-10990

Abexinostat	Inhibitor	99.00%
Abexinostat (CRA 024781) is a novel pan-HDAC inhibitor mostly targeting HDAC1 with K_i of 7 nM. Abexinostat also inhibits metallo-β-lactamase domain-containing protein 2 (MBLAC2) hydrolase activity with an EC₅₀ below 10 nM.

HY-145757

Elevenostat	Inhibitor
Elevenostat (JB3-22) is a selective HDAC11 inhibitor with an IC₅₀ of 0.235 µM. Elevenostat can induce apoptosis of multiple myeloma cells and has anti-tumor effect. In addition, Elevenostat inhibits the maturation of mouse oocytes.

HY-116522

AR420626	Inhibitor	98.29%
AR420626 is a selective agonist of free fatty acid receptor 3 (FFAR3) (IC₅₀=117 nM). AR420626 has anti-inflammatory, anticancer and antidiabetic activities. AR420626 improves neurogenic diarrhea by inhibiting nAChR mediated neural pathways. AR420626 inhibits the growth of HepG2 xenografts and inhibits the proliferation of hepatoma cells by inducing apoptosis. AR420626 also suppresses allergic asthma and eczema and has the ability to activate GPR41 to increase Ca²⁺ signal-mediated glucose uptake and improve diabetes.

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.

HY-109521A

Manganese chloride (tetrahydrate), molecular biology grade,≥99.0% (KT)	Activator	99.08%
Manganese chloride (tetrahydrate), molecular biology grade,≥99.0% (KT) is an orally active and a blood-brain barrier penetrant compound. It affects the activities of multiple enzymes in cells, such as regulating the activities of histone acetyltransferase (HAT) and histone deacetylase (HDAC), thereby affecting gene expression. It has multiple activities such as neurotoxicity, embryotoxicity, and reproductive toxicity. It is currently mainly used in neurodegenerative diseases and toxicology research.

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.

HY-16699

Nexturastat A	Inhibitor	98.28%
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).

HY-13506

M344	Inhibitor	98.86%
M344 (D 237) is an inhibitor of histone deacetylase (IC₅₀=100 nM) and an inducer of terminal cell fifferentiation.

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.

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 K_i values for HDAC1 and HDAC3 are 32 and 5 nM, respectively.

HY-15994

Citarinostat	Inhibitor	99.30%
Citarinostat (ACY241) is a second generation potent, orally active and high-selective HDAC6 inhibitor with an IC₅₀ of 2.6 nM (IC₅₀s of 35 nM, 45 nM, 46 nM and 137 nM for HDAC1, HDAC2, HDAC3 and HDAC8, respectively). Citarinostat has anticancer effects.

HY-15433A

Quisinostat dihydrochloride	Inhibitor	99.05%
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.

HY-111818

TH34	Inhibitor	99.52%
TH34, an HDAC6/8/10 inhibitor with IC₅₀s of 4.6 μM, 1.9 μM, and 7.7 μM respectively, shows high selectivity over HDAC1/2/3.

HY-125771

1-Stearoyl-sn-glycero-3-phosphocholine	Inhibitor	99.53%
1-Stearoyl-sn-glycero-3-phosphocholine is a lysophosphatidylcholine that inhibits HDAC3 activity and phosphorylation of STAT3 in K562 cells. 1-Stearoyl-sn-glycero-3-phosphocholine induces apoptosis and exhibits anticancer activity in chronic myelogenous leukemia (CML) K562 cells.

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.

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.

HY-B0494

Bufexamac	Inhibitor	≥98.0%
Bufexamac is a selective Ⅱb HDAC (HDAC6, HDAC10) and LTA4H dual inhibitor, with K_ds of 0.53 µM and 0.22 µM for HDAC6 and HDAC10. Bufexamac is a nonsteroida anti-inflammatory drug.

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.

TCR CD3 GPCR Adrenergic Agonists, Endothelin, Angiotensin, 5-HT, and Others PKC PKD Rho PLCβ CaMK 14-3-3 14-3-3 HDACII LMB CRM1 HDACII HDACII 14-3-3 HDACII MEF2 p300 Cytokines
Cytokine receptors
Adhesion molecules
(e.e., LFA1) HSP90 p23 HDAC6 HDACi p23 HSP90
HDAC6 Proteasome HDAC1 p53 HDAC1 p53 HATs HDAC Antigen presentation:
Co-stimulatory molecules
(e.g., CD40, CD86)
MHCII expression Anti-viral response: IFN-stimulated
genes (e.g., Rsad2, Ifit2, ISG54) Cyclin E/A, TLR TRIF TRAM HDAC6 MyD88 Mal HDAC
1/2/3 NF-κB HDAC2 HDAC6 MTA-1 HDAC
1/2/3 HATs MKP-1 p38 HDAC
1/8 IRF AP-1 HDAC11 IL-10 HATs HDAC CBP p53 HAT
activity CBP p53 CBP p53 IFNGR IFNγ HDAC
1/2 CIITA IFNα/β IFNAR HDAC1 JAK STAT PLZF HDAC
1/2/3 HATs HDAC HDAC BAX HATs BAX Apoptosis E2F p53 p21 CDK Cyclin HDAC RB HDAC RB E2F DP TF E2F DP TK, DHFR, ... Inflammatory mediators:
Cytokines
(e.g., IL-6, TNFα, Ifnβ) Chemokines (e.g., CXCL10, Ccl2/7)
Other mediators
(e.g., MMP9, Edn-1)

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.

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HDAC

HDAC

HDAC Isoform Specific Products:

HDAC Isoform Specific Products:

HDAC Related Products (626)

Antibodies (16)

HDAC Signaling Pathway

HDAC Isoform Comparison

HDAC Related Products (626):