SMIP004 是一种 SKP2 E3 连接酶抑制剂，可下调 SKP2 并稳定 p27。 SMIP004 是人前列腺癌细胞的癌细胞选择性凋亡诱导剂。
| Cas No. | 143360-00-3 |
| 别名 | N-(4-丁基-2-甲基苯基)乙酰胺,SMIP 004;SMIP-004 |
| 化学名 | N-(4-butyl-2-methylphenyl)acetamide |
| Canonical SMILES | CCCCC1=CC(=C(C=C1)NC(=O)C)C |
| 分子式 | C13H19NO |
| 分子量 | 205.3 |
| 溶解度 | ≥ 20.5 mg/mL in DMSO, ≥ 53.6 mg/mL in EtOH with ultrasonic |
| 储存条件 | Store at -20℃ |
| 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
All other available size: ship with RT , or blue ice upon request |
| 产品描述 | IC50 Value: 1.09 uM (MTT assay in LNCaP-S14 cells) [1]
SMIP004 (N-(4-butyl-2-methyl-phenyl) acetamide) is a novel inducer of cancer-cell selective apoptosis of human prostate cancer cells. Unlike SMIP001, SMIP004 was found to downregulate SKP2 and to stabilize p27, although neither SMIP is a proteasome inhibitor.
in vitro: Whereas SMIP012 and 016 were moderately toxic in normal fibroblasts, SMIPs 001 and 004 showed substantial cancer cell specificity being at least five times more potent in LNCaP-S14 than in IMR90 cells , treatment with either MG132 or SMIP004 increased p27 half-life to > 6 h [1]. Both SMIP001 and 004 led to a strong increase in the recruitment of p27 to CDK2, while SMIP001 also slightly increased coprecipitation of p21 (Figure 6c). SMIP004 also reduced the amounts of cyclins E and A retrieved with CDK2. This was paralleled by a marked downregulation of cyclins E and A upon SMIP004 treatment. SMIP004 decreased the levels of positive cell cycle regulators, upregulated cyclin-dependent kinase inhibitors, and resulted in G1 arrest, inhibition of colony formation in soft agar, and cell death [2].
in vivo: SMIP004 potently inhibits the growth of prostate and breast cancer xenografts in mice [2].
Clinical trial: N/A |
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