| 貨號 | 規(guī)格 | 價格 | 上海 | 北京 | 武漢 | 南京 | 購買數(shù)量 |
|---|---|---|---|---|---|---|---|
S84275-5mg |
≥99% | ￥800.00 | 貨期：2-3天 | - | - | - |
|
S84275-10mg |
≥99% | ￥1400.00 | 貨期：2-3天 | - | - | - |
|
S84275-25mg |
≥99% | ￥2800.00 | 貨期：2-3天 | - | - | - |
|
S84275-50mg |
≥99% | ￥4500.00 | 貨期：2-3天 | - | - | - |
|
S84275-100mg |
≥99% | ￥7200.00 | 貨期：2-3天 | - | - | - |
|
APS-2-79 is a KSR-dependent MEK antagonist. APS-2-79 inhibits ATPbiotin binding to KSR2 within the KSR2-MEK1 complexe with an IC50 of 120 nM. APS-2-79 makes the stabilization of the KSR inactive state antagonizes oncogenic Ras-MAPK signaling
| 產(chǎn)品描述： | APS-2-79 is a KSR-dependent MEK antagonist. APS-2-79 inhibits ATPbiotin binding to KSR2 within the KSR2-MEK1 complexe with an IC50 of 120 nM. APS-2-79 makes the stabilization of the KSR inactive state antagonizes oncogenic Ras-MAPK signaling | ||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 靶點(diǎn)： | KSR2:120 nM (IC50);MEK1;MEK;?MAPK | ||||||||||||||||||||
| 體外研究： | APS-2-79 (5 μM) suppresses KSR-stimulated MEK and ERK phosphorylation in 293H cells. APS-2-79 (1 μM) enhances the efficacy of the clinical MEK inhibitor trametinib within cancer cell lines containing K-Ras mutations | ||||||||||||||||||||
| 參考文獻(xiàn)： | 1. Dhawan NS, et al. Small molecule stabilization of the KSR inactive state antagonizes oncogenic Ras signalling. Nature. 2016 Aug 24;537(7618):112-116. | ||||||||||||||||||||
| 溶解性： | Soluble in DMSO | ||||||||||||||||||||
| 保存條件： | -20℃ | ||||||||||||||||||||
| 配置溶液濃度參考： |
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| 注意： | 部分產(chǎn)品我司僅能提供部分信息，我司不保證所提供信息的權(quán)威性，僅供客戶參考交流研究之用。 |
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北京