Tucidinostat
(Synonyms: 西达本胺; Chidamide; HBI-8000; CS 055) 目录号 : GC37845
Tucidinostat，也称为Chidamide或CS055/HBI-8000，是HDAC1、HDAC2、HDAC3和HDAC10的抑制剂，IC50值分别为95 nM、160 nM、67 nM和78 nM。
Cas No.:1616493-44-7
Sample solution is provided at 25 µL, 10mM.
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Tucidinostat, also known as Chidamide or CS055/HBI-8000, is an inhibitor of HDAC1, HDAC2, HDAC3, and HDAC10, with IC50 values of 95 nM, 160 nM, 67 nM, and 78 nM, respectively. It belongs to the benzamide class of selective HDAC inhibitors and is capable of promoting histone H3 acetylation. Tucidinostat has demonstrated efficacy in inhibiting tumor growth across a range of malignant tumors[1-2].
Tucidinostat(0.25-8uM; 24-96h) inhibited the proliferation of K562 cells in a dose- and time-dependent manner. It achieved this by blocking cells in the G0/G1 phase through downregulation of cyclin-dependent kinase 4 (CDK4). Additionally, Tucidinostat induced apoptosis by upregulating Bax and downregulating Bcl-2[3]. Tucidinostat(0.1-6uM ;72 h) elicited growth inhibition and cell cycle arrest in rituximab-resistant B-cell lymphoma cell lines (RRCL) [4]. Tucidinostat(0, 2.5, and 10 μM; 48 h) significantly upregulated E-cadherin expression in TGF-β-treated cells and suppressed the migration of lung cancer cells[5].
Tucidinostat(25 mg/kg; p.o; thrice weekly for 2 weeks) inhibited the formation of subcutaneous leukemia tumors. Following treatment with Tucidinostat, the tumor size was significantly reduced[6]. Tucidinostat, at a dosage of 5 mg/kg, combined with fluzoparib, more significantly inhibited neoplasm growth compared to monotherapy[7].
[1]. Ning ZQ, Li ZB, et al. Chidamide (CS055/HBI-8000): a new histone deacetylase inhibitor of the benzamide class with antitumor activity and the ability to enhance immune cell-mediated tumor cell cytotoxicity. Cancer Chemother Pharm. 2012;69:901–9.
[2]. Liu L, Chen B, et al. A novel histone deacetylase inhibitor Chidamide induces apoptosis of human colon cancer cells. Biochem Biophys Res Commun. 2010 Feb 5;392(2):190-5. doi: 10.1016/j.bbrc.2010.01.011. Epub 2010 Jan 7. PMID: 20060381.
[3]. Liang S, Zhou X, et al. Chidamide Inhibits Cell Proliferation via the PI3K/AKT Pathway in K562 Cells Based on Network Pharmacology and Experimental Validation. Curr Pharm Des. 2021;27(26):2990-2998. doi: 10.2174/1381612827666210701152250. PMID: 34218775.
[4]. Xue K, Wu JC, et al. Chidamide triggers BTG1-mediated autophagy and reverses the chemotherapy resistance in the relapsed/refractory B-cell lymphoma. Cell Death Dis. 2021 Oct 1;12(10):900. doi: 10.1038/s41419-021-04187-5. PMID: 34599153; PMCID: PMC8486747.
[5]. Lin SH, Wang BY, et al. Chidamide alleviates TGF-β-induced epithelial-mesenchymal transition in lung cancer cell lines. Mol Biol Rep. 2016 Jul;43(7):687-95. doi: 10.1007/s11033-016-4005-z. Epub 2016 May 17. PMID: 27188428.
[6]. Xue K, Wu JC, et al. Chidamide triggers BTG1-mediated autophagy and reverses the chemotherapy resistance in the relapsed/refractory B-cell lymphoma. Cell Death Dis. 2021 Oct 1;12(10):900. doi: 10.1038/s41419-021-04187-5. PMID: 34599153; PMCID: PMC8486747.
[7]. Li X, Yuan X, et al. Chidamide Reverses Fluzoparib Resistance in Triple-Negative Breast Cancer Cells. Front Oncol. 2022 Feb 18;12:819714. doi: 10.3389/fonc.2022.819714. PMID: 35251986; PMCID: PMC8894594.
Tucidinostat，也称为Chidamide或CS055/HBI-8000，是HDAC1、HDAC2、HDAC3和HDAC10的抑制剂，IC50值分别为95 nM、160 nM、67 nM和78 nM。它属于苯甲酰胺类选择性HDAC抑制剂，能够促进组蛋白H3乙酰化。Tucidinostat已被证明对多种恶性肿瘤具有抑制肿瘤生长的功效[1-2]。
Tucidinostat(0.25-8uM; 24-96h) 对K562细胞的增殖具有剂量依赖性和时间依赖性。它下调细胞周期蛋白依赖性激酶4 (CDK4)阻断G0/G1期的细胞。此外，Tucidinostat通过上调Bax和下调Bcl-2诱导细胞凋亡[3]。在利妥昔单抗耐药b细胞淋巴瘤细胞系(RRCL)中，Tucidinostat(0.1-6uM;72 h)可引起生长抑制和细胞周期阻滞[4]。Tucidinostat(0、2.5、10 μM);48 h)显著上调TGF-β处理细胞中E-cadherin的表达，抑制肺癌细胞的迁移[5]。
Tucidinostat(25 mg/kg; p.o; thrice weekly for 2 weeks)抑制皮下白血病肿瘤的形成，应用Tucidinostat治疗后，肿瘤大小明显减小[6]。与单药治疗相比，5 mg/kg剂量的途西替他与氟唑帕尼联用能更显著地抑制肿瘤生长[7]。
| Cell experiment [1]: | |
Cell lines | K562 cells |
Preparation Method | Cells were exposed to Tucidinostat treatment, and subsequent cell proliferation rates were quantitatively assessed. |
Reaction Conditions | 0.25, 0.5, 1, 2, 4 and 8uM; 24, 48, 72 and 96h |
Applications | Tucidinostat showed a dose-dependent and time-dependent inhibition of K562 cell proliferation. |
| Animal experiment [2]: | |
Animal models | Female BALB/c–nude mice(SKM-1 leukemia model) |
Preparation Method | Mice were divided into two groups randomly. One group received oral administration of Tucidinostat at a dose of 25 mg/kg of body weight, Tucidinostat dissolved in 0.2% carboxymethyl cellulose and 0.1% Tween 80 (200 μl). The other group was orally administered 1% DMSO three times weekly for a duration of 2 weeks. |
Dosage form | 25 mg/kg; p.o; thrice weekly for 2 weeks |
Applications | Tucidinostat effectively suppresses the proliferation of acute myeloid leukemia cells in vivo. Following Tucidinostat treatment, a notable reduction in tumor size was observed. |
References: [1]:Liang S, Zhou X, et,al. Chidamide Inhibits Cell Proliferation via the PI3K/AKT Pathway in K562 Cells Based on Network Pharmacology and Experimental Validation. Curr Pharm Des. 2021;27(26):2990-2998. doi: 10.2174/1381612827666210701152250. PMID: 34218775. [2]:Liang S, Zhou X, et,al. Chidamide Inhibits Cell Proliferation via the PI3K/AKT Pathway in K562 Cells Based on Network Pharmacology and Experimental Validation. Curr Pharm Des. 2021;27(26):2990-2998. doi: 10.2174/1381612827666210701152250. PMID: 34218775. | |
| Cas No. | 1616493-44-7 | SDF | |
| 别名 | 西达本胺; Chidamide; HBI-8000; CS 055 | ||
| Canonical SMILES | O=C(C1=CC=C(CNC(/C=C/C2=CN=CC=C2)=O)C=C1)NC(C=CC(F)=C3)=C3N | ||
| 分子式 | C22H19FN4O2 | 分子量 | 390.41 |
| 溶解度 | DMSO: ≥ 50 mg/mL (128.07 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.5614 mL | 12.807 mL | 25.6141 mL |
| 5 mM | 0.5123 mL | 2.5614 mL | 5.1228 mL |
| 10 mM | 0.2561 mL | 1.2807 mL | 2.5614 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
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- Purity: >98.00%
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