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Ruxolitinib

Ruxolitinib

产品编号 T1829   CAS 941678-49-5
别名: 芦可替尼, INCB018424, 鲁索替尼, (R)-Ruxolitinib

Ruxolitinib (INCB018424) 是一种 JAK1/2 抑制剂 (IC50=3.3/2.8 nM),具有有效性和选择性。Ruxolitinib 具有抗肿瘤活性,可以诱导细胞自噬凋亡

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Ruxolitinib Chemical Structure
Ruxolitinib, CAS 941678-49-5
规格 价格/CNY 货期 数量
1 mg ¥ 233 现货
5 mg ¥ 536 现货
10 mg ¥ 828 现货
25 mg ¥ 1,530 现货
50 mg ¥ 2,360 现货
100 mg ¥ 3,810 现货
200 mg ¥ 4,990 现货
500 mg ¥ 7,790 现货
1 g ¥ 10,500 现货
1 mL * 10 mM (in DMSO) ¥ 611 现货
其他形式的 Ruxolitinib:
产品目录号及名称: Ruxolitinib (T1829)
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选择批次  
纯度: 100%
纯度: 99.93%
纯度: 99.83%
纯度: 99.42%
纯度: 99.4%
更多批次查询请联系客服
生物活性
化学信息
存储 & 溶解度
参考文献
产品描述 Ruxolitinib (INCB018424) is a JAK1/2 inhibitor (IC50=3.3/2.8 nM) that is potent and selective. Rixolitinib exhibits antitumor activity and induces autophagy and apoptosis.
靶点活性 JAK2:2.8 nM (cell free), JAK1:3.3 nM (cell free), TYK2:19 nM (cell free)
体外活性 方法:Ba/F3-EpoR-JAK2V617F 细胞用 Ruxolitinib (0-10 μM) 处理 48 h,使用 Cell-Titer Glo 检测的细胞活力。
结果:Ruxolitinib 剂量依赖性降低细胞活力,IC50 为 126 nM。[1]
方法:霍奇金淋巴瘤细胞 HDLM-2 用 Ruxolitinib (10-100 nM) 处理 24 h,使用 Western Blot 方法检测靶点蛋白表达水平。
结果:Ruxolitinib 显著抑制下游活性 p-STAT3 和 p-STAT5,且呈剂量依赖性,而总 STAT3 和 STAT5 水平保持不变。[2]
体内活性 方法:为检测体内抗肿瘤活性,将 Ruxolitinib (3-30 mg/kg,5% dimethyl acetamide, 0.5% methocellulose) 灌胃给药给携带肿瘤 Ba/F3-JAK2V617F 的 BALB/c 小鼠,每天两次,持续三周。
结果:Ruxolitinib 显著降低了脾肿大和炎症细胞因子的循环水平,并优先消除了肿瘤细胞,从而显著延长了生存期,而没有骨髓抑制或免疫抑制作用。[1]
方法:为检测体内抗肿瘤活性,将 Ruxolitinib (150 mg/kg) 口服给药给携带人结直肠肿瘤 LS411N 的 BALB/c nude 小鼠,每两天一次,持续两周。
结果:口服 Ruxolitinib 可显著抑制人结直肠肿瘤的体内生长,而不会引起肝毒性。[3]
激酶实验 The kinase domains of human JAK1 (837-1142), JAK2 (828-1132), JAK3 (781-1124), and Tyk2 (873-1187) were cloned by PCR with N-terminal epitope tags. Recombinant proteins were expressed using Sf21 cells and baculovirus vectors and purified with affinity chromatography. JAK kinase assays used a homogeneous time-resolved fluorescence assay with the peptide substrate (-EQEDEPEGDYFEWLE). Each enzyme reaction was carried out with test compound or control, JAK enzyme, 500nM peptide, adenosine triphosphate (ATP; 1mM), and 2.0% dimethyl sulfoxide (DMSO) for 1 hour. The 50% inhibitory concentration (IC50) was calculated as the compound concentration required for inhibition of 50% of the fluorescent signal. Biochemical assays for CHK2 and c-MET enzymes were performed using standard conditions (Michaelis constant [Km] ATP) with recombinantly expressed catalytic domains from each protein and synthetic peptide substrates. An additional panel of kinase assays (Abl, Akt1, AurA, AurB, CDC2, CDK2, CDK4, CHK2, c-kit, c-Met, EGFR, EphB4, ERK1, ERK2, FLT-1, HER2, IGF1R, IKKα, IKKβ, JAK2, JAK3, JNK1, Lck, MEK1, p38α, p70S6K, PKA, PKCα, Src, and ZAP70) was performed using standard conditions using 200nM INCB018424. Significant inhibition was defined as more than or equal to 30% (average of duplicate assays) compared with control values [1].
细胞实验 Cells were seeded at 2000/well of white bottom 96-well plates, treated with compounds from DMSO stocks (0.2% final DMSO concentration), and incubated for 48 hours at 37°C with 5% CO2. Viability was measured by cellular ATP determination using the Cell-Titer Glo luciferase reagent or viable cell counting. Values were transformed to percent inhibition relative to vehicle control, and IC50 curves were fitted according to nonlinear regression analysis of the data using PRISM GraphPad [1].
动物实验 All of the procedures were conducted in accordance with the US Public Health Service Policy on Humane Care and Use of Laboratory Animals. Mice were fed standard rodent chow and provided with water ad libitum. Ba/F3-JAK2V617F cells (10^5 per mouse) were inoculated intravenously into 6- to 8-week-old female BALB/c mice. Survival was monitored daily, and moribund mice were humanely killed and considered deceased at time of death. Treatment with vehicle (5% dimethylacetamide, 0.5% methocellulose) or INCB018424 began within 24 hours of cell inoculation, twice daily by oral gavage. Hematologic parameters were measured using a Bayer Advia120 analyzed, and statistical significance was determined using Dunnett testing [1].
别名 芦可替尼, INCB018424, 鲁索替尼, (R)-Ruxolitinib
化合物与蛋白结合的复合物

T1829_2

C-Src in complex with Ruxolitinib

分子量 306.36
分子式 C17H18N6
CAS No. 941678-49-5

存储

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

溶解度

H2O: < 1 mg/mL (insoluble or slightly soluble)

DMSO: 57 mg/mL (186 mM)

Ethanol: < 1 mg/mL (insoluble or slightly soluble)

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 3.2641 mL 16.3207 mL 32.6413 mL 81.6033 mL
5 mM 0.6528 mL 3.2641 mL 6.5283 mL 16.3207 mL
10 mM 0.3264 mL 1.6321 mL 3.2641 mL 8.1603 mL
20 mM 0.1632 mL 0.816 mL 1.6321 mL 4.0802 mL
50 mM 0.0653 mL 0.3264 mL 0.6528 mL 1.6321 mL
100 mM 0.0326 mL 0.1632 mL 0.3264 mL 0.816 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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参考文献

1. Quintás-Cardama A, et al. Preclinical characterization of the selective JAK1/2 inhibitor INCB018424: therapeutic implications for the treatment of myeloproliferative neoplasms. Blood. 2010 Apr 15;115(15):3109-17. 2. Lee S, et al. Ruxolitinib significantly enhances in vitro apoptosis in Hodgkin lymphoma and primary mediastinal B-cell lymphoma and survival in a lymphoma xenograft murine model. Oncotarget. 2018 Jan 18;9(11):9776-9788. 3. Li X, et al. Ruxolitinib induces apoptosis of human colorectal cancer cells by downregulating the JAK1/2-STAT1-Mcl-1 axis. Oncol Lett. 2021 May;21(5):352. 4. Datta J, Lamichhane P, Dai X, et al. Combined MEK and STAT3 inhibition reprograms the tumor microenvironment to overcome immunotherapy resistance in pancreatic cancer[J]. bioRxiv. 2021 5. Ryan M M, Patel M, Hogan K, et al. Ruxolitinib inhibits IFNγ licensing of human bone marrow derived Mesenchymal Stromal Cells[J]. Transplantation and Cellular Therapy. 2021, 27(5): 389. e1-389. e10. 6. Chen X, Gao C, Cheng Z, et al. Ruxolitinib exerts neuroprotection via repressing ferroptosis in a mouse model of traumatic brain injury[J]. Experimental Neurology. 2021: 113762. 7. Zhang C, Yan Y, He H, et al. IFN-stimulated P2Y13 protects mice from viral infection by suppressing the cAMP/EPAC1 signaling pathway[J]. Journal of molecular cell biology. 2018 Aug 22. 8. Espinet E, Gu Z, Imbusch C D, et al. Cancer Discovery. 2021, 11(3): 638-659.

文献引用

1. Datta J, Dai X, Bianchi A, et al. Combined MEK and STAT3 inhibition uncovers stromal plasticity by enriching for cancer-associated fibroblasts with mesenchymal stem cell-like features to overcome immunotherapy resistance in pancreatic cancer. Gastroenterology. 2022 2. Datta J, Lamichhane P, Dai X, et al. Combined MEK and STAT3 inhibition reprograms the tumor microenvironment to overcome immunotherapy resistance in pancreatic cancer. Cancer Research. 2022, 82(12_Supplement): 4187-4187. 3. Si H, Wang J, He R, et al. Identification of U937JAK3-M511I Acute Myeloid Leukemia Cells as a Sensitive Model to JAK3 Inhibitor. Frontiers in oncology. 2021, 11: 807200-807200. 4. Alfi O, Hamdan M, Wald O, et al. SARS-CoV-2 Omicron Induces Enhanced Mucosal Interferon Response Compared to other Variants of Concern, Associated with Restricted Replication in Human Lung Tissues. Viruses. 2022, 14(7): 1583. 5. Zhang C, Yan Y, He H, et al. IFN-stimulated P2Y13 protects mice from viral infection by suppressing the cAMP/EPAC1 signaling pathway. Journal of Molecular Cell Biology. 2018 Aug 22 6. Chen X, Gao C, Cheng Z, et al. Ruxolitinib exerts neuroprotection via repressing ferroptosis in a mouse model of traumatic brain injury. Experimental Neurology. 2021: 113762. 7. Wang H, Jia X, Zhang M, et al.Isoliquiritigenin inhibits virus replication and virus-mediated inflammation via NRF2 signaling.Phytomedicine.2023: 154786. 8. Zhang X, Wang J, Wang M, et al.IFN-β Pretreatment Alleviates Allogeneic Renal Tubular Epithelial Cell–Induced NK Cell Responses via the IRF7/HLA-E/NKG2A Axis.The Journal of Immunology.2023 9. Zhang Z D, Shi C R, Li F X, et al.Disulfiram ameliorates STING/MITA-dependent inflammation and autoimmunity by targeting RNF115.Cellular & Molecular Immunology.2024: 1-17. 10. Guo Y, Zhu L, Duan Y, et al.Ruxolitinib induces apoptosis and pyroptosis of anaplastic thyroid cancer via the transcriptional inhibition of DRP1-mediated mitochondrial fission.Cell Death & Disease.2024, 15(2): 125.
Decernotinib NVP-BSK805 Brepocitinib ST271 Zongertinib Ruxolitinib (S enantiomer) AZ7550 Ibrutinib

相关化合物库

该产品包含在如下化合物库中:
抗癌上市药物库 抗癌临床化合物库 抗癌药物库 酪氨酸激酶分子库 抗肝癌化合物库 精选片段库 血管生成库 Mini片段亲电杂环化合物库 激酶抑制剂库 抗胰腺癌化合物库

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
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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

Ruxolitinib 941678-49-5 Angiogenesis Apoptosis Autophagy Chromatin/Epigenetic JAK/STAT signaling Stem Cells Tyrosine Kinase/Adaptors Mitophagy Tyrosine Kinases JAK INCB 18424 芦可替尼 inhibit Mitochondrial Autophagy INCB18424 Janus kinase INCB 018424 INCB-18424 INCB-018424 INCB018424 Inhibitor 鲁索替尼 (R)-Ruxolitinib inhibitor

 

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