2. Metabolic Enzyme/Protease PI3K/Akt/mTOR Stem Cell/Wnt TGF-beta/Smad Apoptosis
  3. Phosphodiesterase (PDE) Akt PKA mTOR Apoptosis Bcl-2 Family Caspase
  4. Kushenol Z

Kushenol Z 是一种 cAMP-PDE/Akt 抑制剂。Kushenol Z 可抑制 cAMP 磷酸二酯酶活性、升高 cAMP 水平、增强 PKA 活性，并通过减弱 Akt 和 PRAS40 的磷酸化来抑制 mTOR 通路。Kushenol Z 可通过线粒体和内质网应激通路诱导非小细胞肺癌细胞凋亡 (apoptosis)，上调 CHOP、调控 Bax/Bcl-2 比值，并激活 caspase-3/7/9/12。Kushenol Z 可用于非小细胞肺癌的相关研究。

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Kushenol Z

Kushenol Z Chemical Structure

CAS No. : 2467875-82-5

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Kushenol Z 相关抗体

Top Publications Citing Use of Products

查看 Phosphodiesterase (PDE) 亚型特异性产品:

查看所有亚型
PDE1 PDE2 PDE3 PDE4 PDE5 PDE6 PDE7 PDE9 PDE10 PDE11 PDE12 PDE8 Autotaxin

查看 Akt 亚型特异性产品:

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Akt Akt1 Akt2 Akt3

查看 PKA 亚型特异性产品:

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PKA PKAR PKACα

查看 mTOR 亚型特异性产品:

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mTOR mTORC1 mTORC2

查看 Bcl-2 Family 亚型特异性产品:

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

查看 Caspase 亚型特异性产品:

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Kushenol Z is a cAMP-PDE/Akt inhibitor. Kushenol Z inhibits cAMP phosphodiesterase activity, elevates cAMP levels, enhances PKA activity, and suppresses the mTOR pathway by attenuating the phosphorylation of Akt and PRAS40. Kushenol Z induces apoptosis in non-small cell lung cancer cells via mitochondrial and endoplasmic reticulum stress pathways, upregulates CHOP, modulates the Bax/Bcl-2 ratio, and activates caspase-3/7/9/12. Kushenol Z is applicable to relevant research on non-small cell lung cancer[1].

IC50 & Target[1]

Caspase-3

 

Caspase-7

 

Caspase-9

 

Caspase-12

 

Bax

 

Bcl-2

 

体外研究
(In Vitro)

Kushenol Z (0-20 μg/mL; 24 h) 可选择性抑制 A549 和 NCI-H226 非小细胞肺癌细胞的增殖，其 IC50 分别为 5.2 μg/mL 和 7.6 μg/mL)，而对 BEAS-2B 正常肺上皮细胞无显著抑制作用[1]。
Kushenol Z (0-20 μg/mL; 12-48 h) 可呈时间依赖性抑制 A549 和 NCI-H226 非小细胞肺癌细胞的增殖[1]。
Kushenol Z (5 μg/mL; 12-48 h) 以时间依赖的方式降低 A549 和 NCI-H226 非小细胞肺癌细胞的活力，处理 24 h 和 48 h 后可观察到细胞活力显著下降[1]。
Kushenol Z (3-6 μg/mL; 24 h) 可在 A549 和 NCI-H226 非小细胞肺癌细胞中诱导细胞凋亡的形态学特征，包括染色质固缩和凋亡小体形成[1]。
Kushenol Z (3-6 μg/mL; 24 h) 可通过上调 Bax/Bcl-2 比值、提高活化型 caspase-3 和活化型 caspase-9 的水平，激活 A549 和 NCI-H226 非小细胞肺癌细胞中的线粒体凋亡通路[1]。
Kushenol Z (3-6 μg/mL; 24 h) 可通过上调剪切型 caspase-12、剪切型 caspase-7 及 CHOP 的表达水平，激活 A549 和 NCI-H226 非小细胞肺癌细胞中的内质网应激凋亡通路[1]。
Kushenol Z (3-6 μg/mL; 24 h) 可呈剂量依赖性升高 A549 和 NCI-H226 非小细胞肺癌细胞内的 cAMP 和 PKA 水平[1]。
Kushenol Z (6 μg/mL; 24 h) 可通过降低 p70 S6K (Thr 389) 的磷酸化水平抑制 A549 非小细胞肺癌细胞中的 mTORC1 信号通路，该效应由 PKA 活性增强介导[1]。
Kushenol Z (6 μg/mL; 24 h) 可通过降低 Akt (Ser 473) 和 PRAS40 (Thr 246) 的磷酸化水平抑制 A549 非小细胞肺癌细胞中的 Akt 信号通路，进而抑制 mTOR 通路[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Kushenol Z 相关抗体:

Cell Proliferation Assay[1]

Cell Line: A549, NCI-H226, BEAS-2B
Concentration: 0, 5, 10, 15 and 20 μg/mL
Incubation Time: 24 h
Result: Selectively inhibited proliferation of A549 and NCI-H226 cells in a dose-dependent manner, with IC50 values of 5.2 μg/mL for A549 cells and 7.6 μg/mL for NCI-H226 cells.
Showed no significant inhibition of BEAS-2B normal lung epithelial cells.

Cell Proliferation Assay[1]

Cell Line: A549, NCI-H226
Concentration: 0, 5, 10, 15 and 20 μg/mL
Incubation Time: 12, 24, 48 h
Result: Inhibited A549 and NCI-H226 cell proliferation in a time-dependent manner, with greater inhibition observed at longer incubation times.

Cell Viability Assay[1]

Cell Line: A549, NCI-H226
Concentration: 5 μg/mL
Incubation Time: 12, 24, 48 h
Result: Reduced A549 cell viability to 85% at 12 h, 60% at 24 h, and 35% at 48 h.
Reduced NCI-H226 cell viability to 85% at 12 h, 70% at 24 h, and 35% at 48 h, with significant decreases at 24 and 48 h compared to 12 h.

Apoptosis Analysis[1]

Cell Line: A549, NCI-H226
Concentration: 3 and 6 μg/mL
Incubation Time: 24 h
Result: Induced morphological changes including cell shrinkage, distortion, and floatage, as well as chromatin condensation and apoptotic body formation in A549 and NCI-H226 cells.\nIncreased the percentage of sub-G1 peak cells in a dose-dependent manner: in A549 cells, sub-G1 peaks were 23.91% at 3 μg/mL and 37.47% at 6 μg/mL; in NCI-H226 cells, sub-G1 peaks were 19.86% at 3 μg/mL and 30.59% at 6 μg/mL.\nIncreased the total apoptotic cell population (Q2 + Q3) in a dose-dependent manner: in A549 cells, total apoptotic cells were 35% at 3 μg/mL and 49.2% at 6 μg/mL; in NCI-H226 cells, total apoptotic cells were 30.5% at 3 μg/mL and 38.9% at 6 μg/mL.

Western Blot Analysis[1]

Cell Line: A549, NCI-H226
Concentration: 3 and 6 μg/mL
Incubation Time: 24 h
Result: Upregulated the Bax/Bcl-2 ratio, and increased levels of cleaved caspase-3 and cleaved caspase-9 in A549 and NCI-H226 cells in a dose-dependent manner.\nIncreased levels of cleaved caspase-12, cleaved caspase-7, and CHOP in A549 and NCI-H226 cells in a dose-dependent manner.

Western Blot Analysis[1]

Cell Line: A549
Concentration: 6 μg/mL
Incubation Time: 24 h
Result: Decreased the phosphorylation of p70 S6K (Thr 389) in A549 cells; this effect was reversed by co-treatment with the PKA inhibitor H-89 (100 nM).\nDecreased the phosphorylation of Akt (Ser 473) and PRAS40 (Thr 246) in A549 cells; this effect was partially reversed by co-treatment with the Akt activator SC79 (10 nM).
分子量

436.50

Formula

C26H28O6
CAS 号
结构分类
初始来源
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

Kushenol Z 相关分类

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Kushenol Z2467875-82-5Phosphodiesterase (PDE)AktPKAmTORApoptosisBcl-2 FamilyCaspasePKBProtein kinase BProtein kinase AMammalian target of Rapamycinendoplasmic reticulum stressNCI-H226BEAS-2BmTOR pathwayA549cAMP-phosphodiesteraseapoptosisnon-small-cell lung cancer cellsInhibitorinhibitorinhibit

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