APS-2-79 HCl
产品说明书
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同义名 : | APS-2-79 (hydrochloride); APS-2-79 HCl |
| CAS号 : | 2002381-31-7 | |
| 货号 : | A364339 | |
| 分子式 : | C23H22ClN3O3 | |
| 纯度 : | 99% | |
| 分子量 : | 423.89 | |
| MDL号 : | - | |
| 存储条件： |
Pure form Keep in dark place, inert atmosphere, room temperature In solvent -20°C:3-6个月-80°C:12个月 |
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| 溶解度 : | - | |
| 动物实验配方： |
| 生物活性 | |||
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| 描述 | The RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathways have been identified as promising therapeutic targets for cancer therapy. Over-activation of these pathways and their components including gene mutations has been considered as one of the major causes of melanoma. Mitogen-activated protein kinase (MEK) is a downstream kinase of RAS pathway found in two different forms MEK1/2[2]. APS-2-79 hydrochloride behaves as a kinase suppressor of Ras (KSR)-dependent antagonist of RAF-mediated MEK phosphorylation. APS-2-79 binds directly to KSR2 within the KSR2-MEK1 complex with an IC50 of 120 ± 23 nM for KSR2[3]. APS-2-79 (1 μM) shifts the cell viability dose response to Trametinib in Ras-mutant cell lines HCT-116 and A549, but not BRAF mutant cell lines SK-MEL-239 and A375. Although the cellular effects of APS-2-79 alone are modest, combination analysis over full concentration matrices reveal that kinase suppressor of Ras (KSR)-inactive state (KSRi) synergizes with Trametinib, and other MEK inhibitors, specifically in KRAS mutant cell lines. APS-3-77, and additional control compounds, do not demonstrate Ras-mutant-specific synergy, supporting the hypothesis that the enhanced activity of Trametinib when combined with APS-2-79 depends on co-modulation of KSR[3]. | ||
| 实验方案 | |||
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| 1mg | 5mg | 10mg | |
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1 mM 5 mM 10 mM |
2.36mL 0.47mL 0.24mL |
11.80mL 2.36mL 1.18mL |
23.59mL 4.72mL 2.36mL |
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