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Selisistat

Selisistat

产品编号 T6111   CAS 49843-98-3
别名: EX-527, 司来司他, SEN0014196

Selisistat (EX-527) 是一种有效且特异性的 SIRT1 抑制剂,IC50值为 38 nM,可用于研究多种亨廷顿病动物和细胞模型的病理学。

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Selisistat Chemical Structure
Selisistat, CAS 49843-98-3
规格 价格/CNY 货期 数量
1 mg ¥ 179 现货
5 mg ¥ 397 现货
10 mg ¥ 528 现货
25 mg ¥ 913 现货
50 mg ¥ 1,330 现货
100 mg ¥ 1,730 现货
200 mg ¥ 2,460 现货
500 mg ¥ 3,550 现货
1 mL * 10 mM (in DMSO) ¥ 437 现货
其他形式的 Selisistat:
产品目录号及名称: Selisistat (T6111)
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纯度: 99.79%
纯度: 99.67%
纯度: 99.66%
纯度: 99.54%
纯度: 99%
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生物活性
化学信息
存储 & 溶解度
参考文献
产品描述 Selisistat (EX-527) is an effective and specific SIRT1 inhibitor (IC50: 38 nM) and shows >200-fold selectivity against SIRT2/3.
靶点活性 SIRT1:38 nM(cell free)
体外活性 Treatment with Selisistat (EX-527) dramatically increased acetylation at lysine 382 of p53 after different types of DNA damage in primary human mammary epithelial cells and several cell lines. Inhibition of SIRT1 catalytic activity by EX-527 had no effect on cell growth, viability, or p53-controlled gene expression in cells treated with etoposide [1]. When the function of SIRT1 is inhibited by EX527 or its expression is suppressed by RNAi, the upregulated level and release of IL-1β and TNF-α by high glucose are further increased [2]. When HCT116 cells were cultured in 0.1% serum, addition of EX-527 caused a 90% increase in cell number after 7 days. In the presence of 10% serum, EX-527 did not change cell number in long term culture [3].
体内活性 The central pretreatment with Ex527 blunted the ghrelin-induced food intake in rats. Mice lacking p53, a target of SIRT1 action, failed to respond to ghrelin in feeding behavior. Ghrelin failed to phosphorylate hypothalamic AMPK when rats were pretreated with Ex527, as it did in p53 KO mice [4]. EX-527 abolished RSV-induced attenuation of microvascular inflammation in ob/ob septic mice [5].
细胞实验 NCI-H460 cells, MCF-7 cells, U-2 OS cells, or HMEC were plated at 2,000 cells per well in opaque-walled 96-well plates for the viability assay and 800 cells per well in 96-well Cytostar-T scintillating microplates for the proliferation assay. Cells were incubated for 1 day (NCI-H460) or 2 days (MCF-7, U-2 OS, and HMEC) prior to exposure to DNA-damaging agents and deacetylase inhibitors. All experiments were performed in triplicate. For viability assays, cells were treated with the indicated compounds for 48 h. Cell viability was then determined using the Cell Titer-Glo luminescent assay, which measures total ATP levels as an index of cell number. Luminescence was measured on a Luminoskan Ascent. For the proliferation assay, 0.5 μCi/ml of [14C]thymidine was added to the medium immediately after the genotoxins and deacetylase inhibitors. Plates were counted at 48 h (HMEC) or 72 h (NCI-H460, MCF-7, and U-2 OS cells) in a Microbeta liquid scintillation counter. Thymidine incorporated by the cells was detected by proximity to the scintillant in the base of the Cytostar-T tissue culture plate [1].
动物实验 Mice were injected with RSV (RSV) 30mg/kg (4ml/kg) or equivalent volume of DMSO (Vehicle) (4ml/kg) intraperitoneally 18 hours pre-sepsis. This dose of RSV in mice was as per documented literature. In one group of mice, RSV pre-treated mice received EX-527 (10 mg/kg intraperitoneally; 4ml/kg, Vehicle: DMSO) within 10 minutes of cecal ligation and puncture [5].
别名 EX-527, 司来司他, SEN0014196
分子量 248.71
分子式 C13H13ClN2O
CAS No. 49843-98-3

存储

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

溶解度

DMSO: 18.7 mg/mL (75 mM)

Ethanol: 12.4 mg/mL (50 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 / Ethanol 1 mM 4.0207 mL 20.1037 mL 40.2075 mL 100.5187 mL
5 mM 0.8041 mL 4.0207 mL 8.0415 mL 20.1037 mL
10 mM 0.4021 mL 2.0104 mL 4.0207 mL 10.0519 mL
20 mM 0.201 mL 1.0052 mL 2.0104 mL 5.0259 mL
50 mM 0.0804 mL 0.4021 mL 0.8041 mL 2.0104 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
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输入分子式,点击计算,可计算出产品的分子量。

参考文献

1. Solomon JM, et al. Inhibition of SIRT1 catalytic activity increases p53 acetylation but does not alter cell survival following DNA damage. Mol Cell Biol. 2006 Jan;26(1):28-38. 2. Jia Y, et al. SIRT1 is a regulator in high glucose-induced inflammatory response in RAW264.7 cells. PLoS One. 2015 Mar 20;10(3):e0120849. 3. Kabra N, et al. SirT1 is an inhibitor of proliferation and tumor formation in colon cancer. J Biol Chem. 2009 Jul 3;284(27):18210-7. 4. Velásquez DA, et al. The central Sirtuin 1/p53 pathway is essential for the orexigenic action of ghrelin. Diabetes. 2011 Apr;60(4):1177-85. 5. Wang X, et al. Resveratrol attenuates microvascular inflammation in sepsis via SIRT-1-Induced modulation of adhesion molecules in ob/ob mice. Obesity (Silver Spring). 2015 Jun;23(6):1209-17. 6. Luo Y, Lu S, Gao Y, et al. Araloside C attenuates atherosclerosis by modulating macrophage polarization via Sirt1-mediated autophagy[J]. Aging (Albany NY). 2020, 12(2): 1704. 7. Chen W, Lin B, Xie S, et al. Naringenin protects RPE cells from NaIO3-induced oxidative damage in vivo and in vitro through up-regulation of SIRT1[J]. Phytomedicine. 2020: 153375.

文献引用

1. Yuan J, Wei Z, Xin G, et al. Vitamin B12 Attenuates Acute Pancreatitis by Suppressing Oxidative Stress and Improving Mitochondria Dysfunction via CBS/SIRT1 Pathway. Oxidative Medicine and Cellular Longevity. 2021, 2021. 2. Lu S, Zhou J, Yang C, et al. γ-glutamylcysteine ameliorates D-gal-induced senescence in PC12 cells and mice via activating AMPK and SIRT1. Food & Function. 2022 3. Luo Y, Lu S, Gao Y, et al. Araloside C attenuates atherosclerosis by modulating macrophage polarization via Sirt1-mediated autophagy. Aging (Albany NY). 2020, 12(2): 1704. 4. Luo Y, Lu S, Gao Y, et al. Araloside C attenuates atherosclerosis by modulating macrophage polarization via Sirt1-mediated autophagy. Aging (Albany NY). 2020, 12(2): 1704. 5. Chen W, Lin B, Xie S, et al. Naringenin protects RPE cells from NaIO3-induced oxidative damage in vivo and in vitro through up-regulation of SIRT1. Phytomedicine. 2020: 153375 6. Zhou J, Yan X, Bi X, et al.γ-Glutamylcysteine rescues mice from TNBS-driven inflammatory bowel disease through regulating macrophages polarization.Inflammation Research.2023: 1-19. 7. Cao P, Wang Y, Zhang C, et al.Quercetin ameliorates non-alcoholic fatty liver disease (NAFLD) via the promotion of AMPK-mediated hepatic mitophagy.The Journal of Nutritional Biochemistry.2023: 109414. 8. Peng X, Yuan H, Chen G, et al.Investigation on the effect of ulinastatin on the apoptosis of vascular smooth muscle cells in rats with aortic dissection based on the Sirt1/FoxO3a pathway.Cellular and Molecular Biology.2023, 69(13): 96-101.
CAY10602 Sirt2-IN-1 SIRT5 inhibitor 8 SRT 2183 Splitomicin OSS_128167 SIRT5 inhibitor 9 MDL-800

相关化合物库

该产品包含在如下化合物库中:
抗癌临床化合物库 抗癌药物库 高选择性抑制剂库 神经退行性疾病化合物库 抑制剂库 已知活性化合物库 细胞重编程化合物库 染色质修饰分子库 抗衰老化合物库 ReFRAME 相关化合物库

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
g
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
计算 重置

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

Selisistat 49843-98-3 Chromatin/Epigenetic DNA Damage/DNA Repair Sirtuin mammalian Huntington's inhibit pathology EX-527 Drosophila 司来司他 deacetylation SEN-0014196 EX 527 SEN0014196 Inhibitor SEN 0014196 disease EX527 inhibitor

 

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