L-165461
L-165461 is a PPARδ and PPARγ agonist with Ki values of 3 nM and 15 nM, respectively. L-165461 can be used for research on diabetes.
For research use only. We do not sell to patients.
- CAS No.: 194608-76-9
- Formula: C23H26ClNO4S
- Molecular Weight:447.97
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
PPARγ 15 nM (Ki) |
PPARδ 3 nM (Ki) |
In Vitro
L-165461 (~16 h) is a potent dual ligand for both PPARγ (Ki = 15 nM) and PPARδ (Ki = 3 nM)[1].
L-165461 (48 h) acts as an agonist for both hPPARγ and hPPARδ, producing robust transactivation of the UAS reporter gene in COS-1 cells expressing either receptor[1].
L-165461 binds to and activates the human PPARδ ligand binding domain with an EC50 of 0.012 µM[3].
L-165461 (4 days) promotes preadipocyte differentiation in 3T3-L1 cells, as measured by aP2 mRNA expression, consistent with its PPARγ binding affinity[1].
L-165461 (50 μM; 1 h) does not inhibit LPS-induced TNF-α or IL-6 production in freshly isolated or 5-day cultured human monocytes[2].
L-165461 (50 μM; 1 h) does not inhibit PMA-induced TNF-α or IL-6 production in freshly isolated or 5-day cultured human monocytes[2].
L-165461 (50 μM; 1 h) does not inhibit LPS-induced TNF-α production in murine RAW 264.7 macrophage-like cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Human peripheral blood monocytes
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Concentration:50 μM
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Incubation Time:1 h (pre-treatment); 4 h (LPS stimulation)
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Result:Failed to inhibit LPS-induced TNF-α or IL-6 synthesis and secretion at concentrations up to 50 μM.
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Cell Line:Human peripheral blood monocytes
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Concentration:50 μM
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Incubation Time:1 h (pre-treatment); 18-24 h (PMA stimulation)
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Result:Failed to inhibit PMA-induced TNF-α or IL-6 synthesis and secretion at concentrations up to 50 μM.
Chemical Information
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CAS No. 194608-76-9
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Molecular Weight 447.97
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Formula C23H26ClNO4S
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SMILES
O=C(CC1=CC=C(C(Cl)=C1)SCCCOC2=C(CCC)C(ON=C3CC)=C3C=C2)O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
L-165461 Related Classifications
HY-10839 Related Classifications
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