L-165041 NEW
Price | $40 | $64 | $129 |
Package | 5mg | 10mg | 25mg |
Min. Order: | |
Supply Ability: | 10g |
Update Time: | 2024-11-19 |
Product Details
Product Name: L-165041 | CAS No.: 79558-09-1 |
Purity: 97.97% | Supply Ability: 10g |
Release date: 2024/11/19 |
Product Introduction
Bioactivity
Name | L-165041 |
Description | L-165041 is a potent and selective agonist of the nuclear receptor PPARβ and PPARδ(Ki = 9 nM, EC50 = ~500 nM ,respectively) |
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]. |
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]. |
Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
Solubility Information | DMSO : 50 mg/mL (124.24 mM) |
Keywords | L 165041 | Peroxisome proliferator-activated receptors | PPAR | L-165041 | L165041 | inhibit | Inhibitor |
Inhibitors Related | PHYTOL | (S)-(+)-Ibuprofen | BADGE | Cinnamyl alcohol | Daidzein | Fenofibrate | Pioglitazone hydrochloride | 5-Aminosalicylic Acid | Naringenin | Fisetin | 2,3-Butanediol | Icariin |
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Company Profile Introduction
Target Molecule Corp. (TargetMol) is a global high-tech enterprise, headquartered in Boston, MA, specializing in chemical and biological research product and service to meet the research needs of global customers.
TargetMol has evolved into one of the biggest global compound library and small molecule suppliers and a customer based on 40+ countries. TargetMol offers over 80 types of compound libraries and a wide range of high-quality research chemicals including inhibitors, activator, natural compounds, peptides, inhibitory antibodies, and novel life-science kits, for laboratory and scientific use. Besides, virtual screening service is also available for customers who would like to conduct the computer-aided drug discovery.
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