Dasatinib
目录号：S1021 别名： BMS-354825
Molecular Weight(MW): 488.01
Dasatinib是一种新型有效的多靶点抑制剂，作用于Abl，Src和 c-Kit，在无细胞试验中IC50分别为 <1 nM，0.8 nM 和 79 nM。
-Vandetanib(ZD6474)-Birinapant-Cell-Death-Dis-20150727.gif)
客户使用该产品的13个实验数据：
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Antitumor activity (A)and body weight (B) relationship for BLU-285 and dasatinib in a P815 KIT D814Y mastocytoma allograft model.
Science, 2017, 9(414), doi: 10.1126/scitranslmed.aao1690. Dasatinib purchased from Selleck.
Combinational treatment of kinase inhibitors induces the similar phenotype produced by PP1. All images are lateral view with dorsal to the top and anterior to the left. The combinational treatment of Dasatinib (D) or U0126 (U) with Sunitinib (SU),PTK787 (PTK), or ZM323881 (Z) resulted in the shrinkage of dorsal aorta.
Cell Res 2011 21, 1080-1087. Dasatinib purchased from Selleck.
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Cytotoxicity by Dasatinib and Nutlin-3 used alone or in combination in B-CLL patient leukemic cells. B-CLL patient leukemic cells were exposed to serial doses of Dasatinib or Nutlin- 3 used either alone or in combination, with a fixed ratio, for 48 hours. Dose-effect plots, to determine drug efficacy, are shown for representative B-CLL samples, including 3 patients carrying 17p- (Pt. #7, Pt. #8, and Pt. #10). The decrease of cell viability, labeled "effect" on the Y-axis, was determined in assays done at least twice in duplicate.
Clin Cancer Res 2011 17, 762-770. Dasatinib purchased from Selleck.
Dasatinib interferes with the p53 transcriptional activity induced by Nutlin-3. Leukemic cell lines were exposed for 24 hours to Dasatinib (10 μM) and Nutlin-3 (10 μM), used either alone or in combination, as indicated. Levels of p53 (A), MDM2 and p21 (B) were assessed by Western blot analysis of total cell lysates. Representative examples of Western blot results are shown. Tubulin staining is shown as loading control; after densitometric analyses, p53 as well as MDM2 and p21 protein levels are expressed as folds of protein modulation, by the indicated treatments, with respect to the control untreated cultures set to 1 (hatched line). *P < 0.05 with respect to the Nutlin-3-treated cultures.
Clin Cancer Res 2011 17, 762-770. Dasatinib purchased from Selleck.
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Role of Akt in Dasatinib cytotoxicity and in DasatinibtNutlin-3 synergy. A, whole cell lysates were prepared from EHEB and BJAB cell lines treated (for 16 hours) as indicated, and hybridized with a human Phospho-Kinase array kit. Spot densities of phospho-proteins were quantified using Image Quant TL software and normalized to those of positive controls (set at 100) on the same membrane. The analysis of modulation of phosphorylation signals for P-ERK1/2, P-p38, and P-Akt are reported (*P < 0.05). Validation of phospho-kinase array results was carried out by Western blot analysis of P-Akt levels.
Clin Cancer Res 2011 17, 762-770. Dasatinib purchased from Selleck.
Impact of the TKI erlotinib, lapatinib, dasatinib, and sorafenib on the viability of MDS/AML cells. MOLM-13 (A) and HL-60 (B) cells were incubated with the indicated doses (given in mM below the x-axis) of the 4 TKI, and cellular viability was assessed by MTT assay after 24, 48 and 72 h of incubation. Changes in viability are given as percentage of cells as compared to non-treated control samples. This experiment was repeated at least three times, yielding comparable results. Graphs show representative results of one experiment carried out in duplicates (mean standard deviation).
Biochem Pharmacol 2011 82, 1457-1466. Dasatinib purchased from Selleck.
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Capacity of the TKI to overcome the AML-typical differentiation blockage. The myeloid cell lines MOLM-13 and HL-60 were incubated for 6 days with 0.01% DMSO (serving as a negative solvent control), 1 μM of ATRA (serving as a positive control), as well as with the indicated doses of the four TKI. (A) Representative May -Gruenwald -Giemsa staining of MOLM-13 cells, (B) quantitation of the percentage of MOLM-13 cells exhibiting at least two morphological signs of differentiation (that is a decrease in cytoplasmic basophilia, a reduction of the nucleo-cytoplasmic ratio, appearance of nuclear lobulation and/or cytoplasmic granules). Percentages were evaluated by examining at least 100 cells/condition; (C) representative FACS overlays of MOLM-13 cells depicting TKI-induced CD11b expression (black line) as compared to the isotype (shaded grey); (D) quantitation of TKI-induced CD11b-expression in MOLM-13 cells; (E) representative slides depicting morphology/staining of MOLM-13 cells assessed in the NBT-reduction assay; (F) respective quantitative assessment demonstrating the NBT-reducing capacity under the different drugs; (G) representative May-Gruenwald-Giemsa staining of HL-60 cells.
Biochem Pharmacol 2011 82, 1457-1466. Dasatinib purchased from Selleck.
Cytotoxicity by Dasatinib treatment in leukemic cells.Leukemic cell lines were exposed to Dasatinib (10 μM). Upon treatment, cell viability (a) was calculated as percentage with respect to the control vehicle cultures (set to 100% for each cell line) and induction of apoptosis (b) was calculated as percentage of Annexin V+/PI+ cells after 48 h of treatment.
Invest New Drugs 2010 30, 417-422. Dasatinib purchased from Selleck.
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Human phospho-kinase array analysis in response to Dasatinib treatment. Whole cell lysates were prepared from EHEB (p53wt) and BJAB (p53mut) B cell lines, either left untreated or exposed to Dasatinib for 24 h, and hybridized with a human Phospho-Kinase array kit. Spot densities of phospho-proteins were quantified using Image Quant TL software and normalized to those of positive controls on the same membrane. In a, intense decreases of signal of P-p38, PERK1/2 and P-CREB in response to Dasatinib are indicated by arrows in the membranes, and intensity of corresponding spots are reported as graphics. In b, analysis of modulation of phosphorylation of STAT family members in response to Dasatinib (spots not shown). The means±SD of three independent experiments are shown. Asterisk indicates P<0.05 against untreated.
Invest New Drugs 2010 30, 417-422. Dasatinib purchased from Selleck.
Cells were either left untreated (Unt.) or exposed to Dasatinib (Das.) for 24 h. Equal amounts of cell lysates were analyzed for ERK1/2, p38 and CREB phosphorylation by Western blot using antibodies specific for the native form of the kinases and for residues that are phosphorylated (P-) in each kinase upon activation. One of three experimentswith similar results is shown. Protein bands were quantified by densitometry and level of PERK1/2, P-p38 and P-CREB expressed as arbitrary units,were calculated for each cell line after normalization to total ERK1/2, p38 and CREB respectively
Invest New Drugs 2010 30, 417-422. Dasatinib purchased from Selleck.
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Effect of dasatinib on endothelial cell actin fiber organization. Subconfluent human microvascular endothelial cells‐1 were treated with dimethyl sulfoxide (A) or dasatinib (B), fixed, permeabilized and stained with phalloıdin (green) for F‐actin or FAK (red) for adhesion plaques. Images were taken in a confocal microscope (1000X).
Cancer Med, 2017, 6(4):809-818. Dasatinib purchased from Selleck.
Inhibition of cell growth upon culturing of primary bone marrow cells from an EMS patient and a healthy control in presence of TKIs in vitro. EMS cells showed reduced cell growth compared to the healthy control cells when cultured with ponatinib, dovitinb or dasatinib. Cell growth was evaluated after 72 hours in culture. All samples were normalized to DMSO controls. Non-linear regression curves were fitted for evaluation of IC50 values. Error bars represent mean values and standard deviation of the analyzed replicates.
Eur J Haematol, 2017, 99(5):442-448. Dasatinib purchased from Selleck.
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Cell vability test result. Different cell lines (A2C12, Beta D5, Gamma A3, Gamma D12, A549, CaCo2,Hep G2) were treated with different concentration of Dasatinib.
Dr. Thomas Kruwel of Fraunhofer-Institute for Toxicology and Experimental Medicine-Dasatinib (BMS-354825) purchased from Selleck. Dasatinib purchased from Selleck.
产品安全说明书
Src抑制剂选择性比较
生物活性
| 产品描述 | Dasatinib是一种新型有效的多靶点抑制剂，作用于Abl，Src和 c-Kit，在无细胞试验中IC50分别为 <1 nM，0.8 nM 和 79 nM。 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| 靶点 |
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| 体外研究 |
在抑制表达野生型Bcr-Abl或全部Bcr-Abl突变型（除了T315I）的Ba/F3增殖时，Dasatinib效果比Imatinib高很多。与Imatinib相比，Dasatinib呈2倍指数增长效力(约325倍)。Dasatinib有效抑制野生型Abl 激酶和全部突变型（除了T315I）。Dasatinib 直接靶向作用于野生型和突变型Abl激酶域，且抑制自磷酸化和底物磷酸化，这种作用存在浓度依赖性。Dasatinib作用于表达野生型 Bcr-Abl的细胞时，效果比Imatinib高325倍多。[1] TgE骨髓细胞菌落百分数从未处理孔的100% 降低到Dasatinib处理孔的4.12%。 有 Dasatinib存在时, WT 和TgE骨髓细胞形成的菌落百分数明显不同。LMP2A的表达可促进 B 淋巴细胞存活和增殖，而Dasatinib通过靶向作用于Lyn 和/或c-Abl 激酶可抑制以上存活和增殖。[2] Dasatinib 处理一系列甲状腺癌细胞，抑制Src信号, 降低生长速度,使细胞周期停滞，且诱导凋亡。使用剂量不断增加的 Dasatinib (0.019 μM 到 1.25 μM) 处理C643, TPC1, BCPAP, 和 SW1736 细胞3天，抑制50%细胞生长，然而抑制K1细胞系生长则需更高浓度Dasatinib。使用10 nM 或50 nM Dasatinib 处理BCPAP，SW1736 和 K1 细胞，导致G1期细胞提高9-22%，而S期细胞百分数则降低7-18%。[3] |
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| Cell Data |
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| 体内研究 | Dasatinib 作用于LMP2A/MYC 双转基因小鼠，可逆转脾肿大。Dasatinib 作用于TgE小鼠 抑制表达LMP2A 的骨髓B 细胞形成的菌落，且使脾脏变小。使用Dasatinib处理Tg6/λ-MYC 小鼠，与对照组相比，脾脏质量明显降低。Dasatinib 作用于LMP2A/MYC 双转基因小鼠，抑制淋巴结肿大。Dasatinib作用于嫁接LMP2A/MYC双转基因小鼠肿瘤细胞的Rag1KO小鼠，可逆转脾肿大。Dasatinib 作用于表达LMP2A的B 淋巴细胞瘤，抑制Lyn磷酸化。[2] |
推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)
| 激酶实验：[1] |
+ 展开
激酶自磷酸化分析: 使用野生型和突变型谷胱甘肽S-转移酶(GST)-Abl融合蛋白 (c-Abl氨基酸220-498位) 进行激酶实验。从谷胱甘肽琼脂糖珠中释放GST-Abl融合蛋白，ATP浓度为5 μM。在用于激酶自磷酸化和体外肽底物磷酸化实验前, 用LAR酪氨酸磷酸酶处理GST-Abl 激酶域融合蛋白。在 30oC下温育1小时后,加入1 mM 钒酸钠，激活LAR磷酸酶。进行免疫印迹分析，比较未处理的GST-Abl激酶和去磷酸化的GST-Abl激酶，使用磷酸化的特点抗体4G10来 确认酪氨酸残基完全去磷酸化(>95%)，使用c-Abl抗体 CST 2862 来确认GST-Abl激酶的平衡负载。实验测定IC50值时所用Dasatinib浓度为0 nM到32 nM。Dasatinib作用于突变型T315I时浓度达到 1,000 nM。在体外肽底物磷酸化实验中使用相同抑制剂浓度。作用于GST-Src激酶和 GST-Lyn激酶的三种抑制剂的浓度范围相同。 |
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| 细胞实验： [1] |
+ 展开
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| 动物实验：[2] |
+ 展开
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溶解度 (25°C)
| 体外 | DMSO | 98 mg/mL (200.81 mM) |
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| Water | Insoluble | |
| Ethanol | Insoluble | |
| 体内 |
从左到右依次将纯溶剂加入产品，现配现用(数据来自Selleck实验检测而非文献)： 4% DMSO+30% PEG 300+5% Tween 80+ddH2O |
5mg/mL |
* 溶解度检测是由Selleck技术部门检测的，可能会和文献中提供的溶解度有所差异，这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。
化学数据
| 分子量 | 488.01 |
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| 化学式 | C22H26ClN7O2S |
| CAS号 | 302962-49-8 |
| 稳定性 | powder |
| in solvent | |
| 别名 | BMS-354825 |
计算器
摩尔浓度计算器
本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系，公式为:
质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)
摩尔浓度计算公式
*在配置溶液时，请务必参考Selleck产品标签上、MSDS / COA（可在Selleck的产品页面获得）批次特异的分子量使用本工具。
稀释计算器
用本工具协助配置特定浓度的溶液，使用的计算公式为：
开始浓度 x 开始体积 = 最终浓度 x 最终体积
稀释公式
稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )
在配置溶液时，请务必参考Selleck产品标签上、MSDS / COA（可在Selleck的产品页面获得）批次特异的分子量使用本工具。.
分子量计算器
通过输入化合物的化学式来计算其分子量：
注：化学分子式大小写敏感。C10H16N2O2 c10h16n2o2
摩尔浓度计算器
临床试验信息
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT03041701 | Recruiting | Rhabdomyosarcoma|Rhabdomyosarcoma- Alveolar|Rhabdomyosarcoma-Embryonal | National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) | July 7 2017 | Phase 1|Phase 2 |
| NCT02011945 | Active not recruiting | Chronic Myeloid Leukemia | Bristol-Myers Squibb | February 7 2014 | Phase 1 |
| NCT02389309 | Recruiting | Solid Tumors | M.D. Anderson Cancer Center | October 5 2015 | Phase 1 |
| NCT02744768 | Recruiting | Acute Lymphoblastic Leukemia | Gruppo Italiano Malattie EMatologiche dell''Adulto | May 31 2017 | Phase 2 |
| NCT01999985 | Active not recruiting | Lung Cancer|Non-small Cell Lung Cancer (NSCLC) | H. Lee Moffitt Cancer Center and Research Institute|Boehringer Ingelheim|Bristol-Myers Squibb | December 31 2013 | Phase 1 |
| NCT01660971 | Active not recruiting | Metastatic Pancreatic Adenocarcinoma|Recurrent Pancreatic Carcinoma|Stage III Pancreatic Cancer AJCC v6 and v7|Stage IV Pancreatic Cancer AJCC v6 and v7 | National Cancer Institute (NCI) | July 30 2012 | Phase 1 |
技术支持
在订购、运输、储存和使用我们的产品的任何阶段，您遇到的任何问题，均可以通过拨打我们的热线电话400-668-6834，或者技术支持邮箱tech@selleck.cn，直接联系到我们。我们会在24小时内尽快联系您。
如果有其他问题，请给我们留言。
常见问题及建议解决方法
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问题 1：
what’s the difference between S1021 and S7782? Which one is better for in vivo studies?
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回答：
Usually, hydrate will be more stable and dissolve better than free base. But this compound (S1021) dissolves better in DMSO than hydrate one (S7782).
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问题 2：
Can I give dasatinib to mice by oral gavage? If so, how to dissolve the drug?
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回答：
Our S1021 Dasatinib in 1% DMSO+30% PEG 300+1% Tween 80 at 30 mg/ml is a suspension which you can administrate to mice via oral gavage. If you want a clear solution, it can be dissolved in 4% DMSO+30% PEG 300+5% Tween 80+ddH2O at 5 mg/ml clearly.
