13585831301
021-59541103 021-60443211
3004967995
13585831301021-59541103 021-604432113004967995
聯系人:高小姐
電話:021-59541103 021-60443211
手機:13585831301
Q Q： 3004967995
Email:3004967995@qq.com
詳細地址：上海嘉定區嘉羅公路1661
化學性質：
| 規格 | 250mg 500mg |
| CAS | 845932-30-1 |
| 別名 | N/A |
| 化學名 | N/A |
| 分子式 | C29H32N4O4S2 |
| 分子量 | 564.72 |
| 溶解度 | Soluble in DMSO |
| 儲存條件 | Store at -20°C |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
| Shipping Condition | Evaluation sample solution : ship with blue ice |
產品描述：
KU 59403 is a potent ATM inhibitor, with an IC50 of 3 nM.
KU 59403 is a novel ATM inhibitor developed from LY294002, which is more potent against ATM than the previous lead KU 55933 (IC50=3 nM vs 13 nM), and has at least 1000 times greater specificity for ATM over other members of the PI3K family tested. KU 59403 is an effective chemosensitiser at a concentration of 1 μM. KU 59403 alone is not significantly cytotoxic to LoVo or SW620 cells (88±7% and 91±6% survival, respectively) but it enhances camptothecin cytotoxicity in both cell lines with greater enhancement being observed in the LoVo compared to the SW620 cells. KU 59403 also significantly enhances the cytotoxicity of fixed concentrations of etoposide (0.1 and 1 μM) or doxorubicin (10 or 100 nM) in these cell lines, with greater enhancement of etoposide in SW620 cells and of doxorubicin in LoVo cells. KU 59403 (1 μM) enhances etoposide (1 μM) cytotoxicity to a similar extent in HCT116 and HCT116-N7 cells, and in the p53 mutant SW620 cells and human breast cancer cell line, MDAMB-231, sensitisation is 11.9±4.7 and 3.8±1.8-fold respectively. Inhibition of IR-induced ATM activity by KU 59403 (1 μM) is approximately 50% in MDA-MB231 cells and >50% in HCT116 cells that have low ATM expression and activity[1].
Tumours in control mice reach 4 times their starting volume (RTV4) at a median time of 6.5 days. Treatment with etopophos alone causes a modest tumour growth delay of 4 days (time to RTV4=10.5 days). This delay is extended to 8.5 days when given with KU 59403 at 12.5 mg/kg i.p. twice daily for 5 days and 11.5 days (time to RTV4=18 days) when given with KU 59403 at 25 mg/kg i.p. twice daily for 5 days. This latter treatment is the most effective dosing schedule for KU 59403 identified; increasing etopophos efficacy by 190%. In contrast, when KU59403 is administered 4 hours after etopophos administration there is no increase in efficacy compared with etopophos alone. In the above studies, neither KU 59403 nor etopophos given as a single agent caused any measurable toxicity and the combination of drugs did not cause unacceptable toxicity. However, the etopophos-induced tumour growth delay is extended to 8.5 days by co-administration of KU 59403, representing a 300% enhancement of etopophos activity that was statistically significant. Toxicity, as measured by body weight loss, is tolerable and transient. In this study irinotecan alone causes an initial modest regression of the SW620 tumour followed by rapid re-growth resulting in a tumour growth delay of 7.5 days, which is extended to 19.5 days by the co-administration of KU 59403. As is clearly indicated from these data, enhancement of the efficacy of etopophos can be obtained in the SW620 and HCT116 xenograft models, and of irinotecan in the SW620 model, by combination with KU 59403 with little enhancement of toxicity[1].
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原創作者：上海莼試生物技術有限公司
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普票匯款信息
賬 戶 名：上海生物
開 戶 行：中國銀行山東省分行營業部
賬 號：2169 2341 6278
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