产品说明书
IMR-1A
 |
同义名 : | - |
| CAS号 : | 331862-41-0 | |
| 货号 : | A253283 | |
| 分子式 : | C13H11NO5S2 | |
| 纯度 : | 99%+ | |
| 分子量 : | 325.36 | |
| MDL号 : | MFCD04083080 | |
| 存储条件： |
粉末 Inert atmosphere,2-8°C 液体 -20°C:3-6个月-80°C:12个月 |
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| 溶解度 : |
DMSO: 2 mg/mL(6.15 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO |
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| 动物实验配方： |
| 生物活性 | |||
|---|---|---|---|
| 描述 | Aberrant activation of the Notch pathway plays a key role in initiation, development, and metastasis of cancers. The inhibitor of mastermind recruitment-1 (IMR-1) is a small-molecule inhibitor of the Notch transcriptional activation complex with an IC50 value of 26μM. IMR-1A is the acid metabolite of IMR-1, exhibiting 50-fold higher potency for Notch than IMR-1, with an IC50 value of 0.5μM. IMR-1A also showed significantly higher affinity to the intracellular domain of Notch (NICD) than IMR-1 (KD: 2.9±0.6μM vs. 11±3μM). Treatment of Notch-dependent cell lines OE33 and 786-0 with IMR-1 (25μM) inhibited Notch-directed transcriptional activation via blocking the occupancy of Maml1 to the Notch transcriptional activation complex, without changing the level of NICD in cells. IMR-1 at a dosage of 15mg/kg blocked tumor establishment in nude mice inoculated with OE19 human esophageal adenocarcinoma cells. In patient-derived esophageal adenocarcinoma xenograft (PDX) models, IMR-1 treatment at 15mg/kg significantly abrogated tumor growth and reduced the expression of Notch target genes compared with DMSO-treated controls[3]. | ||
| 实验方案 | |||
|---|---|---|---|
| 1mg | 5mg | 10mg | |
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1 mM 5 mM 10 mM |
3.07mL 0.61mL 0.31mL |
15.37mL 3.07mL 1.54mL |
30.74mL 6.15mL 3.07mL |
| 参考文献 |
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