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1395347-24-6

中文名稱 1395347-24-6
英文名稱 ISA-2011B
CAS 1395347-24-6
分子式 C22H18ClN3O4
分子量 423.85
MOL 文件 1395347-24-6.mol
更新日期 2024/11/15 18:20:34
1395347-24-6 結(jié)構(gòu)式 1395347-24-6 結(jié)構(gòu)式

基本信息

中文別名
PIP5KΑ抑制劑(ISA-2011B)
英文別名
ISA-2011B
ISA2011B
ISA 2011B
5H-1,3-Dioxolo[4,5-g]pyrazino[1,2-b]isoquinoline-7,10-dione, 5-(5-chloro-1H-indol-3-yl)-8,9,10a,11-tetrahydro-9-methyl-, (5S,10aS)-

物理化學(xué)性質(zhì)

沸點(diǎn)714.9±60.0 °C(Predicted)
密度1.58±0.1 g/cm3(Predicted)
儲(chǔ)存條件-20°C儲(chǔ)存
溶解度DMSO:100.0(Max Conc. mg/mL);235.93(Max Conc. mM)
酸度系數(shù)(pKa)15.58±0.30(Predicted)
形態(tài)Solid
顏色White to off-white
1395347-24-6價(jià)格(試劑級(jí))
報(bào)價(jià)日期產(chǎn)品編號(hào)產(chǎn)品名稱CAS號(hào)包裝價(jià)格
2026/06/05HY-169371395347-24-6
ISA-2011B
1395347-24-61mg1100元
2026/06/05HY-169371395347-24-6
ISA-2011B
1395347-24-65mg2400元
2026/06/05HY-169371395347-24-6
ISA-2011B
1395347-24-610mM * 1mLin DMSO2640元

常見問題列表

生物活性
ISA-2011B是PIP5K1α的抑制劑, 具有抗癌活性。
體外研究

The proliferation rate of PC-3 cells after treatment with ISA-2011B at 10, 20, and 50 μM is significantly reduced to 58.77%, 48.65%, and 21.62% of vehicle-treated controls, respectively. ISA-2011B exhibits the highest binding affinity to PIP5K1α, and to MAP/microtubule affinity-regulating kinase 1 and 4 (MARK1 and MARK4) across 460 kinases. ISA-2011B treatment inhibits PIP5K1α expression by 78.6% in PC-3 cells. ISA-2011B leads to a remarkable reduction in AR-V7 and CDK1 in both nucleus and cytoplasm of 22Rv1 cells. ISA-2011B treatment also abolishes AR expression in the nucleus, without depleting the cytoplasmic AR.

體內(nèi)研究

ISA-2011B significantly inhibits growth of tumor cells in xenograft mice, and is mediated by targeting PIP5K1α-associated PI3K/AKT and the downstream survival, proliferation, and invasion pathways. Overexpression of AR-V7 increases PIP5K1α, promotes rapid growth of PCa in xenograft mice, whereas inhibition of PIP5K1α by its inhibitor ISA-2011B suppresses the growth and invasiveness of xenograft tumors overexpressing AR-V7. ISA-2011B disrupts protein stabilization of AR-V7 which is dependent on PIP5K1α, leading to suppression of invasive growth of AR-V7-high tumors in xenograft mice.

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