2. PI3K/Akt/mTOR Cell Cycle/DNA Damage MAPK/ERK Pathway Stem Cell/Wnt Apoptosis
  3. Akt PI3K PERK p38 MAPK ERK Apoptosis
  4. Anticancer agent 319

Anticancer agent 319 是一种抗癌剂。Anticancer agent 319 抑制肝癌细胞的增殖。Anticancer agent 319 可抑制 AKT 磷酸化，阻断 PI3K/AKT 信号轴；同时可抑制 ERK1/2 磷酸化，阻断 MAPK/ERK 信号轴。Anticancer agent 319 在肝癌细胞中诱导细胞周期 G2/M 期阻滞，诱导细胞凋亡 (apoptosis)，降低细胞的线粒体膜电位。Anticancer agent 319 可用于肝细胞癌的研究。

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Anticancer agent 319

Anticancer agent 319 Chemical Structure

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Anticancer agent 319 相关抗体

Top Publications Citing Use of Products

查看 Akt 亚型特异性产品:

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Akt Akt1 Akt2 Akt3

查看 PI3K 亚型特异性产品:

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PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

查看 p38 MAPK 亚型特异性产品:

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p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

查看 ERK 亚型特异性产品:

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ERK ERK1 ERK2 ERK5 ERK8

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Anticancer agent 319 is an anticancer agent. Anticancer agent 319 inhibits the proliferation of liver cancer cells. Anticancer agent 319 inhibits AKT phosphorylation and blocks the PI3K/AKT signaling axis; meanwhile, it inhibits ERK1/2 phosphorylation and blocks the MAPK/ERK signaling axis. Anticancer agent 319 induces G2/M phase cell cycle arrest, triggers apoptosis, and reduces mitochondrial membrane potential in liver cancer cells. Anticancer agent 319 can be used for the research of hepatocellular carcinoma[1].

体外研究
(In Vitro)

Anticancer agent 319 (Compound 11e) (48-72 h) 可强效抑制人肝癌细胞 HepG2 和 Hep3B 的增殖，其 IC50 值分别为 2.22 μM (72 h, HepG2)、4.55 μM (48 h, HepG2) 和 4.95 μM (48 h, Hep3B)，但对 Huh-7 细胞的增殖无抑制作用[1]。
Anticancer agent 319 (2.5-10 μM; 24-48 h) 呈剂量依赖性抑制人肝癌细胞 HepG2 的迁移[1]。
Anticancer agent 319 (2.5-10 μM; 36-48 h) 在人肝癌 HepG2 细胞中可诱导细胞周期 G2/M 期阻滞，并呈浓度依赖性诱导细胞凋亡，降低细胞的线粒体膜电位[1]。
Anticancer agent 319 (2.5-10 μM; 36 h) 可呈剂量依赖性地抑制 AKT (Ser473) 和 ERK1/2 (Thr202/Tyr204) 的磷酸化，阻断人肝癌 HepG2 细胞中的 PI3K/AKT 和 MAPK/ERK 信号轴[1]。

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

Anticancer agent 319 相关抗体:

Cell Migration Assay [1]

Cell Line: human hepatocellular carcinoma HepG2 cells
Concentration: 2.5, 5 and 10 μM
Incubation Time: 24 h; 48 h
Result: Inhibited HepG2 cell migration in a dose-dependent manner.
Reduced the wound closure rate to 52.96% (2.5 μM), 27.41% (5 μM), and 13.45% (10 μM) after 48 h, compared to 59.11% in the control group.

Cell Cycle Analysis[1]

Cell Line: human hepatocellular carcinoma HepG2 cells
Concentration: 2.5, 5 and 10 μM
Incubation Time: 36 h
Result: Induced G2/M phase arrest at all concentrations.
Increased the SubG1 (apoptotic) population to approximately 22.33% at 5 μM and 10 μM, indicating DNA fragmentation and apoptosis.

Apoptosis Analysis[1]

Cell Line: human hepatocellular carcinoma HepG2 cells
Concentration: 2.5, 5 and 10 μM
Incubation Time: 48 h
Result: Induced characteristic apoptotic nuclear changes, including condensation and fragmentation, in a dose-dependent manner.
Control cells showed uniform, pale blue nuclear staining.\nIncreased the proportion of both early and late apoptotic cells in a concentration-dependent manner.
Caused significant reductions in viable cells compared to the control.

Western Blot Analysis[1]

Cell Line: human hepatocellular carcinoma HepG2 cells
Concentration: 2.5, 5 and 10 μM
Incubation Time: 36 h
Result: Dose-dependently inhibited the phosphorylation of AKT (Ser473) and ERK1/2 (Thr202/Tyr204).
Nearly completely suppressed phosphorylation at the highest concentration.
分子量

657.54

Formula

C33H34Cl2N2O8
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

Anticancer agent 319 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:

Anticancer agent 319Anticancer agent319Anticancer agent-319AktPI3KPERKp38 MAPKERKApoptosisPKBProtein kinase BPhosphoinositide 3-kinaseProtein kinase R-like endoplasmic reticulum kinasePKR-like endoplasmic reticulum kinaseExtracellular signal regulated kinasesPI3K/AKT signaling axisHep3BERK1/2MAPK/ERK signaling axisHepG2AKTAKT1EGFRMMP9hepatocellular carcinomaInhibitorinhibitorinhibit

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