BO-264
产品说明书
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同义名 : | - |
| CAS号 : | 2408648-20-2 | |
| 货号 : | A1262988 | |
| 分子式 : | C18H19N5O3 | |
| 纯度 : | 99%+ | |
| 分子量 : | 353.375 | |
| MDL号 : | MFCD32671323 | |
| 存储条件： |
Pure form Inert atmosphere,Room Temperature In solvent -20°C:3-6个月-80°C:12个月 |
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| 溶解度 : |
DMSO: 50 mg/mL(141.49 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO |
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| 描述 | TACC3 (transforming acidic coiled-coil 3), a transforming acidic coiled-coil (TACC) family member, is frequently upregulated in a broad spectrum of cancers, including breast cancer. It plays critical roles in protecting microtubule stability and centrosome integrity that is often dysregulated in cancers. BO-264 is a potential TACC3 inhibitor having an IC50 of 188 nM. Treatment of JIMT-1 cells with 1 μM BO-264 for 6 hours has led to a considerable stabilization of the cellular TACC3 upon increased temperatures. BO-264 inhibited the viability of basal (MDA-MB-231, MDA-MB-436, CAL51, and HCC1143) and HER2+ (JIMT-1 and HCC1954) breast cancer cell lines at lower doses compared with luminal A (MCF-7, T-47D, and ZR-75-1) and luminal B (BT-474) breast cancer cell lines. Similarly, a significantly lower average colony number of JIMT-1 cells was seen upon treatment with BO-264 for 12 days. Despite a relatively lower sensitivity to TACC3 inhibition in RT4 cells, BO-264 yielded the lowest IC50 value in both models (two human urinary bladder cancer cell lines, RT112 and RT4) as compared with SPL-B and KHS101 (other TACC3 inhibitors), suggesting BO-264 might be a highly relevant therapeutic opportunity to target FGFR3–TACC3 fusion-harboring tumors. Moreover, BO-264 decreased ERK1/2 phosphorylation, which is a marker for activated FGFR signaling along with a strong mitotic arrest at minimum 10× lower doses than other TACC3 inhibitors, suggesting that BO-264 specifically blocks the function of FGFR3–TACC3 fusion protein. BO-264 exhibited a remarkable anticancer activity against more than 90% of the cell lines representing nine different subpanels with GI50 values less than 1 μM. siTACC3-induced mitotic arrest, apoptosis, and DNA damage were fully recapitulated by BO-264 in a dose-dependent manner. Furthermore, treatment of JIMT-1 cells with BO-264 for 48 hours induced a prominent increase (from 4.1% to 45.6%) in the fraction of apoptotic cells[1]. | ||
| 实验方案 | |||
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| 1mg | 5mg | 10mg | |
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1 mM 5 mM 10 mM |
2.83mL 0.57mL 0.28mL |
14.15mL 2.83mL 1.41mL |
28.30mL 5.66mL 2.83mL |
| 参考文献 |
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