| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 200mg | 电议 |
Cell lines | HO-8910 cells |
Preparation Method | HO-8910 cells were treated with different concentrations of Hsp90 inhibitor 17-AAG, and cells treated without 17-AAG were regarded as the control group. |
Reaction Conditions | 17-AAG 0.25、0.5 and 5 μM for 4, 8, 12, and 24 h |
Applications | The levels of Rad50 and Ku80 decreased after 8 h in cells treated with relative low concentration of 17-AAG (0.5 μM). In the groups treated with relative high concentration of 17-AAG (5 μM), Rad50 significantly decreased after 4 h, and Ku80 also decreased after 8 h, indicating that DSBs repair proteins were downregulated in a dose and time-depend manner and Hsp90 inhibition could affect DSBs repair. |
Animal models | Female 4–5weeks old, 18–20 g BALB/c nude mice |
Preparation Method | The mice were randomly assigned to three groups (n = 4/group). The luciferase-expressing HO-8910 cells were injected intraperitoneally into groups. After two weeks, mice were intraperitoneally injected with DDP, DDP combined with 17-AAG (50 mg/kg),once a week for up to 6 weeks. |
Dosage form | 50 mg/kg, once a week for up to 6 weeks |
Applications | A combination of 17-AAG and DDP could inhibit tumor growth more efficiently, The survival time of the mice was significantly prolonged, supporting the notion that 17-AAG combined with DDP could prolong the survival time of mice. |
| 产品描述 | 17-AAG(Geldanamycin), a natural benzoquinone ansamycin antibiotic, is the first established inhibitor of Hsp90. It inhibits Hsp90's ATPase function through binding to its amino-terminal domain[5]. 17-AAG as a potent HSP90 inhibitor with an IC50value of 6 nM in BT474 cells, inhibited the binding of HSP90 to HIF-1α[2]. In a concentration- and time-dependent manner, inhibition of Hsp90 by 17-AAG decreased Akt and eNOS expression. Inhibition of eNOS expression by 17-AAG occurred at the transcriptional level. Furthermore, treatment with 17-AAG decreased basal and vascular endothelial growth factor-stimulated Akt and eNOS phosphorylation. This corresponded with decreased NO production and inhibition of endothelial cell migration and angiogenesis[3].17AAG topically applied to mouse skin, inhibits UVR-induced development of cutaneous squamous cell carcinoma (SCC)[7]. Therapeutic potential of 17-AAG was investigated using nude mice intraperitoneal xenograft. A combination of 17-AAG and DDP could inhibit tumor growth more efficiently, The survival time of the mice was significantly prolonged, supporting the notion that 17-AAG combined with DDP could prolong the survival time of mice[1].17-AAG is able to inhibit the growth of both human glioma cell lines and glioma stem cells in vitro . In addition, 17-AAG can inhibit the growth of intracranial tumors and can synergize with radiation both in tissue culture and in intracranial tumors. This compound was not found to synergize with temozolomide in any of our models of gliomas[6].17-AAG plus trastuzumab is well tolerated and has antitumor activity in patients with HER-2+breast cancer whose tumors have progressed during treatment with trastuzumab. These data suggest that Hsp90 function can be inhibited in vivo to a degree sufficient to cause inhibition of tumor growth[4]. References: |
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