Entinostat (MS-275)

Cat. No. M1791

Synonym:

SNDX-275, MS-27-275

Size	Price	Availability
Free Sample (0.5-1 mg)	USD 0	In stock
10mM*1mL in DMSO	USD 40 USD40	In stock
10mg	USD 40 USD40	In stock
50mg	USD 90 USD90	In stock
100mg	USD 130 USD130	In stock
200mg	USD 210 USD210	In stock

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Quality Control & Documentation

Purity: 99.36%
COA
MSDS
H-NMR
HPLC

Product Information

Biological Activity

Entinostat (MS-275) is an oral and selective class I HDAC inhibitor, with IC50s of 243 nM, 453 nM, and 248 nM for HDAC1, HDAC2, and HDAC3, respectively. Entinostat inhibited in vitro cell growth in all cell lines tested with an IC50 ranging from 50 nM to 1.3 uM. MS-275 showed antiproliferative activity against all human breast cancer cell lines examined and induced TbRII mRNA, but not TGF-b type I receptor mRNA. MS-275 caused an accumulation of acetylated histones H3 and H4 in total cellular chromatin. An increase in the accumulation of acetylated histones H3 and H4 was detected in the TbRII promoter after treatment with MS-275.

Entinostat (MS-275) at 49 mg/kg shows marked antitumor effects against KB-3-1, 4-1St, and St-4 tumor lines, and a moderate effect against Capan-1 tumor. Entinostat at 24.5 mg/kg and 12.3 mg/kg also shows significant effects against these tumors. In addition, oral administration of Entinostat apparently increases the level of histone acetylation in HT-29 tumor xenografts 4-24 h after the administration.

Product Citations

Front Neurosci. 2021 Apr 28;15:641284.

Valproic Acid Induces Autism-Like Synaptic and Behavioral Deficits by Disrupting Histone Acetylation of Prefrontal Cortex ALDH1A1 in Rats
Entinostat (MS-275) purchased from AbMole

Customer Product Validations & Biological Datas

	Source	Int J Clin Exp Pathol (2015). Figure 2. MS-275
	Method	i.v.
	Cell Lines	Sprague-Dawley rats
	Concentrations	12.3, 24.5, 49.0 mg/kg
	Incubation Time	7 days
	Results	There was no hepatocytic macrovesicular steatosis, lobular inflammatory cell infiltration and necrosis in both control group and MS-275 group

Protocol (for reference only)

Cell Experiment
Cell lines	HDACi-treated Y79, Weri-Rb1, and Y79-LUC human RB cell lines
Preparation method	Cell survival assays. For colorimetric analysis, cells were exposed to WST-8 Cell Proliferation Reagent (Dojindo), and absorbance was quantified after 2 h using a SpectraMax microplate reader (Molecular Devices). For bioluminescence analysis (Y79-LUC cells only), cells were exposed to 150 μg/mL D-luciferin, and plates were imaged in an IVIS Imaging System (Xenogen) using a 15-s exposure. Luminescence was quantified using Living Image software (Xenogen). For both assays, cell survival was expressed as a percentage of vehicle-treated control values.
Concentrations	0~100 μM
Incubation time	24, 48, or 72 h

Animal Experiment
Animal models	LHβ-Tag mice model
Formulation	DMSO
Dosages	every other day for 21 d with 20 mg/kg MS-275
Administration	i.p.

Chemical Information

Molecular Weight	376.4
Formula	C21H20N4O3
CAS Number	209783-80-2
Solubility (25°C)	DMSO 40 mg/mL
Storage	-20°C, sealed

Conversion of different model animals based on BSA (PMID: 27057123)

Species	Mouse	Rat	Rabbit	Guinea pig	Hamster	Dog
Weight (kg)	0.02	0.15	1.8	0.4	0.08	10
Body Surface Area (m²)	0.007	0.025	0.15	0.05	0.02	0.5
K_m factor	3	6	12	8	5	20

Animal A (mg/kg) = Animal B (mg/kg) multiplied by	Animal B K_m
	Animal A K_m

For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the K_m factor for a mouse and then divide by the K_m factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.

References

[1] Saito T, et al. Osteoarthritis Cartilage. Histone deacetylase inhibitors suppress mechanical stress-induced expression of RUNX-2 and ADAMTS-5 through the inhibition of the MAPK signaling pathway in cultured human chondrocytes.

[2] Rao-Bindal K, et al. Cell Death Dis. MS-275 sensitizes osteosarcoma cells to Fas ligand-induced cell death by increasing the localization of Fas in membrane lipid rafts.

[3] Kim HN, et al. Eur J Pharmacol. MS-275, a benzamide histone deacetylase inhibitor, prevents osteoclastogenesis by down-regulating c-Fos expression and suppresses bone loss in mice.

[4] Zhan Y, et al. Free Radic Biol Med. P38 MAP kinase functions as a switch in MS-275-induced reactive oxygen species-dependent autophagy and apoptosis in human colon cancer cells.

[5] Z Y Zhang, et al. Neuroscience. MS-275, an Histone Deacetylase Inhibitor, Reduces the Inflammatory Reaction in Rat Experimental Autoimmune Neuritis

[6] Dalgard CL, et al. Clin Cancer Res. Evaluation of the in vitro and in vivo antitumor activity of histone deacetylase inhibitors for the therapy of retinoblastoma.

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