| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
Cell lines | HCT116 colon cancer cells |
Preparation method | The solubility of this compound in DMSO is > 10 mM. 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 | 24 h |
Applications | In HCT116 colon cancer cells, treated with various doses of HBX 41,108 (1, 3, and 10 μmol/L) for 24 h increased p53 levels in a nongenotoxic manner. HBX 41,108 inhibited USP7 activity in HEK293 cells transfected with USP7. HBX 41,108 (0.1-10 μM, 24 h) inhibited HCT116 cancer cell growth and induced apoptotic cell death. HBX 41,108 induced p53-dependent apoptosis in p53 wild-type and null isogenic cancer cell lines. In COS7 cells, HBX 41108 inhibited PPARγ stability induced by USP7 and decreased the basal transcriptional activity of PPARγ by 70%。 |
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 | HBX 41108 is a potent inhibitor of USP7 with IC50 value of 424 nM [1]. Ubiquitin-specific-processing protease 7 (USP7) is a ubiquitin specific protease and removes ubiquitin from specific protein substrates. USP7 can deubiquitinate p53, protecting p53 from Mdm2-mediated degradation and involving the oncogenic stabilization of p53. HBX 41108 is an uncompetitive and reversible USP7 inhibitor. HBX 41108 inhibited USP7-mediated p53 deubiquitination with IC50 value of 0.8 μM in a dose-dependent way and was only weakly active against the aspartic, serine and metalloproteases tested with IC50 > 10 μM. In HCT116 cells, HBX 41108 increased the levels of p53 and p21cip1/waf, which was the product of p53 target genes. In HEK293 cells, HBX 41108 increased the level of polyubiquitinated forms of p53 and reduced Mdm2 levels. In HCT116 colon cancer cells, HBX 41108 inhibited cell proliferation with IC50 value of 1 μM in a dose-dependent way and induced apoptosis in a dose-dependent manner [1]. In COS7 cells, HBX 41108 inhibited PPARγ stability induced by USP7 and decreased the basal transcriptional activity of PPARγ by 70% [2]. References: |
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