CAS NO: | 75747-14-7 |
规格: | 98% |
分子量: | 585.7 |
包装 | 价格(元) |
10mg | 电议 |
50mg | 电议 |
100mg | 电议 |
200mg | 电议 |
Background:
17-AAG is a potent inhibitor of HSP90 with IC50 value of 6 nM in BT474 cells [1].
17-AAG is a synthetic analogue developed from geldanamycin which was found to have significant hepatic toxicity. 17-AAG has an improved toxicity profile and has no hepatic toxicity. 17-AAG can bind to HSP90 and destabilize the client proteins such as HER2, Raf-1, p53 and MAPK signaling. In Multiple myeloma (MM) cells, 17-AAG treatment inhibited cell proliferation and survival. The combination treatment of 17-AAG and bortezomib induced apoptosis in primary MM cells resistant to doxorubicin and bortezomib. The combination of 17-AAG and trastuzumab reduced the expression of ErbB2 in breast cancer cells overexpressing ErbB2. 17-AAG also showed efficacy in thyroid cancer cells and Hodgkin lymphoma cells. Besides that, 17-AAG was found to increased apoptosis in human melanoma xenografts. 17-AAG is now in phase II clinical studies [2].
参考文献:
[1] Kamal A, Thao L, Sensintaffar J, et al. A high-affinity conformation of Hsp90 confers tumour selectivity on Hsp90 inhibitors[J]. Nature, 2003, 425(6956): 407-410..
[2] Dimopoulos M A, Mitsiades C S, Anderson K C, et al. Tanespimycin as antitumor therapy. Clinical Lymphoma Myeloma and Leukemia, 2011, 11(1): 17-22