| 產(chǎn)品描述： | Fimepinostat (CUDC-907) potently inhibits class I PI3Ks as well as classes I and II HDAC enzymes with an IC50 of 19/54/39 nM and 1.7/5.0/1.8/2.8 nM for PI3Kα/PI3Kβ/PI3Kδ and HDAC1/HDAC2/HDAC3/HDAC10 , respectively. |
| 靶點(diǎn)： |
PI3Kα:19 nM (IC50);PI3Kβ:54 nM (IC50);PI3Kδ:39 nM (IC50);PI3Kγ:311 nM (IC50);HDAC1:1.7 nM (IC50);HDAC2:5 nM (IC50);HDAC3:1.8 nM (IC50);HDAC4:409 nM (IC50);HDAC5:674 nM (IC50);HDAC6:27 nM (IC50);HDAC7:426 nM (IC50);HDAC8:191 nM (IC50);HDAC9:554 nM (IC50);HDAC10:2.8 nM (IC50);HDAC11:5.4 nM (IC50);Apoptosis;PI3K;HDAC |
| 體內(nèi)研究： |
Oral administration of Fimepinostat inhibits growth of the Daudi cancer cell xenografts in a dose-dependent manner. Tumor stasis is observed at 100 mg/kg in this model without obvious toxicity. Importantly, in the same model, Fimepinostat achieves better efficacy than GDC-0941, SAHA, or a combination of these 2 compounds given at their maximal tolerated doses (MTD). Furthermore, Fimepinostat causes tumor regression or stasis after intravenous (50 mg/kg) or oral administration (100 mg/kg) in a xenograft tumor model of SU-DHL4 diffuse large B-cell lymphoma (DLBCL) and causes tumor stasis in KRAS-mutant A549 NSCLC cell xenografts |
| 參考文獻(xiàn)： |
1. Qian C, et al. Cancer network disruption by a single molecule inhibitor targeting both histone deacetylase activity and phosphatidylinositol 3-kinase signaling. Clin Cancer Res. 2012 Aug 1;18(15):4104-13. |
| 溶解性： |
DMSO : 50 mg/mL (98.32 mM; Need ultrasonic) DMF : 5 mg/mL (9.83 mM; Need ultrasonic) |
| 保存條件： |
-20℃ |
| 配置溶液濃度參考： |
|
1mg |
5mg |
10mg |
| 1 mM |
1.966 ml |
9.832 ml |
19.664 ml |
| 5 mM |
0.393 ml |
1.966 ml |
3.933 ml |
| 10 mM |
0.197 ml |
0.983 ml |
1.966 ml |
| 50 mM |
0.039 ml |
0.197 ml |
0.393 ml |
|
| 注意： |
部分產(chǎn)品我司僅能提供部分信息，我司不保證所提供信息的權(quán)威性，僅供客戶參考交流研究之用。 |
上海工商
危險品化學(xué)品經(jīng)營許可證（不帶存儲）
營業(yè)執(zhí)照(三證合一)
北京