2. Cell Cycle/DNA Damage Vitamin D Related/Nuclear Receptor Metabolic Enzyme/Protease GPCR/G Protein
  3. PPAR Adenosine Receptor Fatty Acid Synthase (FASN) Endogenous Metabolite
  4. PPAR agonist 7

PPAR agonist 7 is an orally active pan-PPAR agonist, demonstrating potent activation of all three subtypes, PPARα (EC50 = 1.51 μM), PPARδ (EC50 = 1.11 μM), and PPARγ (EC50 = 3.14 μM). PPAR agonist 7 significantly enhances glucose uptake in adipocytes while exhibiting minimal adipogenic activity. PPAR agonist 7 can suppress PPARγ Ser273 phosphorylation in white adipose tissue and upregulate insulin-sensitizing genes. PPAR agonist 7 does not cause weight gain or fluid retention in high-fat diet (HFD)/ Streptozotocin (HY-13753) (STZ)-induced type 2 diabetes mellitus (T2DM) models. PPAR agonist 7 has selective modulation of PPAR signaling pathways without activation of adipogenic gene programs. PPAR agonist 7 can be used for the study of diabetes.

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PPAR agonist 7

PPAR agonist 7 Chemical Structure

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PPAR agonist 7 Related Antibodies

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Description

PPAR agonist 7 is an orally active pan-PPAR agonist, demonstrating potent activation of all three subtypes, PPARα (EC50 = 1.51 μM), PPARδ (EC50 = 1.11 μM), and PPARγ (EC50 = 3.14 μM). PPAR agonist 7 significantly enhances glucose uptake in adipocytes while exhibiting minimal adipogenic activity. PPAR agonist 7 can suppress PPARγ Ser273 phosphorylation in white adipose tissue and upregulate insulin-sensitizing genes. PPAR agonist 7 does not cause weight gain or fluid retention in high-fat diet (HFD)/ Streptozotocin (HY-13753) (STZ)-induced type 2 diabetes mellitus (T2DM) models. PPAR agonist 7 has selective modulation of PPAR signaling pathways without activation of adipogenic gene programs. PPAR agonist 7 can be used for the study of diabetes[1].

In Vitro

PPAR agonist 7 (Compound 1d) (1-10 μM, 24 h) has no significant effect on the viability of 3T3-L1 adipocytes and increases glucose uptake in mature adipocytes in a dose-dependent manner at the tested concentration[1].
PPAR agonist 7 (10 μM, 75 min) can significantly inhibit TNFα-induced phosphorylation of PPARγ at Ser273 in 3T3-L1 cells[1].
PPAR agonist 7 (1-10 μM, 24 h) significantly restores glucose uptake in HepG2 cells exposed to 30 mM glucose and 0.5 μM insulin[1].
PPAR agonist 7 (10 μM, 8 days) significantly reduces the number of lipid droplets in 3T3-L1, and the mRNA levels of key genes for adipogenesis (Ppary, Ap2, Cebpa, Fasn, Cd36, Lpl) are not significantly upregulated[1].

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

PPAR agonist 7 Related Antibodies

Cell Cytotoxicity Assay[1]

Cell Line: 3T3-L1 adipocytes cells
Concentration: 1 μM, 5 μM, 10 μM
Incubation Time: 24 h
Result: Showed no significant effect on the viability of 3T3-L1 adipocytes.

Western Blot Analysis[1]

Cell Line: TNF-α-induced 3T3-L1 cells
Concentration: 10 μM
Incubation Time: Pretreated for 45 min, then stimulation with 50 ng/mL TNF-α for an additional 30 min
Result: Significantly inhibited TNFα-induced phosphorylation of PPARγ at Ser273 in 3T3-L1 cells.

Real Time qPCR[1]

Cell Line: 3T3-L1 adipocytes cells
Concentration: 10 μM
Incubation Time: 8 days
Result: Showed no significant effects on any of these adipogenesis-related genes (Ppary, Ap2, Cebpa, Fasn, Cd36, Lpl).
In Vivo

PPAR agonist 7 (Compound 1d) (5-20 mg/kg, p.o., once daily for 30 days) significantly improved insulin sensitivity, glycemic control, and lipid metabolism in a mice T2DM model without causing weight gain or fluid retention side effects[1].

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

Animal Model: The male C57BL/6J mice (18-22 g, 4-6 weeks) were fed a high-fat diet 12 weeks and then mice were received daily intraperitoneal injections of streptozotocin (STZ; 50 mg/kg) for five consecutive days, following this, the mice were fed for an additional three weeks to establish the STZ/HFD-induced T2DM model[1].
Dosage: 5 mg/kg, 10 mg/kg, 20 mg/kg
Administration: P.o., once daily for 30 days
Result: Significantly improved fasting blood glucose levels and reduced fasting insulin concentrations.
Demonstrated dose-dependent improvements in insulin resistance in this diabetic model.
Significantly elevated fasting plasma adiponectin levels in T2DM mice.
Did not cause significant body weight gain and no effect on hematocrit.
Significantly enhanced glucose clearance and insulin sensitivity.
Significantly reduced plasma TG, TC, LDL-C, and FFA; significantly increased plasma adiponectin levels.
Significantly alleviated hepatocellular steatosis and ballooning degeneration; reduced plasma AST and ALT levels.
Inhibited PPARγ Ser273 phosphorylation in WAT; upregulated insulin-sensitive genes (Adiponectin, Cyp2f2).
Selectively regulated insulin resistance-related genes (Glut4, Irs1), but did not activate adipogenesis genes (Ppary, Fasn).
Molecular Weight

477.59

Formula

C29H35NO5
SMILES

CC(C)(OC1=C(C)C=C(/C=C2OC3=CC(NCC4CC4)=CC=C3C\2=O)C=C1C)C(OC(C)(C)C)=O
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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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PPAR agonist 7 Related Classifications

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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:

PPAR agonist 7PPAR agonist7PPAR agonist-7PPARAdenosine ReceptorFatty Acid Synthase (FASN)Endogenous MetabolitePeroxisome proliferator-activated receptorsP1 receptorInsulin resistanceLipid metabolismPPAR modulatorsSer273 phosphorylationT2DMInhibitorinhibitorinhibit

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