Sesamin

• CAS: 607-80-7
• Catalog Number: ACM607807-2
• Category: Main Products
• Molecular Weight: 354.35
• Molecular Formula: C20H18O6
• Synonyms: Tetrahydro-1,4-bis[3,4-(methylenedioxy)phenyl]-1H,3H-furo[3,4-c]furan
• IUPAC Name: 5-[(3S,3aR,6S,6aR)-3-(1,3-benzodioxol-5-yl)-1,3,3a,4,6,6a-hexahydrofuro[3,4-c]furan-6-yl]-1,3-benzodioxole
• Canonical SMILES: C1[C@H]2[C@H](CO[C@@H]2C3=CC4=C(C=C3)OCO4)[C@H](O1)C5=CC6=C(C=C5)OCO6
• InChI: InChI=1S/C20H18O6/c1-3-15-17(25-9-23-15)5-11(1)19-13-7-22-20(14(13)8-21-19)12-2-4-16-18(6-12)26-10-24-16/h1-6,13-14,19-20H,7-10H2/t13-,14-,19+,20+/m0/s1
• InChI Key: PEYUIKBAABKQKQ-AFHBHXEDSA-N
• Boiling Point: 504.4±50.0 °C
• Melting Point: 121-125 °C
• Density: 1.385±0.06 g/ml
• Appearance: White powder
• Exact Mass: 354.11000
• Safety Description: S22-S24/25

Case Study

Sesamin for the Preparation of Sesamin-Loaded Sodium Caseinate Nanoparticles

Liu W-Y, et al. Food Bioscience, 2025, 68, 106386.

Sesamin-loaded sodium caseinate nanoparticles (S-CNPs) were developed using a simple coacervation method. The preparation involved dissolving sodium caseinate (NaCas) in deionized water, followed by the addition of lysine and sesamin dissolved in dimethylformamide. Calcium chloride was used to induce the formation of nanoparticles, with mannitol serving as a cryoprotectant during lyophilization. The resulting nanoparticles demonstrated an optimal size of 137 nm, a polydispersity index (PDI) of 0.20, and a zeta potential of -15.6 mV. The encapsulation efficiency of sesamin was 90%, and the stability studies revealed that the sesamin content remained above 90% after 28 days, indicating that the nanoparticles effectively protected sesamin from degradation.

Sesamin Alleviates Lipid Accumulation via PINK1/Parkin-Mediated Mitophagy in HepG2 Cells

Dong M, et al. Biochemical and Biophysical Research Communications, 2024, 708, 149815.

This study explores sesamin's protective effects against lipid accumulation in HepG2 cells induced by oleic acid (OA), a model for hepatic steatosis. The results reveal that sesamin effectively reduces lipid levels, including triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), while enhancing high-density lipoprotein cholesterol (HDL-C) levels.
Sesamin restores impaired autophagy and mitophagy, which are crucial in managing intracellular lipid accumulation. It was shown to modulate key lipid metabolism-related genes such as PCSK9, FABP1, CD36, and SOX4, improving fatty acid metabolism. Notably, sesamin enhances mitophagy by activating the PINK1/Parkin pathway, thereby improving mitochondrial homeostasis and mitigating lipid accumulation. This process was verified using transmission electron microscopy (TEM), Western blotting, and immunofluorescence techniques. The findings suggest that sesamin exerts its lipid-lowering effects by restoring mitochondrial function and autophagic processes, highlighting its therapeutic potential in preventing or treating hepatic steatosis.

Sesamin as a Neuroprotective Agent Against Lead-Induced Behavioral Deficits

Ghaderi S, et al. Brain Research Bulletin, 2024, 206, 110852

Sesamin exhibits neuroprotective potential by mitigating lead (Pb)-induced behavioral impairments. In a controlled study, male rats were administered 500 ppm Pb acetate via drinking water for eight weeks, with concurrent oral sesamin supplementation (30 mg/kg/day). Behavioral assessments revealed that Pb exposure resulted in heightened anxiety and depressive behaviors, along with impaired object recognition memory. However, locomotor activity remained unaffected. Notably, oxidative stress markers, including lipid peroxidation, were elevated in the cerebral cortex and hippocampus, while antioxidant defenses were suppressed. The administration of sesamin effectively reversed these neurotoxic effects by reducing oxidative damage and restoring enzymatic and non-enzymatic antioxidant levels. The study established a significant correlation between oxidative stress and behavioral deficits, highlighting sesamin's antioxidative mechanism as a primary factor in its neuroprotective role.

Sesamin as a Potential Therapeutic Agent for Hepatic Lipotoxicity and Lipid Metabolism Disorders

Pham TH, et al. Biochemical Pharmacology, 2023, 216, 115768.

Sesamin has garnered significant attention for its antioxidant, anti-inflammatory, and anticancer properties. The present case study focuses on the molecular mechanisms through which sesamin exerts hepatoprotective effects, particularly via the estrogen receptor alpha (ERα)-mediated signaling pathway.
A study employing an in vitro hepatic steatosis model using palmitate sodium-induced HepG2 cells demonstrated sesamin's efficacy in ameliorating lipotoxicity and reducing intracellular reactive oxygen species (ROS) production. The compound was found to modulate critical regulators of lipid metabolism, including fatty acid synthase (FASN), sterol regulatory element-binding protein 1c (SREBP-1c), forkhead box protein O-1 (FOXO1), and adipose triglyceride lipase (ATGL). By downregulating FASN and SREBP-1c, sesamin effectively suppressed lipogenesis while enhancing lipolysis, promoting a balanced lipid metabolism.
Molecular docking analysis further elucidated sesamin's interaction with ERα, suggesting that its beneficial effects are mediated through the Ca2+/calmodulin-dependent protein kinase kinase β (CaMKKβ)/AMP-activated protein kinase (AMPK) signaling pathway. Activation of this pathway enhances lipid catabolism and reduces hepatic steatosis, reinforcing sesamin's role in preventing fatty liver disease progression.