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10058-F4

现货
Catalog No.
A1169
C-Myc-Max二聚化抑制剂
组合的产品项目
规格价格库存 数量
10mM (in 1mL DMSO)
¥ 550.00
现货
5mg
¥ 450.00
现货
10mg
¥ 700.00
现货
50mg
¥ 2,200.00
现货

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Background

10058-F4 is a novel small-molecule inhibitor of c-Myc. 10058-F4 prevented the binding of c-Myc/Max dimers to its DNA targets, inhibited leukemic proliferation, and induced apoptosis through mitochondrial pathway, such as downregulation of Bcl-2, upregulation of Bax and release of cytoplasmic cytochrome C. [1]

10058-F4 blocks the C-MYC/Max heterodimerization which is required for c-Myc activity as a transcription factor. 10058-F4 efficiently inhibits the induction of PGC-1β mRNA by both HRG and IGF-1 and also abolishes the induction of PGC-1β protein levels by HRG and IGF-1, confirming that the induction of PGC-1b protein by these growth factors is a transcriptional event requiring C-MYC activity.[2] 10058-F4 acts not only to block c-Myc function through the mechanism of c-Myc/Max heterodimer dissociation, but it also resulted in decreased c-Myc mRNA levels (65%, n = 3) in lymphoma cells.[3]

References:
[1] Huang MJ, Cheng YC, Liu CR, Lin SF, Liu H. E. A small-molecule c-Myc inhibitor, 10058-F4, induces cell-cycle arrest, apoptosis, and myeloid differentiation of human acute myeloid leukemia. Experimental Hematology. 2006; 34: 1480–1489.
[2] Ching-yi Chang, Dmitri Kazmin, Jeff S. Jasper, Rebecca Kunder, William J. Zuercher, Donald P. McDonnell. The Metabolic Regulator ERRα, a Downstream Target of HER2/IGF-1R, as a Therapeutic Target in Breast Cancer. Cancer Cell. 18 October 2011. 20(4): 500-510.
[3] Ilsa Gomez-Curet, R. Serene Perkins, Ryan Bennett, Katherine L. Feidler, Stephen P. Dunn, Leslie J. Krueger. c-Myc inhibition negatively impacts lymphoma growth. Journal of Pediatric Surgery. January 2006. 41(1): 207-211.

Chemical Properties

Physical AppearanceA solid
StorageStore at -20°C
M.Wt249.35
Cas No.403811-55-2
FormulaC12H11NOS2
Solubility≥24.9mg/mL in DMSO
Chemical Name(5E)-5-[(4-ethylphenyl)methylidene]-2-sulfanylidene-1,3-thiazolidin-4-one
SDFDownload SDF
Canonical SMILESCCC1=CC=C(C=C1)C=C2C(=O)NC(=S)S2
运输条件试用装:蓝冰运输。 其他可选规格:常温运输或根据您的要求用蓝冰运输。
一般建议为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。

试验操作

细胞实验 [1]:

细胞系

HL-60、U937和NB-4细胞

制备方法

在DMSO中的溶解度大于12.5 mg/mL。若配制更高浓度的溶液,一般步骤如下:请将试管置于37 °C加热10分钟和/或将其置于超声波浴中震荡一段时间。原液于-20 °C可放置数月。

反应条件

0、30、60、100和150 μM;72小时

实验结果

10058-F4呈剂量依赖性地作用于所有AML细胞系(HL-60、U937和NB-4)。在100 μM的剂量下,经72小时处理后,10058-F4显著诱导AML细胞凋亡。此外,在所有AML细胞系中,10058-F4降低了c-Myc蛋白水平。

动物实验 [2]:

动物模型

携带DU145或PC-3人类前列腺癌异种移植物的SCID小鼠

给药剂量

20或30 mg/kg;静脉注射;每日1次,每周5日,持续2周

实验结果

在携带PC-3异种移植物的小鼠中,静脉注射20或30 mg/kg 10058-F4,最大平均%TC值分别为72.3%和72.9%。相似地,在携带DU145异种移植物的小鼠中,30mg/kg 10058-F4相应的最大平均%TC值为85%。在上述2个模型中,10058-F4效果微弱。

注意事项

请于室内测试所有化合物的溶解度。虽然化合物的实际溶解度可能与其理论值略有不同,但仍处于实验系统误差的允许范围内。

References:

[1]. Huang MJ, Cheng YC, Liu CR, Lin SF, Liu H. E. A small-molecule c-Myc inhibitor, 10058-F4, induces cell-cycle arrest, apoptosis, and myeloid differentiation of human acute myeloid leukemia. Experimental Hematology. 2006; 34: 1480–1489.

[2]. Guo J, Parise RA, Joseph E, Egorin MJ, Lazo JS, Prochownik EV, Eiseman JL. Efficacy, pharmacokinetics, tisssue distribution, and metabolism of the Myc-Max disruptor, 10058-F4 [Z,E]-5-[4-ethylbenzylidine]-2-thioxothiazolidin-4-one, in mice. Cancer Chemother Pharmacol. 2009 Mar;63(4):615-25.

生物活性

描述 10058-F4是一种细胞通透性的c-Myc-Max二聚化小分子抑制剂。
靶点 c-Myc-Max dimerization          
IC50            

质量控制

化学结构

10058-F4