2. Cell Cycle/DNA Damage Vitamin D Related/Nuclear Receptor Metabolic Enzyme/Protease
  3. PPAR
  4. PPARγ agonist 17

PPARγ agonist 17 (Compound C1) 是一种有口服活性的 PPARγ 激动剂。PPARγ agonist 17 增强PPARγ 活性并阻断 HT-29 细胞周期于 G2/M 期，抑制细胞迁移并诱导细胞凋亡。PPARγ agonist 17 在癌细胞中具有广谱抗增殖活性，且毒性相对正常细胞较低，不能穿过血脑屏障。

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PPARγ agonist 17 Chemical Structure

PPARγ agonist 17 Chemical Structure

CAS No. : 3054652-58-0

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PPARγ agonist 17 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

PPARγ agonist 17 (Compound C1) is a PPARγ agonist. PPARγ agonist 17 enhances PPARγ activity and blocks the cell cycle in G2/M phase, inhibits cell migration and induces apoptosis in HT-29 cells. PPARγ agonist 17 has a broad spectrum anti-proliferative activity in cancer cells with relatively low toxicity in normal cells which cannot cross the blood-brain barrier[1].

体外研究
(In Vitro)

PPARγ agonist 17 (0-1000 μM, 48 小时) 对HCT-116、HT-29、HCT-8、MCF-7、MDA-MB-231表现出良好的抗增殖活性，且不损害 293T 和 L02细胞[1]。
PPARγ agonist 17 (4-8 μM) 显著增强 HT-29 细胞中 PPARγ 的活性。PPARγ agonist 17 (2-8 μM，24 小时) 显著降低 EdU 阳性细胞比例，有效抑制 HT-29 细胞增殖，使细胞周期阻滞于 G2/M 期，抑制 cyclin D1和 CDK4 的表达。PPARγ agonist 17 以剂量依赖性方式显著抑制 HT-29 细胞集落形成的数量和大小，并诱导细胞凋亡。 PPARγ agonist 17 (2-4 μM，0-48 小时) 抑制HT-29细胞迁移[1]。
PPARγ agonist 17 表现出相对较低的毒性，无致瘤作用和低 AMES 毒性 (无致突变性)，并且急性口服毒性比 18β-GA 和罗格列酮 (HY-17386 , ROS) 相对较低[1]。
PPARγ agonist 17 不能穿过血脑屏障，从而避免了中枢神经系统毒性[1]。
PPARγ agonist 17 表现出足够的人肝微粒体 (HLM) 稳定性和合适的T1/2，表明它在人肝微粒体中具有足够的代谢稳定性[1]。

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

PPARγ agonist 17 相关抗体:

Cell Proliferation Assay[1]

Cell Line: HT-29
Concentration: 2, 4, 8 μM
Incubation Time: 24 h
Result: Inhibited the number and size of HT-29 cell colony formation in a dose-dependent manner.

Cell Proliferation Assay[1]

Cell Line: HCT-116, HT-29, HCT-8, MCF-7, MDA-MB-231, 293 T, L02
Concentration: 0, 0.1, 1, 10, 100, 1000 μM
Incubation Time: 48 h
Result: Showed anti-proliferative activity against HCT-116, HT-29, HCT-8, MCF-7, MDA-MB-231 with IC50 values of 25.02 μM, 12.25 μM, 33.13 μM, 15.23 μM, 18.58 μM., without damaging 293 T and L02 cells.
Had an anti-proliferative activity against the HT-29 cell line that is 12 times that of its parent skeleton 18β-GA and ROS.

Cell Migration Assay [1]

Cell Line: HT-29
Concentration: 2, 4 μM
Incubation Time: 0, 24, 48 h
Result: Could significantly slow the healing of scratches in a dose-dependent manner, indicating its ability to inhibit the migration of HT-29 cells.

Apoptosis Analysis[1]

Cell Line: HT-29
Concentration: 2, 4, 8 μM
Incubation Time: 24 h
Result: Induced apoptosis of HT-29 cells.

Cell Cycle Analysis[1]

Cell Line: HT-29
Concentration: 2, 4, 8 μM
Incubation Time: 24 h
Result: Could significantly block HT-29 cell cycle in G2/M phase in a dose-dependent manner.

Western Blot Analysis[1]

Cell Line: HT-29
Concentration: 2, 4, 8 μM
Incubation Time: 24 h
Result: Significantly inhibited the expression of cyclin D1 and CDK4.
Significantly up-regulated the expression level of proapoptotic protein BAX and down-regulated the expression level of anti-apoptotic protein Bcl2, thereby activating downstream caspase-3, leading to an increase in the levels of cleaved caspase-3 and cytochrome C.

Western Blot Analysis[1]

Cell Line: HT-29
Concentration: 2, 4, μM
Incubation Time: 0, 24, 48 h
Result: Could effectively regulate the expression of the migration-related proteins, such as up-regulating the expression of E-cadherin and down-regulating the expression of β-catenin and vimentin.
分子量

766.02

Formula

C48H63NO7
CAS 号
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

PPARγ agonist 17 相关分类

  • 摩尔计算器

  • 稀释计算器

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Keywords:

PPARγ agonist 173054652-58-0PPARγ agonist17PPARγ agonist-17PPARPeroxisome proliferator-activated receptorsPPARγapoptosisanti-proliferativeHCT-116HT-29HCT-8MCF-7MDA-MB-231cell cycleantitumorInhibitorinhibitorinhibit

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