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Entinostat

产品编号 T6233 CAS 209783-80-2

别名: 恩替诺特, SNDX-275, MS-275

Entinostat (MS-275) 是一种可口服的 HDAC class I 选择性抑制剂，抑制HDAC1、HDAC2和HDAC3的IC50分别为 243 nM、453 nM 和 248 nM。

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Entinostat, CAS 209783-80-2

规格	价格/CNY	货期
10 mg	￥ 379	现货
50 mg	￥ 828	现货
100 mg	￥ 1,255	现货
200 mg	￥ 2,263	现货
1 mL * 10 mM (in DMSO)	￥ 268	现货

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选择批次

纯度: 99.52%

纯度: 99.11%

纯度: 98%

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生物活性

化学信息

存储 & 溶解度

参考文献

相关产品

产品描述	Entinostat (MS-275) (MS-275) is an inhibitor of HDACs that inhibits HDAC1 and HDAC3 (IC50s: 0.18/0.74 μM).
靶点活性	HDAC1:0.18 μM(cell free), HDAC3:0.74 μM(cell free)
体外活性	MS275 is partial inhibitors of HeLa nuclear extract HDAC activity, however, showing full and potent inhibition of HDAC1 and 3 isoenzymes. MS275 display a substrate competitive inhibition of HDAC1 (Ki: 1.3 μM) [1]. MS-275 inhibited partially purified human HDA and caused hyperacetylation of nuclear histones in various tumor cell lines. MS-27-275 induced p21(WAF1/CIP1) and gelsolin and changed the cell cycle distribution, decrease of S-phase cells, and increase of G1-phase cells. The in vitro sensitivity spectrum of MS-27-275 against various human tumor cell lines showed a pattern different than that of a commonly used antitumor agent, 5-fluorouracil [2]. MS-275 displayed dose-dependent effects in human leukemia and lymphoma cells and primary acute myelogenous leukemia blasts in relation to differentiation and apoptosis. When administered at a low concentration (e.g., 1 micro M), MS-275 exhibited potent antiproliferative activity, inducing p21(CIP1/WAF1)-mediated growth arrest and expression of differentiation markers (CD11b) in U937 cells [3].
体内活性	MS-27-275 administered orally strongly inhibited the growth in seven of eight tumor lines implanted into nude mice, although most of these did not respond to 5-fluorouracil [2]. MS-275 administration (3.5 mg/kg i.p.) to Experimental autoimmune neuritis (EAN) rats once daily from the appearance of first neurological signs greatly reduced the severity and duration of EAN and attenuated local accumulation of macrophages, T cells and B cells, and demyelination of sciatic nerves [4].
激酶实验	The HDAC enzyme activity assay was done as described. Briefly, 40 μl HeLa cell nuclear extract, 29 μl enzyme buffer [15 mM Tris HCl pH 8.1, 0.25 mM EDTA, 250 mM NaCl, 10% (v/v) glycerol]; for recombinant HDAC isoenzymes, 0.1 mg/ml bovine serum albumin (BSA was added) and 1 μl compound were added per well of a microtiter plate. The reaction was started by addition of 30 μl substrate (Ac-NH-GGK(Ac)-AMC final 25 μM). After incubation for 90 min at 30°C, reaction was terminated by adding 25 μl stop solution (50 mM Tris HCl pH 8, 100 mM NaCl, 0.5 mg/ml trypsin, 2 μM TSA). After 40 min incubation at room temperature, fluorescence was measured using a Wallac Victor 1420 multilabel counter (Excitation 355 nm, Emission 460 nm). The HDAC1, 3, 6 and 8 assays were done with slight modifications. About 14 ng/well HDAC1, 2 ng/well HDAC3 or 10 ng/well HDAC6 were incubated with 6, 25 or 10 lM Ac-NH-GGK(Ac)-AMC, respectively, for 2 or 3 hr at 30°C. In contrast, 100 ng/well HDAC8 were incubated with 50 μM Ac-NH-RHK(Ac)K(Ac)-AMC for 3 hr at 30°C. Termination of the reaction and all further steps were done as described earlier for HeLa cell nuclear extracts. For the enzyme kinetic studies with HDAC1, selected HDAC inhibitor (around IC50 value), as well as Ac-NH-GGK(Ac)-AMC substrate (up to 100 μM) concentrations, were evaluated under standard conditions as described earlier [1].
细胞实验	Cancer cells (5 × 10^3) were seeded into each well of 96-well plates and were cultured with graded concentrations of the drugs for 3 days. The cells were stained with 0.1 mg/ml neutral red for 1 h 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 was measured. The IC50 value was determined by plotting growth inhibition of the cells against the logarithm of the drug concentration [2].
动物实验	A2780 cells (9 × 10^6) grown in vitro were suspended in PBS and were injected subcutaneously into the flank of nude mouse. For the other tumor lines, KB-3-1, HCT-15, 4-1St, Calu-3, St-4, Capan-1, and HT-29, tumors were passaged several times before starting in vivo antitumor testing, and a tumor lump (2–3 mm in diameter) was transplanted subcutaneously into the flank of a nude mouse by using a trocar needle. Treatment (four or five mice in each experimental group) with the drugs was started after the tumors were confirmed to have grown in the body (tumor size, 20–100 mm3). MS-27-275 and compound 2, both dissolved with 0.05 N HCl, 0.1% Tween 80, and 5-fluorouracil (5-FU) and diluted with physiological saline, were administered orally once daily 5 days per week for 4 weeks. Tumor length and width were monitored twice weekly, and tumor volume was calculated as described [2].

别名	恩替诺特, SNDX-275, MS-275
分子量	376.41
分子式	C21H20N4O3
CAS No.	209783-80-2

存储

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度

DMSO: 37.6 mg/mL (100 mM)

溶液配制表

可选溶剂	浓度体积质量	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.6567 mL	13.2834 mL	26.5668 mL	66.4169 mL
	5 mM	0.5313 mL	2.6567 mL	5.3134 mL	13.2834 mL
	10 mM	0.2657 mL	1.3283 mL	2.6567 mL	6.6417 mL
	20 mM	0.1328 mL	0.6642 mL	1.3283 mL	3.3208 mL
	50 mM	0.0531 mL	0.2657 mL	0.5313 mL	1.3283 mL
	100 mM	0.0266 mL	0.1328 mL	0.2657 mL	0.6642 mL

计算器

摩尔浓度计算器

稀释计算器

配液计算器

分子量计算器

质量

浓度

容积

分子量

浓度 (起始)

容积 (起始)

浓度 (终)

容积 (终)

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配液浓度

参考文献

1. Beckers T, et al. Distinct pharmacological properties of second generation HDAC inhibitors with the benzamide or hydroxamate head group. Int J Cancer. 2007 Sep 1;121(5):1138-48. 2. Saito A, et al. A synthetic inhibitor of histone deacetylase, MS-27-275, with marked in vivo antitumor activity against human tumors. Proc Natl Acad Sci U S A, 1999, 96(8), 4592-4597. 3. Rosato RR, et al. The histone deacetylase inhibitor MS-275 promotes differentiation or apoptosis in human leukemia cells through a process regulated by generation of reactive oxygen species and induction of p21CIP1/WAF1 1. Cancer Res. 2003 Jul 1;63(13):3637-45. 4. Zhang ZY, et al. MS-275, an histone deacetylase inhibitor, reduces the inflammatory reaction in rat experimental autoimmune neuritis. Neuroscience. 2010 Aug 11;169(1):370-7. 5. Moreno-Yruela C, Zhang D, Wei W, et al. Class I Histone Deacetylases (HDAC1‒3) are Histone Lysine Delactylases[J]. bioRxiv. 2021 6. Wellinger L C, Hogg S J, Newman D M, et al. BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity[J]. bioRxiv. 2021 7. Lagosz K B, Bysiek A, Macina J M, et al. HDAC3 Regulates Gingival Fibroblast Inflammatory Responses in Periodontitis[J]. Journal of dental research. 2019: 0022034519885088.

文献引用

1. Moreno-Yruela C, Zhang D, Wei W, et al. Class I Histone Deacetylases (HDAC1‒3) are Histone Lysine Delactylases. Science advances. 2022, 8(3): eabi6696. 2. Wellinger L C, Hogg S J, Newman D M, et al. BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity. Cancer Immunology Research. 2022, 10(1): 87-107. 3. Wellinger L C, Hogg S J, Newman D M, et al. Bet inhibition enhances TNF-mediated antitumor immunity. Cancer Immunology Research. 2022, 10(1): 87-107 4. Zierfuss B, Weinhofer I, Buda A, et al. Targeting foam cell formation in inflammatory brain diseases by the histone modifier MS‐275. Annals of Clinical and Translational Neurology. 2020, 7(11): 2161-2177 5. Zhang L, Shi J, Du D, et al. Ketogenesis acts as an endogenous protective programme to restrain inflammatory macrophage activation during acute pancreatitis. eBioMedicine. 2022, 78: 103959. 6. Jiang X C, Tu F H, Wei L Y, et al. Discovery of a Novel G-Quadruplex and Histone Deacetylase (HDAC) Dual-Targeting Agent for the Treatment of Triple-Negative Breast Cancer. Journal of Medicinal Chemistry. 2022 7. Lagosz K B, Bysiek A, Macina J M, et al. HDAC3 Regulates Gingival Fibroblast Inflammatory Responses in Periodontitis. Journal of Dental Research. 2019: 0022034519885088 8. Wang C, Huang M, Lin Y, et al.ENO2-derived phosphoenolpyruvate functions as an endogenous inhibitor of HDAC1 and confers resistance to antiangiogenic therapy.Nature Metabolism.2023: 1-22. 9. Villoria-González A, Zierfuss B, Parzer P, et al.Efficacy of HDAC Inhibitors in Driving Peroxisomal β-Oxidation and Immune Responses in Human Macrophages: Implications for Neuroinflammatory Disorders.Biomolecules.2023, 13(12): 1696.

剂量换算

对于不同动物的给药剂量换算，您也可以参考 更多...

体内实验配液计算器

请在以下方框中输入您的动物实验信息后点击计算，可以得到母液配置方法和体内配方的制备方法：比如您的给药剂量是10 mg/kg，每只动物体重20 g，给药体积100 μL，一共给药动物10 只，您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。

母液配置方法：2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 50 μL DMSO 主液，加入 300 μL PEG300，混匀澄清，再加 50 μL Tween 80，混匀澄清，再加 600 μL ddH2O, 混匀澄清。

第一步：请输入动物实验的基本信息

剂量

mg/kg

每只动物体重

给药体积

μL

动物数量

第二步：请输入动物体内配方组成，不同的产品配方组成不同，如有配方需求，可先联系我们提供正确的体内配方。

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

计算重置

计算结果如下:

工作液浓度: mg/ml;

母液配置方法: mg 药物溶于 μL DMSO (母液浓度为 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 μL DMSO 主液，加入 μL PEG300，混匀澄清，再加 μL Tween 80，混匀澄清，再加 μL ddH₂O, 混匀澄清。

备注:

要按顺序从左向右依次添加助溶剂。可配合物理方法，如涡流、超声波或热水浴使之帮助溶解。

技术支持

您可能有的问题的答案可以在抑制剂处理说明中找到，包括如何准备库存溶液，如何存储产品，以及基于细胞的分析和动物实验需要特别注意的问题。

Keywords

Entinostat 209783-80-2 Apoptosis Autophagy Chromatin/Epigenetic DNA Damage/DNA Repair HDAC MS275 恩替诺特 SNDX 275 Inhibitor inhibit SNDX275 SNDX-275 MS-275 MS 275 Histone deacetylases inhibitor

我们的所有产品和服务仅用于科学研究，不能被用于人体，我们也不向个人提供产品和服务。

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Entinostat

存储

溶解度

溶液配制表

计算器

输入分子式，点击计算，可计算出产品的分子量。

参考文献

文献引用

相关产品

相关化合物库

剂量换算

体内实验配液计算器

技术支持

Keywords