ISA-2011B

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

ISA-2011B 是 PIP5K1α 的抑制剂，可用于抗癌研究。

ISA-2011B is an inhibitor of PIP5K1α and can be used in anticancer studies.(In Vitro):ISA-2011B treatment abolished AR expression in the nucleus, without depleting the cytoplasmic AR . The proliferation rate of PC-3 cells after treatment with ISA-2011B at 10, 20, and 50 μM is obviously reduced to 58.77%, 48.65%, and 21.62% of vehicle-treated controls, respectively. ISA-2011B leads to a remarkable reduction in AR-V7 and CDK1 in both nucleus and cytoplasm of 22Rv1 cells. ISA-2011B shows 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 .(In Vivo):In xenograft mice, ISA-2011B disrupts protein stabilization of AR-V7 which is dependent on PIP5K1α, leading to suppression of invasive growth of AR-V7-high tumors. 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 obviously suppresses the growth of tumor cells in xenograft mice and is mediated by targeting PIP5K1α-associated PI3K/AKT and the downstream survival, proliferation, and invasion pathways .

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.

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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Others

Other Targets

estrogen receptor

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1395347-24-6

423.85

C22H18ClN3O4

>98% (HPLC)

In Vitro:?DMSO : 100 mg/mL (235.93 mM)

[H][C@@]12Cc3cc4OCOc4cc3[C@H](N1C(=O)CN(C)C2=O)c1c[nH]c2ccc(Cl)cc12

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(-20℃)

With Ice Pack

≥ 2 years