Cat. No.: HY-N15190

Sesaminol

Sesaminol is an orally active antioxidant. Sesaminol induces G1 phase arrest and inhibits cancer cell growth by binding to ANT2, inhibiting mTORC1, and promoting cyclin D1 degradation; it also activates Nrf2/NQO1, inhibits ROS- and neurotoxin-induced apoptosis (apoptosis), reduces α-synuclein (α-synuclein) and Aβ oligomerization/fibril formation, and promotes M2 microglial polarization. Sesaminol can be used in research on cancer, Parkinson's disease, obesity, Alzheimer's disease, colitis, cognitive decline, and liver diseases.

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CAS No.: 74061-79-3
화학식: C₂₀H₁₈O₇
분자량:370.35

보관:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (314 KB)

Sesaminol Chemical Structure

CAS No.: 74061-79-3

Amount: USD 0.00

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- 제품 설명
- In Vitro
- In Vivo
Chemical Information
순도&문서
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

제품 설명

All mTOR Isoforms :

All α-synuclein Isoforms :

In Vitro

Anti-cancerProtein/Amino Acid MetabolismApoptosisAβ/Tau/α-Synuclein AggregationCell Cycle RegulationInnate ImmunityCytokines & ChemokinesLysosomal MetabolismOxidative StressLipid MetabolismMitochondrial FunctionMitochondrial Oxidative PhosphorylationOthers

Anti-cancer

Sesaminol (12.5-100 μM; 24 h) decreases cyclin D1 and RB phosphorylation in MCF7 cells, and 50 μM Sesaminol also decreases cyclin D1 in A549 and RKO cells^[1].
Sesaminol (50 μM; 3 h) reduces cyclin D1 mRNA levels in MCF7 cells^[1].
Sesaminol (50 μM) inhibits mTORC1 signaling in MCF7 cells in a time-dependent manner^[1].
Sesaminol (24 h) does not reduce intracellular ATP levels in MCF7 cells^[1].
Sesaminol (2.5-10 µM; 24 h) improves lipid handling and inhibits inflammatory signaling in PA+OA-exposed HepG2 cells^[9].
Sesaminol (10 µM; 24 h) restores PA+OA-suppressed PPARα and Slc27a5 protein expression in HepG2 cells^[9].
Sesaminol (10 µM; 24 h) promotes the binding of PPARα to the Slc27a5 promoter in HepG2 cells^[9].
Sesaminol (10 µM) increases BODIPY-C16 uptake in HepG2 cells^[9].
Sesaminol (10 µM; 24 h) restores the NAD⁺/NADH ratio in HepG2 cells after lipid overload^[9].
Sesaminol (10 µM; 24 h) upregulates Pparα and Cpt1a mRNA in PA+OA-exposed HepG2 cells^[9].
Sesaminol (40 μM; 24 h) enhances MFN2 immunofluorescence and reduces DRP1/Parkin immunofluorescence in HepG2 cells^[10].

Anti-cancer

Protein/Amino Acid Metabolism

Sesaminol (50 μM; 6 h) promotes the proteasomal degradation of cyclin D1 in MCF7 cells, as MG132 restores cyclin D1 levels after 6 h^[1].

Apoptosis

Sesaminol (1 μg/mL; 2 h) protects SH-SY5Y cells against 20 μM 6-OHDA-induced apoptotic morphological changes in PI staining^[3].

Aβ/Tau/α-Synuclein Aggregation

Sesaminol (25 µM; 24 h) inhibits human Aβ_1-42 amyloid fibril formation, as measured by ThT fluorescence^[5].
Sesaminol (25 µM; 24 h) prevents human Aβ_1-42 fibril formation, as visualized by TEM^[5].
Sesaminol (25 µM; 24 h) attenuates human Aβ_1-42 oligomer formation^[5].

Cell Cycle Regulation

Sesaminol (30 µg/mL; 48 h after induction) inhibits DNA synthesis during mitotic clonal expansion of 3T3-L1 cells^[6].

Innate Immunity

Sesaminol (10 μM) requires HIF-1α to suppress inflammation and promote M2 polarization in LPS-exposed BV2 microglia^[8].

Innate Immunity

Apoptosis

Sesaminol (pre-incubation for 24 h; co-culture for 24 h)-pre-exposed BV2 microglia protect HT-22 neurons by restoring neurological function proteins and reducing inflammation and apoptosis^[8].

Innate Immunity

Cytokines & Chemokines

Sesaminol (5-10 μM; 16 h) shifts BV2 microglia toward an M2-dominant phenotype under LPS or IL-4 stimulation^[8].
Sesaminol (16 h after stimulation) promotes M2 marker expression in BV2 microglia^[8].

Innate Immunity

Cytokines & Chemokines

Aβ/Tau/α-Synuclein Aggregation

Lysosomal Metabolism

Sesaminol (10 μM; pre-incubation for 16 h and incubation for 16 h) promotes Aβ phagocytosis by BV2 microglia in a LAMP1-dependent manner^[8].

Innate Immunity

Oxidative Stress

Sesaminol (10 μM) reverses LPS-induced transcriptomic changes in BV2 microglia^[8].

Innate Immunity

Oxidative Stress

Aβ/Tau/α-Synuclein Aggregation

Sesaminol (5-10 μM; 24 h) inhibits Aβ-induced oxidative stress and inflammatory signaling in BV2 microglia^[8].

Lipid Metabolism

Sesaminol (10-20 µM; 4 h) induces Ucp1 mRNA expression in primary iWAT SVF-derived white adipocytes, reaching up to approximately 6.5-fold at 20 µM, without increasing Trilaurin (HY-126573) content^[4].
Sesaminol (30 µg/mL; 8 days) reduces lipid accumulation and GPDH activity in differentiated 3T3-L1 adipocytes^[6].
Sesaminol (30 µg/mL; the first 2 days of the 8-day differentiation process) exhibits the strongest inhibitory effect on lipid accumulation in 3T3-L1 adipocytes^[6].
Sesaminol (30 µg/mL; C/EBPβ exposure for 24 h) inhibits C/EBPβ protein in 3T3-L1 adipocytes and downregulates C/EBPα and PPARγ mRNA and protein^[6].
Sesaminol (10 µM; 24 h) reduces neutral lipid accumulation in PA+OA-exposed HepG2 cells in a Slc27a5-dependent manner^[9].

Mitochondrial Function

Anti-cancer

Sesaminol (40 μM; 24 h) increases mitochondrial content and ROS levels in HepG2 cells^[10].
Sesaminol (40 μM; 24 h) does not significantly alter the levels of mitochondrial dynamics marker proteins in HepG2 cells^[10].

Mitochondrial Function

Lipid Metabolism

Sesaminol (4 days) inhibits myogenic differentiation and shifts C2C12 myoblasts toward an adipocyte-like phenotype, while increasing the expression of mitochondrial markers^[4].

Mitochondrial Oxidative Phosphorylation

Sesaminol (20 µM; differentiation days 4 to 7) increases Ucp1, Pgc1a, and CytC expression and uncoupled oxygen consumption in BAT SVF-derived brown adipocytes^[4].

Oxidative Stress

Sesaminol (1 μg/mL; 2 h) inhibits 20 μM 6-OHDA-induced intracellular ROS production in SH-SY5Y cells^[3].
Sesaminol (1 μg/mL; 6 h) inhibits the 20 μM 6-OHDA-induced increase in the GSSG/GSH ratio in SH-SY5Y cells^[3].
Sesaminol (1 μg/mL; 2 h) promotes Nrf2 nuclear translocation in SH-SY5Y cells exposed to 20 μM 6-OHDA for 3 h^[3].
Sesaminol (1 μg/mL; 2 h) enhances NQO1 activity in SH-SY5Y cells exposed to 20 μM 6-OHDA for 6 h^[3].
Sesaminol (30 µg/mL; 4-26 h after induction) inhibits intracellular ROS levels in 3T3-L1 preadipocytes^[6].
Sesaminol (30 µg/mL) upregulates HO-1 and GCLC mRNA expression in 3T3-L1 adipocytes^[6].
Sesaminol (30 µg/mL; 24 h after induction) promotes Nrf2 nuclear translocation in 3T3-L1 cells^[6].
Sesaminol (10-100 μM; 5 min) exhibits concentration-dependent antioxidant activity in the luminol chemiluminescence quenching assay, reducing luminescence to approximately 50% of the control at 10 μM and to basal levels at 100 μM^[7].
Sesaminol (12.5-100 μM; 1 h) induces less than 10% linear DNA formation in the plasmid DNA nicking assay, with over 90% remaining in the ccc form, indicating very low pro-oxidant activity^[7].

Others

Sesaminol (100 mM; 24 h) directly binds ANT2 in MCF7 whole-cell extracts and purified recombinant FLAG-ANT2^[1].
Sesaminol (1-5 μg/mL; 2 h) protects SH-SY5Y cells against 20 μM 6-OHDA-induced loss of viability in the MTT assay^[3].
Sesaminol (8 days) downregulates myogenic genes during adipogenic differentiation of C2C12 myoblasts^[4].
Sesaminol (20-100 µg/mL; 24 h) shows no cytotoxicity to 3T3-L1 preadipocytes at concentrations below 40 µg/mL^[6].
Sesaminol (30 µg/mL) reduces the expression of cyclin E1, cyclin E2, and CDK2 in 3T3-L1 adipocytes^[6].
Sesaminol (30 µg/mL; 4-24 h after induction) inhibits the centromeric localization of C/EBPβ in 3T3-L1 cells^[6].
Sesaminol (30 µg/mL) increases AMPK phosphorylation in 3T3-L1 adipocytes^[6].
Sesaminol (0.5-100 μM; 12 h) is not toxic to BV2 microglial cells at concentrations up to 10 μM and begins to induce significant cytotoxicity at 25 μM^[8].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cycle Analysis^[1]

Cell Line:

MCF7
Concentration:

12.5, 25, 50, 100 μM
Incubation Time:

24 h
Result:

Dose-dependently accumulated MCF7 cells in G1 phase.

Western Blot Analysis^[1]

Cell Line:

MCF7, MCF-10A, WI-38, MDA-MB-231, SK-MEL-28, A549, RKO
Concentration:

12.5, 25, 50, 100 μM (MCF7 concentration course); 50 μM (MCF7 time course); 50 μM (MCF-10A, WI-38, MDA-MB-231, SK-MEL-28, A549, RKO); 100 μM (MDA-MB-231, SK-MEL-28)
Incubation Time:

24 h (MCF7 concentration course); 3, 6, 12, 24 h (MCF7 time course); 6 h (MCF-10A, WI-38, MDA-MB-231, SK-MEL-28, A549, RKO); 24 or 48 h (MDA-MB-231, SK-MEL-28 at 100 μM)
Result:

In MCF7, sesaminol dose-dependently reduced cyclin D1 and caused dephosphorylation of RB at Ser780 and Ser807/811.
At 50 μM, sesaminol time-dependently reduced cyclin D1, and RB was converted to the hypophosphorylated form.
At 50 μM for 6 h, cyclin D1 was remarkably reduced in A549 and RKO cells; no reduction was observed in WI-38, MDA-MB-231, or SK-MEL-28 cells; MCF-10A cells showed little apparent cyclin D1 expression with or without sesaminol.
At 100 μM for 24 or 48 h, cyclin D1 was reduced in MDA-MB-231 and SK-MEL-28 cells.

Real Time qPCR^[1]

Cell Line:

MCF7
Concentration:

50 μM
Incubation Time:

3 h
Result:

Suppressed cyclin D1 mRNA expression; data obtained with DMSO were taken as 1.0.

Western Blot Analysis^[1]

Cell Line:

MCF7
Concentration:

50 μM
Incubation Time:

6 h
Result:

MG132 restored the sesaminol-induced reduction in cyclin D1.

Cell Viability Assay^[3]

Cell Line:

human neuroblastoma SH-SY5Y cells
Concentration:

0.25, 0.5, 1, 5, 10 μg/mL (cytotoxicity evaluation); 1 or 5 μg/mL (with 20 μM 6-OHDA); 1 μg/mL (subsequent experiments)
Incubation Time:

2 h (sesaminol pre-exposure before 6-OHDA)
Result:

Did not affect SH-SY5Y cell viability from 0.25 to 10 μg/mL. 20 μM 6-OHDA significantly reduced cell viability.
Pre-exposure with 1 or 5 μg/mL sesaminol restored viability to the control level.

Apoptosis Analysis^[3]

Cell Line:

SH-SY5Y cells
Concentration:

1 μg/mL
Incubation Time:

2 h (sesaminol pre-exposure); 1 h (PI staining at 37 °C)
Result:

6-OHDA alone produced morphological abnormalities such as nuclear aggregation.
These abnormalities were alleviated by 2 h sesaminol pre-exposure.

Immunofluorescence^[3]

Cell Line:

SH-SY5Y cells
Concentration:

1 μg/mL
Incubation Time:

2 h (sesaminol); 3 h (6-OHDA); overnight at 4 °C (anti-Nrf2 antibody); 1 h (secondary antibody)
Result:

Control cells showed almost no nuclear Nrf2 expression, and 6-OHDA alone showed slight expression.
Cells pre-exposed to sesaminol showed strong Nrf2 expression in the cytoplasm and nuclei.

Cell Viability Assay^[6]

Cell Line:

3T3-L1 preadipocytes
Concentration:

20, 40, 60, 80, 100 µg/mL; below 40 µg/mL
Incubation Time:

24 h
Result:

Did not significantly affect 3T3-L1 preadipocyte viability at concentrations below 40 µg/mL.

Cell Differentiation Assay^[6]

Cell Line:

differentiated 3T3-L1 adipocytes
Concentration:

30 µg/mL; below 40 µg/mL
Incubation Time:

8 days
Result:

Decreased lipid accumulation in differentiated 3T3-L1 adipocytes at 30 µg/mL; reduced red-stained intracellular lipid granules were quantified spectrophotometrically.

Cell Differentiation Assay^[6]

Cell Line:

3T3-L1 preadipocytes
Concentration:

30 µg/mL
Incubation Time:

8-day differentiation period; first 2 days
Result:

Significantly suppressed triacylglycerol accumulation, particularly during the first two days of differentiation.

Cell Proliferation Assay^[6]

Cell Line:

3T3-L1 cells
Concentration:

30 µg/mL
Incubation Time:

48 h post-induction
Result:

Inhibited DNA synthesis during mitotic clonal expansion; no rise in DNA content at 48 h post-induction, unlike control cells.

Immunofluorescence^[6]

Cell Line:

3T3-L1 cells
Concentration:

30 µg/mL
Incubation Time:

4, 16, and 24 h after differentiation induction
Result:

Suppressed centromeric localization of C/EBPβ at all examined time points (4, 16, and 24 h after induction).

Immunofluorescence^[6]

Cell Line:

3T3-L1 cells
Concentration:

30 µg/mL
Incubation Time:

4, 16, and 24 h after induction; significant increase at 24 h post-differentiation
Result:

Increased nuclear Nrf2 levels at 24 h post-differentiation compared with control.
Compound C significantly reduced the increased Nrf2 levels.
Nuclear/whole cell ratio supported enhanced Nrf2 nuclear translocation.

Cell Viability Assay^[8]

Cell Line:

murine BV2 microglial cells
Concentration:

0.5, 1, 2.5, 5, 10, 25, 50, 100 μM
Incubation Time:

12 h
Result:

Nontoxic up to 10 μM.
25 μM sesaminol began to induce significant cytotoxicity.

Western Blot Analysis^[9]

Cell Line:

HepG2 cells
Concentration:

10 µM
Incubation Time:

24 h
Result:

PA+OA exposure markedly suppressed PPARα and Slc27a5 protein levels; sesaminol fully restored both to baseline.

Real Time qPCR^[9]

Cell Line:

HepG2 cells
Concentration:

10 µM
Incubation Time:

24 h
Result:

qPCR results revealed that sesaminol elevated Pparα and Cpt1a transcripts under PA and OA challenge, increases that were abolished by GW6471, confirming the PPARα-dependent mechanism.

Western Blot Analysis^[10]

Cell Line:

HepG2 human hepatoma cells
Concentration:

40 μM
Incubation Time:

24 h (SML); overnight at 4°C (primary antibodies)
Result:

Immunoblotting analyses did not reveal significant changes in mitochondrial dynamics markers.

In Vivo

Aβ/Tau/α-Synuclein AggregationCarbohydrate MetabolismLipid MetabolismCytokines & ChemokinesInnate ImmunityOxidative StressMitochondrial FunctionMitochondrial Oxidative Phosphorylation

Aβ/Tau/α-Synuclein Aggregation

Sesaminol (0.0008-0.008%; diet; ad libitum; from day -7 to day 29) prevents Rotenone (HY-B1756)-induced motor and intestinal dysfunction and attenuates α-synuclein and colonic mucosal pathology in a mouse model of Parkinson's disease^[3].

Carbohydrate Metabolism

Lipid Metabolism

Cytokines & Chemokines

Sesaminol (5 mg/kg; intraperitoneal injection; continuously for 14 days starting from the 4th week of the 6-week HFD modeling) ameliorates chronic HFD-induced obesity in C57BL/6J mice and improves glucose tolerance, insulin sensitivity, and serum lipid/adipokine profiles^[4].

Carbohydrate Metabolism

Lipid Metabolism

Cytokines & Chemokines

Innate Immunity

Sesaminol (50 mg/kg; oral gavage; once daily; 12 weeks) ameliorates HFD-induced MAFLD in male C57BL/6J mice by reducing body weight, improving glucose and insulin homeostasis, lowering hepatic and serum lipids, inhibiting inflammation, and activating the PPARα/Slc27a5 axis^[9].

Innate Immunity

Sesaminol (50 mg/kg; oral; once daily; for 5 consecutive days) reverses LPS-induced acute cognitive impairment and hippocampal neuroinflammation in male C57BL/6J mice^[8].

Innate Immunity

Carbohydrate Metabolism

Lipid Metabolism

Sesaminol (5 mg/kg BW; i.p.; 14 days) alleviates HFD-induced NAFLD/MAFLD by improving metabolic parameters, reducing hepatic lipids and inflammation, and remodeling the phospholipid profile^[10].

Innate Immunity

Oxidative Stress

Sesaminol (100 mg/kg body weight/day; intragastric administration; once daily; for 14 days) attenuates chronic ethanol-induced colonic oxidative stress, inflammation, colonic lesions, and increased intestinal permeability in mice^[7].

Innate Immunity

Oxidative Stress

Aβ/Tau/α-Synuclein Aggregation

Sesaminol (10-50 mg/kg; intragastric administration; 14 weeks) dose-dependently ameliorates age-related cognitive decline and reduces oxidative stress, neuroinflammation, M1 microglial polarization, and hippocampal Aβ load in middle-aged male C57BL/6 mice^[8].

Lipid Metabolism

Sesaminol (5 mg/kg; intraperitoneal injection; daily; for 10 days) prevents acute HFD-induced weight gain and promotes BAT function and iWAT browning in C57BL/6J mice^[4].

Lipid Metabolism

Cytokines & Chemokines

Innate Immunity

Sesaminol (50 mg/kg; intragastric administration; once daily; 5 days) attenuates acute binge alcohol-induced liver injury and inflammation and improves hepatic lipid handling and liver function in male C57BL/6J mice^[9].

Lipid Metabolism

Innate Immunity

Sesaminol (50 mg/kg; intragastric administration; once daily; 5 days) protects male C57BL/6J mice against acute binge alcohol-induced liver injury through the PPARα/Slc27a5 axis, and PPARα blockade abolishes this protective effect^[9].

Lipid Metabolism

Mitochondrial Function

Mitochondrial Oxidative Phosphorylation

Sesaminol (2 mg/kg; i.p.; 1 week or 2 weeks) increases hepatic mitochondrial content and OXPHOS proteins and alters lipid metabolism in mice fed a normal diet^[10].

Mitochondrial Function

Mitochondrial Oxidative Phosphorylation

Lipid Metabolism

Sesaminol (2 mg/kg; intraperitoneal injection; for 7 days) stimulates brown adipose tissue activity and subcutaneous white adipose tissue browning, and enhances mitochondrial function and oxygen consumption in C57BL/6J mice fed a standard diet^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

C57BL6/J (male, 7-week-old)^[3]
Dosage:

0.0008% in diet (L); 0.008% in diet (H)
Administration:

diet; ad libitum; from day -7 to day 29
Result:

Prevented rotenone-induced motor and intestinal dysfunction and reduces α-synuclein and colonic mucosal pathology in a mouse model of Parkinson's disease.

Animal Model:

C57BL/6J (male)^[4]
Dosage:

2 mg/kg BW
Administration:

intraperitoneal; for 7 days
Result:

Stimulated brown fat activity and browning of subcutaneous white adipose tissue in chow-fed C57BL/6J mice, enhancing mitochondrial function and oxygen consumption.

Animal Model:

C57BL/6J (male)^[4]
Dosage:

5 mg/kg BW
Administration:

intraperitoneal; daily; for 10 days along with HFD
Result:

Protected against acute HFD-induced weight gain and promotes BAT function and iWAT browning in C57BL/6J mice.

Animal Model:

C57BL/6J (male)^[4]
Dosage:

5 mg/kg BW
Administration:

intraperitoneal; for 14 days from the 4th week of a 6-week HFD challenge
Result:

Ameliorated chronic HFD-induced obesity and improves glucose tolerance, insulin sensitivity, and serum lipid/adipokine profiles in C57BL/6J mice.

Animal Model:

C57BL/6NCr (male, 8 weeks old, average body weight 23.0 g)^[7]
Dosage:

2.5 mg per mouse per day (100 mg/kg body weight per day)
Administration:

oral gavage; once daily; for 14 days; in 1 mL LDCLD
Result:

In group ES, the microscopic colonic lesion score was lower than in ethanol-only group E and slightly higher than in groups C and S.
Colonic 8-OHdG levels were lower in group ES than in group E and higher than in groups C and S.
Colonic MDA + HAE levels were lower in group ES than in group E and slightly higher than in groups C and S.
Colonic CYP2E1 and iNOS levels were lower in group ES than in group E, while colonic HO-1 levels and Nrf2 activation were higher in group ES than in group E and restored toward control levels.
Colonic TNF-α, IL-6, and MCP-1 mRNA and protein levels were lower in group ES than in group E.
NF-κB p65 activation was lower in group ES than in group E.
Colonic ZO-1, occludin, and claudin-1 levels were higher in group ES than in group E, and plasma LPS levels were lower in group ES than in group E.
On day 15, group ES body weight was 25.1 g, liver/body weight ratio was 3.77%, liver TG was 66.0 mg/g protein, plasma AST was 44.1 U/L, plasma ALT was 45.3 U/L, and plasma TG was 0.57 mmol/L.

Animal Model:

C57BL/6 (male, 12 months old; young control 2 months old)^[8]
Dosage:

10 mg/kg; 50 mg/kg
Administration:

gavage; for 14 weeks
Result:

Dose-dependently ameliorated age-related cognitive decline and reduces oxidative stress, neuroinflammation, M1 microglial polarization, and hippocampal Aβ load in middle-aged male C57BL/6 mice.

Animal Model:

C57BL/6J (male, 8 weeks old)^[8]
Dosage:

50 mg/kg
Administration:

oral; once daily; for 5 consecutive days
Result:

Reversed LPS-induced acute cognitive impairment and hippocampal neuroinflammation in male C57BL/6J mice.

Animal Model:

C57BL/6J (male, 7-week-old at purchase, acclimated for 1 week)^[9]
Dosage:

50 mg/kg body weight
Administration:

oral gavage; once daily; 12 weeks
Result:

Ameliorated HFD-induced MAFLD in male C57BL/6J mice by reducing body weight, improving glucose and insulin homeostasis, lowering hepatic and serum lipids, inhibiting inflammation, and activating the PPARα/Slc27a5 axis.

Animal Model:

C57BL/6J (male)^[9]
Dosage:

50 mg/kg
Administration:

oral gavage; once daily; 5 days
Result:

Attenuated acute binge alcohol-induced liver injury and inflammation and improves hepatic lipid handling and liver function in male C57BL/6J mice.

Animal Model:

C57BL/6J (male, 7-week-old)^[9]
Dosage:

50 mg/kg
Administration:

oral gavage; once daily; 5 days
Result:

Protected male C57BL/6J mice against acute binge alcohol-induced liver injury through the PPARα/Slc27a5 axis, and PPARα blockade abolishes this protective effect.

Animal Model:

C57BL/6 (male; 2-3 months old)^[10]
Dosage:

2 mg/kg BW
Administration:

i.p.; for 1 week or 2 weeks
Result:

Increased hepatic mitochondrial content and OXPHOS proteins and alters lipid metabolism in mice fed a normal diet.

Animal Model:

C57BL/6 (male)^[10]
Dosage:

5 mg/kg BW
Administration:

i.p.; for 14 days, starting from the sixth week of the 8-week HFD challenge
Result:

Alleviated HFD-induced NAFLD/MAFLD by improving metabolic parameters, reducing hepatic lipids and inflammation, and remodeling the phospholipid profile.

Related Protocols :

Chemical Information

CAS No. 74061-79-3
분자량 370.35
화학식 C₂₀H₁₈O₇
SMILES

OC1=C(C=C2C(OCO2)=C1)[C@@H]3[C@]4([H])[C@@](CO3)([H])[C@@H](C5=CC=C(OCO6)C6=C5)OC4
Structure Classification
- Phenylpropanoids
- Lignans
Initial Source
선적

Room temperature in continental US; may vary elsewhere.
보관

Please store the product under the recommended conditions in the Certificate of Analysis.

순도&문서

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (314 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Watanabe M, et al. The pleiotropic regulation of cyclin D1 by newly identified sesaminol-binding protein ANT2. Oncogenesis. 2017 Apr 03;6(4):e311.

[2]. Sheng H, et al. Modifying effect of dietary sesaminol glucosides on the formation of azoxymethane-induced premalignant lesions of rat colon. Cancer letters. 2007 Feb 08;246(1-2):63-8.

[3]. Kaji H, et al. Sesaminol prevents Parkinson's disease by activating the Nrf2-ARE signaling pathway. Heliyon. 2020 Nov;6(11):e05342. [Content Brief]

[4]. Divakaran SJ, et al. Sesaminol induces brown and beige adipocyte formation through suppression of myogenic program. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2020 May;34(5):6854-6870.

[5]. Katayama S, et al. Effects of Sesaminol Feeding on Brain Aβ Accumulation in a Senescence-Accelerated Mouse-Prone 8. Journal of agricultural and food chemistry. 2016 Jun 22;64(24):4908-13.

[6]. Nakamatsu S, et al. Sesaminol Inhibits Adipogenesis by Suppressing Mitotic Clonal Expansion and Activating the Nrf2-ARE Pathway. Nutrients. 2025 Oct 15;17(20):3242.

[7]. Ohira H, et al. Suppression of colonic oxidative stress caused by chronic ethanol administration and attenuation of ethanol-induced colitis and gut leakiness by oral administration of sesaminol in mice. Food & function. 2022 Sep 22;13(18):9285-9298.

[8]. Zheng L, et al. Sesaminol Ameliorates Age-Related Cognitive Decline and Neuroinflammation by Modulating Microglial Polarization and Enhancing Aβ Phagocytosis in Mice. Journal of agricultural and food chemistry. 2026 Feb 04;74(4):3624-3641.

[9]. Zheng L, et al. Sesaminol Ameliorates Metabolic and Alcohol-Related Liver Injury by Activating the PPARα/Slc27a5 Axis-Driven Hepatic Fatty Acid β-Oxidation. Molecular nutrition & food research. 2026 May;70(10):e70506. [Content Brief]

[10]. Rajendran R, et al. Sesaminol alters phospholipid metabolism and alleviates obesity-induced NAFLD. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2024 Jul 31;38(14):e23835.

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Sesaminol

All mTOR Isoforms

All α-synuclein Isoforms