| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
Cell lines | HL-60, U937 and NB-4 cells |
Preparation method | The solubility of this compound in DMSO is > 12.5 mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 ℃ for several months. |
Reacting condition | 0, 30, 60, 100 and 150 μM; 72 hrs |
Applications | All AML cell lines (HL-60, U937 and NB-4) were sensitive to 10058-F4 in a dose-dependent manner. At the dose of 100 μM, 10058-F4 significantly induced apoptosis of AML cell after the 72-hr treatment. In addition, 10058-F4 decreased levels of c-Myc proteins in all AML cell lines. |
Animal models | SCID mice bearing DU145 or PC-3 human prostate cancer xenografts |
Dosage form | 20 or 30 mg/kg; i.v.; q.d., 5 days per week, for 2 weeks |
Applications | In mice bearing PC-3 xenografts, intravenous treatment with 20 or 30 mg/kg 10058-F4 resulted in the maximum mean %TC values of 72.3 and 72.9%, respectively. Similarly, in mice bearing DU145 xenografts, 30 mg/kg 10058-F4 resulted in a maximum mean %TC value of 85%. 10058-F4 showed lack of effect in both models. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| 产品描述 | 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: |
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