2. Protein Tyrosine Kinase/RTK Apoptosis
  3. VEGFR Apoptosis
  4. VEGFR-2-IN-73

VEGFR-2-IN-73 是一种强效且高选择性的 VEGFR-2 抑制剂，其对 VEGFR-2 的抑制作用 (IC50 = 0.0787 μM) 显著优于对 EGFR 的抑制作用 (IC50 = 1.31 μM)。VEGFR-2-IN-73 在多种癌细胞系中均表现出强大的抗增殖活性。VEGFR-2-IN-73 可诱导 G2/M 期和 Pre-G1 期细胞周期阻滞，并显著促进细胞凋亡 (apoptosis)。VEGFR-2-IN-73 可用于抗癌领域的研究，例如结直肠癌、肝细胞癌和乳腺癌。

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VEGFR-2-IN-73

VEGFR-2-IN-73 Chemical Structure

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Customer Review

VEGFR-2-IN-73 相关抗体

Top Publications Citing Use of Products

查看 VEGFR 亚型特异性产品:

查看所有亚型
VEGFR1/Flt-1 VEGFR2/KDR/Flk-1 VEGFR3/Flt-4

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

VEGFR-2-IN-73 is a potent and selective VEGFR-2 inhibitor, showing selectively inhibition of VEGFR-2 (IC50 = 0.0787 μM) over EGFR (IC50 = 1.31 μM). VEGFR-2-IN-73 demonstrates potent antiproliferative activity across multiple cancer cell lines. VEGFR-2-IN-73 induces G2/M and Pre-G1 phase arrest and significantly enhances apoptosis. VEGFR-2-IN-73 can be used in cancer research, such as colorectal carcinoma, hepatocellular carcinoma, and breast cancer[1].

IC50 & Target[1]

VEGFR-2

0.0787 μM (IC50)

体外研究
(In Vitro)

VEGFR-2-IN-73 (compound 15) (2 天) 对 HCT-116、HepG-2 和 MCF-7 癌细胞系表现出强细胞毒性(IC50 分别为 3.66、3.31 和 4.29 μM)，而对正常 WI-38 细胞则表现出极小的细胞毒性 (IC50 > 69 μM)，显示出良好的选择性特征[1]。
VEGFR-2-IN-73 (3.31-4.29 μM，72 小时) 可有效诱导 HCT-116、HepG-2 和 MCF-7 细胞的 G2/M 期和 Pre-G1 期周期阻滞，并显著触发细胞凋亡，其作用与 Doxorubicin (HY-15142A) 相当[1]。
VEGFR-2-IN-73 与 VEGFR-2 的预测结合能 (-24.27 kcal/mol) 远低于Sorafenib (HY-10201) (-20.88 kcal/mol)，显示出更优的结合亲和力[1]。

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

VEGFR-2-IN-73 相关抗体:

Cell Cycle Analysis[1]

Cell Line: HCT-116, HepG-2, and MCF-7 Cells
Concentration: 3.66, 3.31, and 4.29 μM for HCT-116, HepG-2, and MCF-7 Cells, respectively
Incubation Time: 72 h
Result: Induced a significant increase in the Hep-G2 cell population in the G2/M (from 12.73 % to 38.49 %) and Pre-G1 (from 1.92 % to 22.80 %) phases.
Induced a significant increase in the HCT-116 cell population in the G2/M (from 5.45 % to 22.72 %) and Pre-G1 (from 1.91 % to 16.05 %) phases.
Significantly increased the population of MCF-7 Cells in the G2/M and Pre-G1 phases from 9.55 % and 2.14 % to 31.58 % and 14.29 %, respectively.
Reduced the proportion of cells in the G0-G1 and S phases compared to the control in Hep-G2, HCT-116, and MCF-7 cell lines.

Apoptosis Analysis[1]

Cell Line: HCT-116, HepG-2, and MCF-7 Cells
Concentration: 3.66, 3.31, and 4.29 μM for HCT-116, HepG-2, and MCF-7 Cells, respectively
Incubation Time: 72 h
Result: Induced a total apoptosis rate of 16.05 % in HCT-116 cells (early: 5.64 %; late: 8.72 %).
Induced a total apoptosis rate of 22.8 % in HepG-2 cells (early: 6.38 %; late: 13.9 %).
Induced a total apoptosis rate of 14.29 % in MCF-7 cells (early: 5.86 %; late: 6.77 %).
Triggered apoptosis in HCT-116, HepG-2, and MCF-7 Cells, with an efficacy comparable to Doxorubicin.
分子量

559.70

Formula

C29H29N5O3S2
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

VEGFR-2-IN-73 相关分类

  • 摩尔计算器

  • 稀释计算器

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Help & FAQs
  • 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:

VEGFR-2-IN-73VEGFRApoptosisVascular endothelial growth factor receptorVEGFR-2antiproliferativeapoptosiscell cycle arrestHCT-116HepG-2MCF-7Inhibitorinhibitorinhibit

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