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MedChemExpress - Model 5-Heptadecylresorcinol - 41442-57-3
5-Heptadecylresorcinol (AR-C17), a phenolic lipid component, is also an orally active mitochondrial protector. 5-Heptadecylresorcinol improves mitochondrial function via sirtuin3 signaling pathway, thus alleviates endothelial cell damage and apoptosis. 5-Heptadecylresorcinol induces sirtuin3-mediated autophagy. 5-Heptadecylresorcinol reduces the atherosclerotic plaques in the aortic root region of mice heart. 5-Heptadecylresorcinol can be used for research of atherosclerosis prevention and obesity[1][2].MCE products for research use only. We do not sell to patients.
5-Heptadecylresorcinol
MCE China:5-Heptadecylresorcinol
Brand:MedChemExpress (MCE)
Cat. No.HY-N2673
CAS:41442-57-3
Synonyms:5-n-Heptadecylresorcinol; AR-C17
Purity:99.83%
Storage:Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Shipping:Room temperature in continental US; may vary elsewhere.
Description:5-Heptadecylresorcinol (AR-C17), a phenolic lipid component, is also an orally active mitochondrial protector. 5-Heptadecylresorcinol improves mitochondrial function via sirtuin3 signaling pathway, thus alleviates endothelial cell damage and apoptosis. 5-Heptadecylresorcinol induces sirtuin3-mediated autophagy. 5-Heptadecylresorcinol reduces the atherosclerotic plaques in the aortic root region of mice heart. 5-Heptadecylresorcinol can be used for research of atherosclerosis prevention and obesity.
In Vitro:5-Heptadecylresorcinol (0, 0.5, 1, and 2 µM; 24 h) alleviates mitochondrial dysfunction through upregulation of SIRT3 in HUVECs[1]. 5-Heptadecylresorcinol alleviates inflammatory conditioned medium (CM) induced adipocyte lipolysis and mitochondrial damage, accompanied by attenuated mitochondrial reactive oxygen species production and mitochondrial membrane depolarization[2]. 5-Heptadecylresorcinol (5, 10 and 15 μM; 24 h) significantly prevents CM-induced adipocyte lipolysis by decreasing the release of glycerol in 3T3-L1 adipocytes[2]. 5-Heptadecylresorcinol (5, 10 and 15 μM; 24 h) ameliorates mitochondrial dysfunction in adipocytes induced by CM[2].
In Vivo:5-Heptadecylresorcinol (30 mg/kg, 150 mg/kg; po daily for 16 weeks) improves the lipid metabolism in HFD-fed ApoE−/− mice[1]. 5-Heptadecylresorcinol (30 mg/kg, 150 mg/kg; po daily for 16 weeks) increases the body weight of mouse, and alleviates adipose tissue macrophage infiltration and mitochondrial dysfunction[2].
IC50 & Target:SIRT3
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References:
[1]. Rakshit D, et al. The Pharmacological Activity of Garlic (Allium sativum) in Parkinson's Disease: From Molecular Mechanisms to the Therapeutic Potential. ACS Chem Neurosci. 2023 Mar 15;14(6):1033-1044. [Content Brief]
[2]. Yoo DY, et al. Neuroprotective effects of Z-ajoene, an organosulfur compound derived from oil-macerated garlic, in the gerbil hippocampal CA1 region after transient forebrain ischemia. Food Chem Toxicol. 2014 Oct;72:1-7. [Content Brief]
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