ISA-2011B

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白,专注于信号通路和疾病研究领域。

ISA-2011B  纯度: 99.94%

ISA-2011B是PIP5K1α的抑制剂, 具有抗癌活性。

ISA-2011B

ISA-2011B Chemical Structure

CAS No. : 1395347-24-6

规格 价格 是否有货 数量
10 mM * 1 mL in DMSO ¥3077 In-stock
1 mg ¥1100 In-stock
5 mg ¥3300 In-stock
10 mg ¥5000 In-stock
50 mg ¥15000 In-stock
100 mg ¥21000 In-stock
200 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

ISA-2011B 相关产品

相关化合物库:

  • Bioactive Compound Library Plus
  • Anti-Cancer Compound Library

生物活性

ISA-2011B is a PIP5K1α inhibitor with promising anticancer effects .

体外研究
(In Vitro)

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[1]. 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[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

体内研究
(In Vivo)

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[1]. 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[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

分子量

423.85

Formula

C22H18ClN3O4

CAS 号

1395347-24-6

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : 100 mg/mL (235.93 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.3593 mL 11.7966 mL 23.5933 mL
5 mM 0.4719 mL 2.3593 mL 4.7187 mL
10 mM 0.2359 mL 1.1797 mL 2.3593 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效
储备液的保存方式和期限:-80°C, 6 months; -20°C, 1 month。-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液,再依次添加助溶剂:

——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用; 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂: 0.5% CMC-Na/saline water

    Solubility: 4 mg/mL (9.44 mM); Suspended solution; Need ultrasonic

  • 2.

    请依序添加每种溶剂: 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (5.90 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (5.90 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀;向上述体系中加入50 μL Tween-80,混合均匀;然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠,完全溶解于 100 mL ddH₂O 中,得到澄清透明的生理盐水溶液

  • 3.

    请依序添加每种溶剂: 10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (5.90 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (5.90 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中,混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中,再用生理盐水定容至 10 mL,完全溶解,澄清透明
  • 4.

    请依序添加每种溶剂: 10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (5.90 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (5.90 mM,饱和度未知) 的澄清溶液,此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中,混合均匀。

*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
  • [1]. Semenas J, et al. The role of PI3K/AKT-related PIP5K1α and the discovery of its selective inhibitor for treatment of advanced prostate cancer. Proc Natl Acad Sci U S A. 2014 Sep 2;111(35):E3689-98.

    [2]. Sarwar M, et al. Targeted suppression of AR-V7 using PIP5K1α inhibitor overcomes MDV3100 resistance in prostate cancer cells. Oncotarget. 2016 Sep 27;7(39):63065-63081.

Cell Assay
[2]

Cells are grown in phenol red-free RPMI-1640 medium 24 hours and then are treated with drugs alone or in combination for 24 hours or 48 hours. MDV3100 at 5 μM or ISA-2011B at 20 μM or 50 μM final concentrations or solvent DMSO 1% is used. For treatment of 22Rv1 cells with MG132, a proteasome inhibitor, cells are treated with MG132 at 1 μM. For combination treatment of MG132 and ISA-2011B, cells are pre-treated with MG132 for 30 min at 1 μM prior to treatment of ISA-2011B[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Administration
[1]

Mice: BALB/c nude mice aged 8 to 12 wk are used in the experiments. Tumor cells are implanted into the mice. Tumor xenografts are treated with vehicle (control), RP-56976 (10 mg/kg), ISA-2011B (40 mg/kg), and RP-56976 (10 mg/kg) in combination with ISA-2011B (40 mg/kg) every second day[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

参考文献
  • [1]. Semenas J, et al. The role of PI3K/AKT-related PIP5K1α and the discovery of its selective inhibitor for treatment of advanced prostate cancer. Proc Natl Acad Sci U S A. 2014 Sep 2;111(35):E3689-98.

    [2]. Sarwar M, et al. Targeted suppression of AR-V7 using PIP5K1α inhibitor overcomes MDV3100 resistance in prostate cancer cells. Oncotarget. 2016 Sep 27;7(39):63065-63081.

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