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L-165041

Catalog No. T7159 CAS 79558-09-1

L-165041 is a potent and selective agonist of the nuclear receptor PPARβ and PPARδ(Ki = 9 nM, EC50 = ~500 nM ,respectively)

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L-165041, CAS 79558-09-1

Pack Size	Availability	Price/USD
2 mg	In stock	$ 42.00
5 mg	In stock	$ 56.00
10 mg	In stock	$ 82.00
25 mg	In stock	$ 178.00
50 mg	In stock	$ 336.00
100 mg	In stock	$ 562.00
1 mL * 10 mM (in DMSO)	In stock	$ 65.00

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Description	L-165041 is a potent and selective agonist of the nuclear receptor PPARβ and PPARδ(Ki = 9 nM, EC50 = ~500 nM ,respectively)
Targets&IC50	PPARβ:9 nM(ki) , PPARδ:500 nM(EC50)
In vitro	L-165041 inhibited VEGF-induced cell proliferation and migration in human umbilical vein ECs (HUVECs). L-165041 also inhibited angiogenesis in the Matrigel plug assay and aortic ring assay. Flow cytometric analysis indicated that L-165041 reduced the number of ECs in the S phase and the expression levels of cell cycle regulatory proteins such as cyclin A, cyclin E, CDK2, and CDK4; phosphorylation of the retinoblastoma protein was suppressed by pretreatment with L-165041. The PPARδ ligand L-165041 inhibits VEGF-stimulated angiogenesis by suppressing the cell cycle progression independently of PPARδ[1].
In vivo	L-165041 lowered hepatic expression of PPARgamma, apolipoprotein B, interleukin 1 beta (IL-1beta), and interleukin-6. In contrast, L-165041 increased hepatic expressions of PPARdelta, lipoprotein lipase (LPL), and ATP-binding cassette transporter G1 (ABCG1).L-165041 might be effective in preventing Western diet-induced hepatic steatosis by regulating genes involved in lipid metabolism and the inflammatory response[2].
Cell Research	Cell cycle distribution was determined by flow cytometry. Synchronized HUVECs were pretreated with L-165041 (1 or 5μM) 6 h prior to the addition of VEGF (10 ng/ml). The cells were harvested 16 h after VEGF addition and washed with PBS. The cells were then incubated with buffer containing 0.1% Triton X-100 and 0.1% trisodium citrate for 30 min. Cells were rinsed with PBS and then stained with 50 μg/ml propidium iodide for 20 min at room temperature. In total, 1*10^4 cells were analyzed with the FACScan system . At least three independent experiments were performed[1].
Animal Research	The effect of PPARdelta ligand L-165041 on Western diet-induced fatty liver using low-density lipoprotein receptor-deficient (LDLR(-/-)) mice. LDLR(-/-) mice received either L-165041 (5mg/kg/day) or vehicle (0.1N NaOH) with Western diet for 16 weeks. L-165041 drastically reduced lipid accumulation in the liver, decreasing total hepatic cholesterol and triglyceride content compared to the vehicle group[1].

Molecular Weight	402.44
Formula	C22H26O7
CAS No.	79558-09-1

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 50 mg/mL (124.24 mM)

References and Literature

1. Park J H , Lee K S , Lim H J , et al. The PPARδ ligand L-165041 inhibits vegf-induced angiogenesis, but the antiangiogenic effect is not related to PPARδ[J]. Journal of Cellular Biochemistry, 2012, 113(6):1947-1954. 2. Lim H J , Park J H , Lee S , et al. PPARδ ligand L-165041 ameliorates Western diet-induced hepatic lipid accumulation and inflammation in LDLR?/? mice[J]. European Journal of Pharmacology, 2009, 622(1-3):45-51.

Related compound libraries

This product is contained In the following compound libraries：

Anti-COVID-19 Compound Library Anti-Obesity Compound Library DNA Damage & Repair Compound Library Transcription Factor-Targeted Compound Library Metabolism Compound Library Anti-Pancreatic Cancer Compound Library Anti-Cancer Compound Library Anti-Diabetic Compound Library NO PAINS Compound Library Lipid Metabolism Compound Library

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Keywords

L-165041 79558-09-1 DNA Damage/DNA Repair Metabolism PPAR L 165041 Peroxisome proliferator-activated receptors L165041 inhibit Inhibitor inhibitor

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