2. Cell Cycle/DNA Damage Cytoskeleton Metabolic Enzyme/Protease Apoptosis
  3. Microtubule/Tubulin Carbonic Anhydrase Apoptosis MDM-2/p53
  4. Anticancer agent 314

Anticancer agent 314 是一种多靶点抗癌剂，具有微管蛋白 (tubulin) 聚合抑制活性 (IC50 = 6.35 μM)，以及对人碳酸酐酶 (carbonic anhydrase) IX (Ki = 27.1 nM) 和 XII (Ki = 20.9 nM) 的抑制活性。Anticancer agent 314 可结合至微管蛋白的秋水仙碱结合口袋，并通过酶活性位点内的锌配位作用抑制肿瘤相关碳酸酐酶亚型。Anticancer agent 314 可诱导细胞周期 G2/M 期阻滞、通过 p53 依赖信号通路介导的细胞凋亡 (apoptosis)，并在多种癌细胞中表现出广谱抗增殖活性。Anticancer agent 314 可用于癌症相关研究，例如白血病、黑色素瘤、卵巢癌。

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Anticancer agent 314

Anticancer agent 314 Chemical Structure

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Anticancer agent 314 相关抗体

Top Publications Citing Use of Products

查看 Carbonic Anhydrase 亚型特异性产品:

查看所有亚型
CA CA I CA Ⅱ CA IX CA XII CA VII CA VI CA VA CA VB CA XIII CA XIV

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Anticancer agent 314 is a multi-target anticancer agent with tubulin polymerization inhibitory activity (IC50 = 6.35 μM) and human carbonic anhydrase IX (Ki = 27.1 nM) and XII (Ki 20.9 = nM) inhibitory activity. Anticancer agent 314 binds to the colchicine-binding pocket of tubulin and inhibits tumor-associated carbonic anhydrase isoforms via zinc coordination within enzyme active sites. Anticancer agent 314 induces G2/M phase cell cycle arrest, apoptosis via p53-dependent signaling, and broad-spectrum antiproliferative activity across multiple cancer cells. Anticancer agent 314 can be used for the research of cancer, such as leukemia, melanoma, ovarian cancer[1].

IC50 & Target[1]

hCA XII

20.9 nM (Ki)

hCA IX

27.1 nM (Ki)

体外研究
(In Vitro)

Anticancer agent 314 (Compound 13n) 可强效抑制重组人肿瘤相关碳酸酐酶亚型 hCA IX (Ki = 27.1 nM) 和 hCA XII (Ki = 20.9 nM)[1]。
Anticancer agent 314 (1.5-100 μM) 可强效抑制无细胞体系中的微管蛋白聚合，其 IC50 为 6.35 μM[1]。
Anticancer agent 314 (0.01-100 μM) 在 NCI-60 人肿瘤细胞系组中表现出广谱抗增殖活性，其 GI50 值范围为 2.48 至 31.00 μM[1]。
Anticancer agent 314 对 WI-38 人正常肺成纤维细胞的细胞毒性较低，其 IC50 为 68.62 μM[1]。
Anticancer agent 314 (6.35 μM; 24 h) 可强效将人乳腺癌 MCF-7 细胞阻滞于细胞周期的 G2/M 期，使 G2/M 期细胞比例升高至 31.97%[1]。
Anticancer agent 314 (6.35 μM; 24 h) 可在人乳腺癌 MCF-7 细胞中诱导强烈的细胞凋亡，使总凋亡细胞比例升高至 24.68%[1]。
Anticancer agent 314 (6.35 μM; 24 h) 可激活 MCF-7 人乳腺癌细胞中 p53 依赖的凋亡通路，上调 p53、Bax 及活化型 caspase-7 的水平，同时下调 Bcl-2 的水平[1]。

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

Anticancer agent 314 相关抗体:

Cell Cycle Analysis[1]

Cell Line: MCF-7 human breast cancer cells
Concentration: 6.35 μM
Incubation Time: 24 h
Result: Increased the G2/M phase population from 13.81% (control) to 31.97% (treated).
Suppressed the G0/G1 phase population from 63.58% to 52.76%.
Reduced the S phase population from 22.61% to 15.27%.

Apoptosis Analysis[1]

Cell Line: MCF-7 human breast cancer cells
Concentration: 6.35 μM
Incubation Time: 24 h
Result: Increased the total apoptotic cell population from 0.67% (control) to 24.68% (treated), with 9.51% early apoptotic cells and 15.17% late apoptotic cells.

ELISA Assay[1]

Cell Line: MCF-7 human breast cancer cells
Concentration: 6.35 μM
Incubation Time: 24 h
Result: Increased p53 protein levels 3.43-fold relative to control cells.
Increased Bax levels 12.34-fold relative to control cells.
Reduced Bcl-2 levels 4.37-fold relative to control cells.
Increased caspase-7 activation 7.35-fold relative to control cells.
分子量

460.47

Formula

C22H16N6O4S
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 314 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 314Anticancer agent314Anticancer agent-314Microtubule/TubulinCarbonic AnhydraseApoptosisMDM-2/p53Carbonate dehydratasehuman carbonic anhydrase XIIcolchicine-binding pocketmelanomap53-dependent signalingovarian cancerG2/M phase cell cycle arrestleukemiatubulin polymerizationhuman carbonic anhydrase IXMCF-7 human breast cancer cellsInhibitorinhibitorinhibit

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