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

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.

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PPARγ agonist 17 Chemical Structure

PPARγ agonist 17 Chemical Structure

CAS No. : 3054652-58-0

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Description

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].

In Vitro

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. 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 T1/2, 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.

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.
Molecular Weight

766.02

Formula

C48H63NO7

CAS No.
SMILES

C[C@]12[C@@](C(C=C3[C@]2(CC[C@@]4([C@@]3([H])C[C@](CC4)(C(O)=O)C)C)C)=O)([H])[C@@]5([C@@](C(C)([C@H](CC5)OC(CC6=CC=CC(NC(COC7=C(C)C=CC(C)=C7)=O)=C6)=O)C)([H])CC1)C

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    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.

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Product Name:
PPARγ agonist 17
Cat. No.:
HY-173166
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