PPARγ agonist 17

PPARγ agonist 17 (0-1000 μM, 48 h) exhibits good anti-proliferative activity against HCT-116, HT-29, HCT-8, MCF-7, MDA-MB-231, without damaging 293 T and L02^[1].
PPARγ agonist 17 (4-8 μM) significantly enhances PPARγ activity in HT-29 cells. PPARγ agonist 17 (2-8 μM, 24 h) significantly reduces the proportion of EdU positive cells, and effectively inhibits the proliferation of HT-29 cells, and blocks the cell cycle in G2/M phase, inhibits the expression of cyclin D1 and CDK4. PPARγ agonist 17 significantly inhibits the number and size of HT-29 cell colony formation in a dose-dependent manner, and induces apoptosis^[1].
PPARγ agonist 17 (2-4 μM, 0-48 h) inhibits HT-29 cell migration^[1].
PPARγ agonist 17 demonstrates relatively low toxicity, with no tumorigenic effects and low-AMES toxicity (non-mutagenic), as well as comparatively lower acute oral toxicity than 18β-Glycyrrhetinic acid (HY-N0180) and Rosiglitazone (HY-17386, ROS) ^[1].
PPARγ agonist 17 cannot cross the blood-brain barrier, thus avoiding central nervous system toxicity^[1].
PPARγ agonist 17 shows adequate human liver microsomal (HLM) stability and a suitable T_1/2, indicating that it has sufficient metabolic stability in human liver microsomes^[1].

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