| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 200mg | 电议 |
Cell lines | Small-cell lung cancer (SCLC) cell (NCI-H889, NCI-H1963, NCI-H1417, NCI-H146, NCI-187, DMS79, NCI-1048, NCI-H82, NCI-H196, H69AR, and DMS114) lines. |
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. |
Reaction Conditions | 48 h; 10 μM |
Applications | The ability of ABT-737 to inhibit cell proliferation with single-agent activity was evaluated against a panel of 11 kinds of SCLC cell lines. Ac-DEVD-AMC, a substrate for activated caspase 3, was used to treatment of H146 cells for 24 h. A dose-dependent increase in apoptosis coincided with a dose-dependent decrease in cell viability following ABT-737 treatment suggesting that ABT-737 inhibits cell proliferation through the induction of apoptosis. |
Animal models | Lymphoma-prone Eμ- myc transgenic mice |
Dosage form | 75 mg/kg body weight; the tail injection. |
Applications | All B-lymphoid subsets in the ABT-737-treatment (75 mg/kg) cohort were significantly decreased, compared with the vehicle-treated animals, in both the bone marrow and the spleen. Eμ- myc animals treated with ABT-737 contained significantly (**P |
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 | ABT-737 is a novel and potent inhibitor of B-cell lymphoma 2 (BCL-2) family proteins, which are critical for cell survival and overexpressed in many tumor cells, with high affinity towards BCL-XL, BCL-2, and BCL-w but no affinity towards less homologous proteins, such as BCL-B, MCL-1, and A1. ABT-737 has shown single-agent activity against lymphoma and small-cell lung cancer as well as substantial antimyeloma activity bothin vitroandin vivo. In recent studies, acute myeloid leukemia blast, origenitor, and stem cells are effectively killed by ABT-737 with normal hematopoietic cells intact. The disruption of the BCL-2/BAX complex and BAK-dependent but BIM-independent activation of the intrinsic apoptotic pathway could also be induced by ABT-737. Reference [1].Marina Konopleva, Rooha Contractor, Twee Tsao, Ismael Samudio, Peter P. Ruvolo, Shinichi Kitada, Xingming Deng, Dayong Zhai, Yue-Xi Shi, Thomas Sneed, Monique Verhaegen, Maria Soengas, Vivian R. Ruvolo, Teresa McQueen, Wendy D. Schober, Julie C. Watt, Tilahun Jiffar, Xiaoyang Ling, Frank C. Marini, David Harris, Martin Dietrich, Zeev Estrov, James McCubrey, W. Stratford May, John C. Reed, and Michael Andreeff. Mechanisms of apoptosis sensitivity and resistance to the BH3 mimetic ABT-737 in acute myeloid leukemia. Cancer Cell 2006: 10; 375-388 |
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