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Trichostatin A

CAS号

58880-19-6

分子式

C17H22N2O3

主要靶点

HDAC

仅限科研使用

Cat No : CM00558

Print datasheet

Synonyms

inhibit|HDAC|Histone deacetylases|曲古柳菌素A|曲古抑菌素A|Trichostatin A|TSA|Inhibitor

验证数据展示

  • CAS No.: 58880-19-6

    Trichostatin A
    CAS#: 58880-19-6

产品信息

CAS号 58880-19-6
分子式 C17H22N2O3
主要靶点 HDAC
主要通路 表观遗传|DNA 损伤和修复
分子量 302.37
纯度 98.3%， 此纯度可做参考，具体纯度与批次有关系，可咨询客服
储存条件 store at low temperature,store under nitrogen | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice.
别名 inhibit|HDAC|Histone deacetylases|曲古柳菌素A|曲古抑菌素A|Trichostatin A|TSA|Inhibitor

靶点活性

HDAC:1.8 nM

体内活性

方法：为检测体内抗肿瘤活性，将 Trichostatin A (500 μg/kg) 皮下注射给 NMU 诱导乳腺癌肿瘤的大鼠，每天一次，持续四周。 结果：Trichostatin A 在体内具有显著的抗肿瘤活性。Trichostatin A 处理的大鼠肿瘤具有良性表型，纤维腺瘤或管状腺瘤，这表明 Trichostatin A 的抗肿瘤活性可能归因于分化的诱导。[1] 方法：为检测体内抗肿瘤活性，将 Trichostatin A (0.5-1 mg/kg，每周两次) 和 Quercetin (10 mg/kg，每周三次) 腹腔注射给携带人肺腺癌肿瘤 A549 的裸鼠，持续十三周。 结果：高剂量 Trichostatin A 显著抑制肿瘤生长，而低剂量 Trichostatin A 和 Quercetin 单独使用没有效果。然而，低剂量 Trichostatin A 和 Quercetin 联合治疗显著抑制了肿瘤生长。[3]

体外活性

方法：八种乳腺癌细胞 MCF-7、T-47D、ZR-75-1、BT-474、MDA-MB-231、MDA-MB-453、CAL 51 和 SK-BR-3 用 Trichostatin A (10?12?-10?5 M) 处理 96 h，使用 SRB 方法检测细胞活力。 结果：Trichostatin A 抑制八种乳腺癌细胞系的增殖，平均 IC50=124.4±120.4 nM（范围 26.4-308.1 nM）。[1] 方法：食管鳞状细胞癌细胞 EC9706 和 EC1 用 Trichostatin A (0.3-1μM) 处理 48 h，使用 Flow Cytometry 方法检测细胞凋亡情况。 结果：在 0.3 和 0.5 μM Trichostatin A 的剂量下，早期凋亡的百分比没有显著增加。但与对照组相比，1.0 μM Trichostatin A 处理可显著诱导早期细胞凋亡。此外，中晚期凋亡的百分比以浓度依赖的方式增加。[2] 方法：食管鳞状细胞癌细胞 EC9706 和 EC1 用 Trichostatin A (0.3-1μM) 处理 60 min，使用 Western Blot 方法检测靶点蛋白表达水平。 结果：Trichostatin A 以剂量依赖的方式降低 PI3K 的蛋白水平以及 p-Akt 和 p-ERK1/2。组蛋白H4的乙酰化以浓度依赖性方式增加。[2]

溶解度

Ethanol:3 mg/mL (9.92 mM);DMSO:50 mg/mL (165.36 mM)

细胞实验

Cells are exposed to various concentrations of Trichostatin A for 96 hours. After treatment, cell proliferation is estimated using the sulforhodamine B colorimetric assay. Cell viability is determined by trypan blue exclusion. (Only for Reference)

参考文献

1.Vigushin DM, et al. Trichostatin A is a histone deacetylase inhibitor with potent antitumor activity against breast cancer in vivo. Clin Cancer Res. 2001 Apr;7(4):971-6.
2.Ma J, et al. Trichostatin A, a histone deacetylase inhibitor, suppresses proliferation and promotes apoptosis of esophageal squamous cell lines. Mol Med Rep. 2015 Jun;11(6):4525-31.
3.Chan ST, et al. Quercetin enhances the antitumor activity of trichostatin A through upregulation of p53 protein expression in vitro and in vivo. PLoS One. 2013;8(1):e54255.
4.Huang W, et al. J Biol Chem, 2005, 280(11), 120047-120054.
5.Avila AM, et al. J Clin Invest, 2007, 117(3), 659-671.
6.Li X, Pan L, Wang B, et al. The Histone Deacetylases HosA and HdaA Affect the Phenotype and Transcriptomic and Metabolic Profiles of Aspergillus niger[J]. Toxins. 2019, 11(9): 520.
7.Meng Y, Qian X, Zhao L, et al. Trichostatin A downregulates bromodomain and extra-terminal proteins to suppress osimertinib resistant non-small cell lung carcinoma[J]. Cancer Cell International. 2021, 21(1): 1-12.
8.Xu K, Sun G, Li M, et al. Glibenclamide Targets Sulfonylurea Receptor 1 to Inhibit p70S6K Activity and Upregulate KLF4 Expression to Suppress Non-Small Cell Lung Carcinoma[J]. Molecular cancer therapeutics. 2019, 18(11): 2085-2096.
9.Su Q, Li T, He P F, et al. Trichostatin A ameliorates Alzheimer’s disease-related pathology and cognitive deficits by increasing albumin expression and Aβ clearance in APP/PS1 mice[J]. Alzheimer's Research & Therapy. 2021, 13(1): 1-15.

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