Product Categories

Entinostat (MS-275, SNDX-275)

MS-275 is an HDAC inhibitor of HDAC1 and HDAC3 with IC50 of 0.51 μM and 1.7 μM, respectively.

Catalog No.S1053

9 Reviews 18 Product Citations

: Tel: +1-832-582-8158[email protected]

Entinostat (MS-275, SNDX-275) Chemical Structure
Molecular Weight: 376.41

Validation & Quality Control

Customer Reviews(9) in vivo invitation

HAUSP KO cells are more sensitive to HDACi-induced apoptosis.(A) HDAC inhibition induces apoptosis in HAUSP KO cells.HAUSP WT or KO cells were treated with or without MS-275 at the indicated concentration for 72 hours, then fixed and stained with propidium iodide. Flow cytometric analyses were used to profile sub-G1, G1, and G2-M cell populations. Apoptotic cells were quantified after the indicated clones were treated with either 5 or 10 μM MS-275. The means and SDs of three independent experiments were plotted (*P<0.001, t test). (B) HDAC inhibition induces apoptosis in HAUSP KO cells but leads to G2-M arrest in WT cells.Cell cycle profiles of HAUSP WT or KOcells that were treated or not with 5 μM MS-275. (C)HDAC inhibition increases the abundance of apoptotic cell markers. The indicated cells were treated with or without MS-275 for 72 hours.Cell lysates were blotted with antibodies against cleaved caspase 3 and β-actin. (D) Ectopic overexpression of DNMT1 in HAUSP KO cells suppresses apoptosis. HAUSP KO clones or HAUSP KO cells inducibly

overexpressingDNMT1 were treatedwith 10 μM MS-275. Apoptotic cell populations were quantified by fluorescence-activated cell sorting (FACS) analyses (*P < 0.001, t test). Cell lysates from these cells were blotted with the indicated antibodies. (E) HDAC inhibition arrests the growth of HAUSP KO cells. DLD1, HAUSP KO, and KO cells ectopically expressing HAUSP were treated with the indicated concentration of MS-275 for 4 days. Cell numbers were determined and data from eight replicates were plotted (**P <0.001, t test). (FandG) HDACi inhibits tumor xenograft formation ofHAUSP KOcells.Athymic nudemice (five in each group)were injectedsubcutaneously and bilaterallywith cells of the indicated genotypes. Mice were treated with or without MS-275 at 15mg/kg for 4 weeks. Tumors were harvested and photographed (F). Tumor sizes of the indicated groupsweremeasuredweekly and theaveragevolumes at each timepoint were plotted (G).MANOVA analyses were performed to determine whether there was an overall difference of the tumor sizes, as well as whether there was a difference in development over time of tumor sizes between the two groups (P < 0.0001).

Sci Signal , 2010, 3, ra80. Entinostat (MS-275, SNDX-275) purchased from Selleck

Quality Control & MSDS

Related Compound Libraries

Entinostat (MS-275, SNDX-275) is available in the following compound libraries:

Cambridge Cancer Compound Library(96-well) Chemical Library (96-well) Epigenetics Compound Library (96-well) Inhibitor Library (96-well)

Product Information

Compare HDAC Inhibitors

Research Area
Research Area
Dr. Antonino Maria Sparta demonstrates a breakthrough in leukemia research by utilizing two inhibitors produced by Selleck Chemicals.

Cat.No.	Product Name	Solubility (25°C)
S1053	Entinostat (MS-275, SNDX-275)	<1 mg/mL	75 mg/mL	<1 mg/mL
S1047	Vorinostat (SAHA)	<1 mg/mL	53 mg/mL	3 mg/mL
S1030	Panobinostat (LBH589)	<1 mg/mL	70 mg/mL	<1 mg/mL
S3020	Romidepsin (FK228 ,depsipeptide)	<1 mg/mL	10 mg/mL	<1 mg/mL
S1045	Trichostatin A (TSA)	<1 mg/mL	23 mg/mL	<1 mg/mL
S1122	Mocetinostat (MGCD0103)	<1 mg/mL	13 mg/mL	<1 mg/mL
S2627	Tubastatin A HCl	<1 mg/mL	74 mg/mL	<1 mg/mL
S1085	Belinostat (PXD101)	<1 mg/mL	64 mg/mL	<1 mg/mL
S2170	ITF2357 (Givinostat)	<1 mg/mL	95 mg/mL	3 mg/mL
S1095	LAQ824 (NVP-LAQ824, Dacinostat)	<1 mg/mL	76 mg/mL	<1 mg/mL
S1194	CUDC-101	<1 mg/mL	20 mg/mL	<1 mg/mL
S1515	SB939 (Pracinostat)	<1 mg/mL	72 mg/mL	27 mg/mL
S2012	PCI-34051	<1 mg/mL	59 mg/mL	<1 mg/mL
S1422	Droxinostat	<1 mg/mL	49 mg/mL	49 mg/mL
S1484	MC1568	<1 mg/mL	13 mg/mL	<1 mg/mL
S1090	PCI-24781	<1 mg/mL	80 mg/mL	<1 mg/mL
S1096	JNJ-26481585	<1 mg/mL	79 mg/mL	<1 mg/mL
S1168	Valproic acid sodium salt (Sodium valproate)	33 mg/mL	33 mg/mL	33 mg/mL
S2818	CI994 (Tacedinaline)	<1 mg/mL	≥54 mg/mL	<1 mg/mL
S2244	AR-42 (HDAC-42)	<1 mg/mL	63 mg/mL	63 mg/mL
S2779	M344	<1 mg/mL	62 mg/mL	4 mg/mL
S2759	PI3K/HDAC InhibitorⅠ	<1 mg/mL	102 mg/mL	<1 mg/mL
S8001	Rocilinostat (ACY-1215)	<1 mg/mL	87 mg/mL	<1 mg/mL
S8043	Scriptaid	<1 mg/mL	65 mg/mL	<1 mg/mL
S4125	Sodium Phenylbutyrate	37 mg/mL	8 mg/mL	<1 mg/mL

Product Description

Biological Activity Protocol Chemical Information Customer Reviews Product Citations Tech Support & FAQs

Biological Activity

Description	MS-275 is an HDAC inhibitor of HDAC1 and HDAC3 with IC50 of 0.51 μM and 1.7 μM, respectively.
Targets	HDAC1	HDAC3
IC50	0.51 μM	1.7 μM ^[2]
In vitro	MS-275 shows inhibitory to HDACs by 2'-amino group. MS-275 induces accumulation of p21^WAF1/CIP1 and gelsolin in K562 cell. MS-275 could reduce S-phase cells and induce G1-phase cells in A2780 cell. MS-275 inhibits the proliferation of human tumor cell lines including A2780, Calu-3, HL-60, K562, St-4, HT-29, KB-3-1, Capan-1, 4-1St and HCT-15 with IC50 from 41.5 nM to 4.71 μM, which due to HAD-inhibition. ^[1] MS-275 is not sensitive to other HDACs (4, 6, 8 and 10) with IC50 about/above 100 μM. ^[2] MS-275 shows great inhibition to human leukemia and lymphoma cells, including U937, HL-60, K562, and Jurkat. MS-275 also decreases expression of cyclin D1 and the antiapoptotic proteins Mcl-1 and XIAP. ^[3]
In vivo	MS-275 exhibits great antitumor activity against human tumor xenografts except HCT-15 at 49 mg/kg. ^[1] MS-275 demonstrates promising therapeutic potential in both solid and hematologic malignancies, as well as regulation of physiologic and aberrant gene expression. ^[4] MS-275, combination with IL-2, has great antitumor activity to renal cell carcinoma xenograft model, which due to decreased T regulatory cells and increased splenocytes. ^[5]
Clinical Trials	MS-275 is currently in Phase I/II clinical trials in recurrent advanced non-small cell lung cancer, combining with 5-azacytidine.
Features

Protocol(Only for Reference)

Kinase Assay:
^[6]

Standard HDAC Assays	Rat liver enzyme is diluted 1:6 with HDAC buffer. Recombinant human HDACs are diluted 1:4 in HDAC buffer. For standard HDAC assays, 60 μL of HDAC buffer is mixed with 10 μL of diluted enzyme solution at 30 °C. The HDAC reaction is started by adding 30 μL substrate solution in HDAC buffer followed by 30 min of incubation at 30 °C. The reaction is stopped by adding 100 μL trypsin solutions (10 mg/ml trypsin in 50 mM Tris-HCl [pH 8.0], 100 mM NaCl, 2 μM TSA). After a 20 min incubation period at 30 °C, the release of AMC is monitored by measuring the fluorescence at 460 nm (λ_ex = 390 nm). Fluorescence intensity is calibrated using free AMC. For standard time course experiments, 20 pmol of substrate is used in the initial 100 μL HDAC reaction. K_m and V_max values are determined by measuring the fluorescence AMC generated by enzymatic cleavage of 2–50 pmol of substrate. The experimental data are analyzed using a Hanes plot. The AMC signals are recorded against a blank with buffer and substrate but without the enzyme.

Standard HDAC Assays

Rat liver enzyme is diluted 1:6 with HDAC buffer. Recombinant human HDACs are diluted 1:4 in HDAC buffer. For standard HDAC assays, 60 μL of HDAC buffer is mixed with 10 μL of diluted enzyme solution at 30 °C. The HDAC reaction is started by adding 30 μL substrate solution in HDAC buffer followed by 30 min of incubation at 30 °C. The reaction is stopped by adding 100 μL trypsin solutions (10 mg/ml trypsin in 50 mM Tris-HCl [pH 8.0], 100 mM NaCl, 2 μM TSA). After a 20 min incubation period at 30 °C, the release of AMC is monitored by measuring the fluorescence at 460 nm (λ_ex = 390 nm). Fluorescence intensity is calibrated using free AMC. For standard time course experiments, 20 pmol of substrate is used in the initial 100 μL HDAC reaction. K_m and V_max values are determined by measuring the fluorescence AMC generated by enzymatic cleavage of 2–50 pmol of substrate. The experimental data are analyzed using a Hanes plot. The AMC signals are recorded against a blank with buffer and substrate but without the enzyme.

Cell Assay:
^[2]

Cell lines	A2780, Calu-3, HL-60, K562, St-4, HT-29, KB-3-1, Capan-1, 4-1St and HCT-15 cells
Concentrations	~ 10 μM
Incubation Time	3 days
Method	Cancer cells (5 × 10³) are seeded into each well of 96-well plates and cultured with graded concentrations of MS-275 for 3 days. The cells are stained with 0.1 mg/mL neutral red for 1 hour in a CO₂-incubator, and, after aspiration of the medium, OD540 of the neutral red solubilized with 50 μL of ethanol and 150 μL of 0.1 M Na₂HPO₄ is measured. The IC50 value is determined by plotting growth inhibition of the cells against the logarithm of the drug concentration.

Animal Study:
^[1]

Animal Models	A2780, HT-29, HTC-15, KB-3-1, 4-1St, St-4, Capan-1 and Calu-3 cells are injected subcutaneously into the flank of nude mice.
Formulation	Dissolved with 0.05 N HCl, 0.1% Tween 80
Dosages	12.3, 24.5 and 49 mg/kg
Administration	Administered orally once daily 5 days per week for 4 weeks

References

Chemical Information

Download Entinostat (MS-275, SNDX-275) SDF

Molecular Weight (MW)	376.41
Formula	C₂₁H₂₀N₄O₃
CAS No.	209783-80-2
Synonyms	SNDX-275

Solubility (25°C) DMSO 75 mg/mL Water <1 mg/mL Ethanol <1 mg/mL
Storage	2 years -20°CPowder
	2 weeks4°Cin DMSO
	6 months-80°Cin DMSO

Chemical Name	pyridin-3-ylmethyl 4-((2-aminophenyl)carbamoyl)benzylcarbamate

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Research Area

Customer Reviews (9)

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Rating

Source

Biochemical and Biophysical Research Communications, 414 (2011) 25–30. Entinostat (MS-275, SNDX-275) purchased from Selleck

Method

qRT-PCR

Cell Lines

HEK-293cells

Concentrations

0.37-10uM

Incubation Time

Results

Analysis of mRNA changes following MS-275 treatment revealed a different profile than what was observed with the paninhibitors. Class I specific HDAC inhibition increased both total and exon 7 included mRNA. However, the fold increases of the total transcript exceeded that of exon 7 included.

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Rating

Source

J Am Heart Assoc, 2012, 1(3), e000901.. Entinostat (MS-275, SNDX-275) purchased from Selleck

Method

Western blot

Cell Lines

human aortic SMCs

Concentrations

Incubation Time

Results

Both TSA and MS-275 significantly suppressed the induction of S MC proteins by Notch activation.

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Rating

Source

Mol Pain , 2010, 6, 51. Entinostat (MS-275, SNDX-275) purchased from Selleck

Method

Immunoblot, Immunofluorescent histochemistry

Cell Lines

lumbar spinal cord

Concentrations

0.5 μg

Incubation Time

30 min

Results

As shown in Fig. A and B, the relative H3K9 acsignals in animals injected either with SAHA or with MS-275 were largely enhanced in comparison to that in animals receiving i.t. saline. Using an antibody specific to acety-lated H3 lysine 9/18 (H3K9/18ac) for immunohisto-chemistry, we further observed that 30 min after the injection, the signals of H3K9 /18ac robustly increased in the lumbar spinal cord (Fi g. C)

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Rating

Source

Breast Cancer Res Treat , 2010, 131(3), 777-789. Entinostat (MS-275, SNDX-275) purchased from Selleck

Method

Western blot

Cell Lines

MDA-MB-231 cells, MDA-MB-468 cells

Concentrations

0.5-10 μM

Incubation Time

24 h

Results

In both MDA-MB-231 and MDA-MB-468 cell lines, exposure to MS-275 and other compounds produced significant global increase of nuclear H3K4me2,which is the specific substrate of LSD1.The enhanced level of histone methylation by HDAC inhibitors parallels the increase of acetylation of histone 3

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Rating

Source

Dr. Zhang of Tianjin Medical University. Entinostat (MS-275, SNDX-275) purchased from Selleck

Method

Western blot

Cell Lines

MDA-MB-231 cells

Concentrations

0-20 μM

Incubation Time

Results

Western blot analysis of Acetyl-H3 and H3. 0-20μM MS-275 was added.

Click to enlarge

Rating

Source

Breast Cancer Res Treat , 2010, 131(3), 777-789. Entinostat (MS-275, SNDX-275) purchased from Selleck

Method

MTT growth inhibition and drug combination index (CI) analysis

Cell Lines

MDA-MB-231 cells

Concentrations

Incubation Time

48 h

Results

At very low dose combination (fractional growth inhibition,Fa=0.9), synergistic growth inhibition (CI<1) was observed between pargyline and HDAC inhibitors SAHA,TSA,MS-275, and LBH-589.At median or higher dose combination (Fa = 0.5 or 0.75), pargyline exhibited synergy with all the HDAC inhibitors tested (CI<1)

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Inhibition of HDAC1-mediated DNMT1 deacetylation promotes DNMT1 proteasomal degradation. (A) Knockout of HAUSP potentiates HDAC inhibitor (HDACi)-induced DNMT1 degradation. Parental or HAUSP KO DLD1 cells were treated or not with 5 μM HDACi MS-275 for 72 hours and cell lysates were blotted with the indicated antibodies. (B) HDAC inhibition induces DNMT1 ubiquitination. HAUSP WT or KO cells were treated with or without HDACi for 24 hours and MG132 for 12 hours before being harvested to make cell lysates. DNMT1 immunoprecipitates were blotted with an antibody against ubiquitin. Because the abundance of DNMT1 in the HAUSP KO cells is lower than in WT cells, more KO cells were used than WT cells to obtain equal amounts of precipitated DNMT1 proteins. (C) DNMT1 is acetylated after HDACi treatment. DNMT1 immunoprecipitates from cells treated with HDACi were blotted with an antibody against acetylated lysine (Ac-K). (D) A DNMT1 acetylation site mutant is resistant to HDACi-induced degradation. HEK 293 cells were transfected with WT DNMT1 or a DNMT1 mutant lacking four known acetylation sites (K173R, K1113R, K115R, and K117R) and treated with MS-275 for 48 hours and with CHX for 24 hours. Cell lysates were blotted with the indicated antibodies. (E) Knockdown of HDAC1 decreases the abundance of DNMT1. RKO cells were treated with the indicated concentration of doxycycline (Dox) for 48 hours to induce expression of an shRNA directed against HDAC1. Western blots were performed with the indicated antibodies. (F) Knockdown of HDAC1 leads to increased acetylation of DNMT1. RKO cells expressing an inducible HDAC1 shRNA were treated with or without Dox (4 mg/ml) for 36 hours and then with MG132 for 12 hours. DNMT1 immunoprecipitates were blotted with an antibody against Ac-K. Cell lysates were also blotted with antibodies against HDAC1 and b-actin.

Rating

Source

Sci Signal, 2010, 3, ra80. Entinostat (MS-275, SNDX-275) purchased from Selleck

Method

Western blot

Cell Lines

HAUSP WT cells, HAUSP KO cells, HEK 293 cells, RKO cells

Concentrations

5 μM

Incubation Time

24/48/72 h

Results

The HDAC inhibitor MS-275 directly destabilizes DNMT1 by enhancing its ubiquitination (Fig. A and B).We then showed that acetylation of DNMT1 plays a direct role in this process. HDAC Inhibitor MS-275 increased DNMT1 acetylation (Fig.C). The functional importance of DNMT1 acetylation was then demonstrated by showing that inhibition of HDAC activity failed to induce degradation of a DNMT1 mutant in which the four previously identified acetylated lysines were altered to arginines (Fig. D). inducible knockdown of HDAC1 in RKO colorectal cancer cells led to reduced DNMT1 abundance, consistent with a similar observation made in a breast cancer cell line (Fig. E). Knockdown of HDAC1 led to increased DNMT1 acetylation (Fig. 2F). These data suggest that HDAC1 deacetylates DNMT1, thus protecting it from proteasomal degradation.

Click to enlarge

Rating

Source

Sci Signal , 2010, 3, ra80. Entinostat (MS-275, SNDX-275) purchased from Selleck

Method

Western blot

Cell Lines

HEK 293 cells

Concentrations

5 μM

Incubation Time

24 h

Results

HDAC inhibitor MS-275 increased the interaction between endogenous and transfected DNMT1 and UHRF1 (Fig. A to C). Furthermore, overexpression of UHRF1 led to increased ubiquitination of DNMT1 (Fig. D). UHRF1-mediated ubiquitination was required for HDAC inhibitor(MS-275)-induced degradation of DNMT1. In addition, knockdown of UHRF1 by three different siRNAs blocked HDAC inhibitor-induced degradation of DNMT1 (Fig. E). Conversely, overexpression of UHRF1 reduced the abundance of a DNMT1 mutant lacking the HAUSP interaction domain (DNMT1 D ) (Fig. F).

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Rating

Source

Sci Signal , 2010, 3, ra80. Entinostat (MS-275, SNDX-275) purchased from Selleck

Method

Flow cytometric analyses, Western blot, MANOVA analyses, Tumor Volume Measurements

Cell Lines

HAUSPKO cells

Concentrations

5/10 μM

Incubation Time

72 h

Results

We treated wild-type and HAUSP knockout cells with HDAC inhibitor MS-275, which induced 5 to 10 times as many apoptotic cells in HAUSP knockout cells relative to wild-type cells (Fig. A). Furthermore, HDAC inhibition increased the number of apoptotic cells (sub-G 1 cells) (Fig. B) and increased the abundance of apoptotic cell markers including cleaved caspases 3, 6, and 9, and poly(adenosine diphosphate-ribose) polymerase (PARP) (Fig. C). Furthermore, degradation of DNMT1 was the major cause of cell death, because ectopic overexpression of DNMT1 in the HAUSP knockout cells partially rescued HDAC inhibitor-induced apoptosis (Fig. D). Moreover, HAUSP knockout cells were more sensitive to growth arrest caused by MS-275 (Fig. E)when grown in cell culture.

Product Citations (18)

Chemoproteomics profiling of HDAC inhibitors reveals selective targeting of HDAC complexes. [Bantscheff M, et al. Nat Biotechnol 2011;29(3), 255-265]
PubMed: 21258344
Role of checkpoint kinase 1 (Chk1) in the mechanisms of resistance to histone deacetylase inhibitors. [Lee JH, et al. Proc Natl Acad Sci U S A 2011;108(49):19629-34]
PubMed: 22106282
Selective class I histone deacetylase inhibition suppresses hypoxia-induced cardiopulmonary remodeling through an antiproliferative mechanism. [Cavasin MA, et al. Circ Res 2012;110(5):739-48]
PubMed: 22282194

Schizophrenia is associated with dysregulation of a Cdk5 activator that regulates synaptic protein expression and cognition. [Engmann O, et al. Brain 2011;134(Pt 8):2408-21]
PubMed: 21772061
Histone deacetylase inhibitors preserve white matter structure and function during ischemia by conserving ATP and reducing excitotoxicity. [Baltan S, et al. J Neurosci 2011;31(11):3990-9]
PubMed: 21411642
DNMT1 stability is regulated by proteins coordinating deubiquitination and acetylation-driven ubiquitination. [Du Z, et al. Sci Signal 2010;3(146), ra80]
PubMed: 21045206
IL-10 Regulates Il12b Expression via Histone Deacetylation: Implications for Intestinal Macrophage Homeostasis. [Kobayashi T, et al. J Immunol 2012;189(4):1792-9]
PubMed: 22786766
RSK2Ser227 at N-terminal kinase domain is a potential therapeutic target for multiple myeloma. [Shimura Y, et al. Mol Cancer Ther 2012;11(12):2600-9]
PubMed: 23012246
Inhibitors of histone demethylation and histone deacetylation cooperate in regulating gene expression and inhibiting growth in human breast cancer cells. [Huang Y, et al. Breast Cancer Res Treat 2012;131(3), 777-789]
PubMed: 21452019
Histone Deacetylase Inhibitors (HDACis) That Release the Positive Transcription Elongation Factor b (P-TEFb) from Its Inhibitory Complex Also Activate HIV Transcription. [Bartholomeeusen K, et al. J Biol Chem 2013;288(20), 14400-14407]
PubMed: 23539624
Histone deacetylase inhibitors downregulate checkpoint kinase 1 expression to induce cell death in non-small cell lung cancer cells. [Brazelle W, et al. PLoS One 2010;5(12), e14335]
PubMed: 21179472
Enhancement of vaccinia virus based oncolysis with histone deacetylase inhibitors. [MacTavish H, et al. PLoS One 2010;5(12), e14462]
PubMed: 21283510
Inhibition of class II histone deacetylases in the spinal cord attenuates inflammatory hyperalgesia. [Bai G, et al. Mol Pain 2010;6, 51]
PubMed: 20822541
Histone deacetylase inhibitors preserve function in aging axons. [Baltan S, et al. J Neurochem 2012;123 Suppl 2:108-15]
PubMed: 23050648
Epithelial to mesenchymal transition in an epidermal growth factor receptor-mutant lung cancer cell line with acquired resistance to erlotinib. [Suda K, et al. J Thorac Oncol 2011;6(7):1152-61]
PubMed: 21597390
Sca-1 is an early-response target of histone deacetylase inhibitors and marks hematopoietic cells with enhanced function. [Walasek MA, et al. Exp Hematol 2013;41(1):113-23.e2]
PubMed: 22989761
Differential regulation of theSMN2 gene by individual HDAC proteins. [Evans MC, et al. Biochem Biophys Res Commun 2011;414(1):25-30]
PubMed: 21925145
Histone Deacetylase Activity Selectively Regulates Notch-Mediated Smooth Muscle Differentiation in Human Vascular Cells. [Tang Y, et al. J Am Heart Assoc 2012;1(3):e000901]
PubMed: 23130137

Tech Support & FAQs

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Entinostat (MS-275, SNDX-275)