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AAPK-25 是选择性的Aurora/PLK 激酶双重抑制剂,显示出抗肿瘤活性。它可造成有丝分裂延迟并阻滞前中期细胞,通过生物标志物组蛋白 H3Ser10磷酸化反应,导致细胞凋亡激增。


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AAPK-25 是选择性的Aurora/PLK 激酶双重抑制剂,显示出抗肿瘤活性。它可造成有丝分裂延迟并阻滞前中期细胞,通过生物标志物组蛋白 H3Ser10磷酸化反应,导致细胞凋亡激增。
| 规格 | 价格 | 库存 | 数量 |
|---|---|---|---|
| 1 mg | ¥ 749 | In stock | |
| 5 mg | ¥ 1,850 | In stock | |
| 10 mg | ¥ 2,780 | In stock | |
| 25 mg | ¥ 4,550 | In stock | |
| 50 mg | ¥ 6,380 | In stock | |
| 100 mg | ¥ 8,580 | In stock | |
| 200 mg | ¥ 11,600 | In stock | |
| 1 mL x 10 mM (in DMSO) | ¥ 1,780 | In stock |
AAPK-25 相关产品
| 产品描述 | AAPK-25, a potent and selective dual inhibitor of Aurora/PLK, causes mitotic delay and cell arrest in prometaphase, via phosphorylation of the biomarker histone H3Ser10, followed by a surge in apoptosis. AAPK-25 targets Aurora A, Aurora B, and Aurora C with Kd values ranging from 23-289 nM, and PLK1, PLK2, and PLK3 with Kd values ranging from 55-456 nM. AAPK-25 has antitumor activity. |
| 靶点活性 | ERK:5.32 μM (kd), Aurora C:289 nM (kd), PI3K:7.11 μM (kd), CDK:8.02 μM , PLK2:272 nM (kd), PLK1:55 nM (kd), Aurora B:78 nM (kd), Aurora A:23 nM (kd), PLK3:456 nM (kd) |
| 体外活性 | AAPK-25抑制HCT-116、Calu6、A549和MCF-7细胞增长(IC50s分别为0.4、5.3、11.6和2.3 μM)。在HCT-116细胞系中,AAPK-25按剂量依赖性诱导凋亡。AAPK-25显著增加组蛋白H3Ser10的磷酸化,表明明显的有丝分裂阻塞。AAPK-25对有丝分裂纺锤体检查点具有显著抑制作用。 |
| 体内活性 | AAPK-25在BALB/c裸鼠肿瘤异种移植模型中提高了存活率。 |
| 分子量 | 442.32 |
| 分子式 | C21H13Cl2N3O2S |
| CAS No. | 2247919-28-2 |
| Smiles | Clc1ccc(cc1Cl)C(=O)Nc1ccc2cc(ccc2c1)C(=O)Nc1nccs1 |
| 密度 | 1.536 g/cm3 (Predicted) |
| 颜色 | White |
| 物理性状 | Solid |
| 存储 | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature. | |||||||||||||||||||||||||||||||||||
| 溶解度信息 | DMSO: 50 mg/mL (113.04 mM), Sonication is recommended. | |||||||||||||||||||||||||||||||||||
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