S80284 |
CUDC-907 |
源葉(MedMol) | 98% |
- 提示:詳情請下載說明書。
- 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。
輸入產(chǎn)品批號:
本計算器可幫助您計算出特定溶液中溶質(zhì)的質(zhì)量、溶液濃度和體積之間的關(guān)系,公式為:
質(zhì)量 (mg) = 濃度 (mM) x 體積 (mL) x 分子摩爾量 (g/mol)