2. PI3K/Akt/mTOR Stem Cell/Wnt MAPK/ERK Pathway Metabolic Enzyme/Protease NF-κB Immunology/Inflammation
  3. Akt ERK p38 MAPK MMP NADPH Oxidase Reactive Oxygen Species (ROS) Keap1-Nrf2
  4. Adonixanthin

Adonixanthin  (Synonyms: (3S,3′R)-Adonixanthin)

Cat. No.: HY-W750654
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Adonixanthin ( (3S,3'R)-Adonixanthin), a carotenoid, is an orally active anti-oxidative and anti-carcinogenic agent. Adonixanthin shows an ability to suppress cell proliferation and migration in three types of glioblastoma cells Adonixanthin exerts cytoprotective effects against various types of damage and inhibits the increased production of ROS. Adonixanthin protects against light-induced cell damage through not only an anti-oxidative response but also through Nrf2 activation. Adonixanthin suppresses glioblastoma progression and adonixanthin improves blood-brain barrier hyper-permeability in an autologous blood ICH model. Adonixanthin can be used for the study of glioblastoma (GBM) and intracerebral hemorrhage (ICH).

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Adonixanthin

Adonixanthin Chemical Structure

CAS No. : 4418-73-9

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Adonixanthin Related Antibodies

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NOX1 NOX2 NOX4 NOX5 DUOX1

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Description

Adonixanthin ( (3S,3'R)-Adonixanthin), a carotenoid, is an orally active anti-oxidative and anti-carcinogenic agent. Adonixanthin shows an ability to suppress cell proliferation and migration in three types of glioblastoma cells Adonixanthin exerts cytoprotective effects against various types of damage and inhibits the increased production of ROS. Adonixanthin protects against light-induced cell damage through not only an anti-oxidative response but also through Nrf2 activation. Adonixanthin suppresses glioblastoma progression and adonixanthin improves blood-brain barrier hyper-permeability in an autologous blood ICH model. Adonixanthin can be used for the study of glioblastoma (GBM) and intracerebral hemorrhage (ICH)[1].

In Vitro

Adonixanthin (0.1-10 μM, 96 h) inhibits the proliferation of murine glioblastoma cell line GL261 and human glioblastoma cell line U251MG[1].
Adonixanthin (10 μM, 72 h) reduces the proportion of BrdU-positive cells in GL261 cells[1].
Adonixanthin (10 μM, 48 h) suppresses the migration of GL261 and U251MG cells[1].
Adonixanthin (10 μM, 6 h) decreases the phosphorylation levels of p-ERK1/2 and p-Akt in GL261 cells[1].
Adonixanthin (10 μM, 6-48 h) increases p-p38 phosphorylation, reduces cyclin D1 expression, increases p27 expression, and decreases the expression of MMP-2, Nox4 and fibronectin in GL261 cells, with no significant effect on MMP-9[1].
Adonixanthin (0.1-1 µM, 4 h) significantly reduces hemoglobin-induced cell death and ROS production in human brain endothelial cells (HBMVECs), and upregulates HO-1 and VE-cadherin levels[2].
Adonixanthin (0.1-1 µM, 28 h) significantly decreases collagenase-induced cell death in HBMVECs, inhibits ERK1/2 phosphorylation, and upregulates VE-cadherin levels[2].
Adonixanthin (0.1-1 µM, 25 h) concentration-dependently reduces H₂O₂-induced and LPS-induced cell death in SH-SY5Y cells[2].
Adonixanthin inhibits the activation of Epstein-Barr virus early antigen in Raji cells at concentrations resulting in an IC50 of 329 in molar ratio/Hyptadienic acid (TPA) (HY-N4024) without significant cytotoxicity[3].
Adonixanthin (167 μM) inhibits AMVN-induced methyl linolate peroxidation[3].
Adonixanthin (1-100 μM) shows singlet oxygen quenching activity in the methylene blue-sensitized photooxidation system in ethanol, with an IC50 of 11.1 μM[3].
Adonixanthin (20 μM, 6 h) upregulates the mRNA expression of Nrf2-controlled genes and increases Nrf2 in the nucleus in 661 W cells[4].
Adonixanthin (10 μM) protects against light-induced cell death and reduces ROS production induced by light exposure in 661 W cells, which is canceled by Nrf2 silencing[4].

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

Adonixanthin Related Antibodies

Cell Migration Assay [1]

Cell Line: GL261 and U251MG cells
Concentration: 10 μM
Incubation Time: 48 h
Result: Suppressed the migration of GL261 and U251MG cells.

Western Blot Analysis[1]

Cell Line: GL261 cells
Concentration: 10 μM
Incubation Time: 6, 48 h
Result: Decreased the phosphorylation levels of p-ERK1/2 and p-Akt.
Increased p-p38 phosphorylation.
Reduced cyclin D1 expression.
Increased p27 expression.
Decreased the expression of MMP-2, fibronectin and Nox4.

Western Blot Analysis[2]

Cell Line: human brain endothelial cells (HBMVECs)
Concentration: 1 μM
Incubation Time: 28 h
Result: Inhibited ERK1/2 phosphorylation.
Upregulated VE-cadherin levels.

Real Time qPCR[4]

Cell Line: 661 W cells
Concentration: 20 μM
Incubation Time: 6 h
Result: Upregulated the mRNA expression of Nrf2-controlled genes Ho-1, Nqo-1, and Gclm.
In Vivo

Adonixanthin (10-30 mg/kg, p.o., once daily, 10 days) significantly suppresses tumour progression in C57BL/6J mice with orthotopic glioblastoma[1].
Adonixanthin (100 mg/kg, p.o., once daily, 7 days) improves blood-brain barrier hyperpermeability in autologous blood injection intracerebral hemorrhage (ICH) model mice[2].
Adonixanthin (50 μg (85 nmol), applied topically, 1 hour before each TPA treatment for 20 weeks) significantly reduces the incidence and number of papillomas in DMBA (HY-W011845)-initiated and Hyptadienic acid (TPA) (HY-N4024)-promoted mouse skin carcinogenesis[3].

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

Animal Model: GL261 cells (1 × 105 in 2 µL PBS) were intracranially implanted into male C57BL/6J mice (8 weeks old; body weight 22-27 g))[1]
Dosage: 10, 30 mg/kg
Administration: p.o. once daily for 10 days
Result: Suppressed tumour progression and reduced tumour area and volume.
Showed no significant effect on body weight.
Animal Model: Male ddY mice aged 8-9 weeks were administered twenty-five microliters of blood over 5 min, with the needle left in place for 3 min and then slowly removed over 2 min[2]
Dosage: 100 mg/kg
Administration: p.o. once daily for 7 days until 12 h before ICH induction
Result: Improves blood-brain barrier hyperpermeability.
Reduced Evans blue leakage.
Ameliorated neurological deficits.
Increased Garcia scores.
Reduced the number of limb errors in the grid walk test.
Animal Model: ICR mice (6-week old) were treated with DMBA (100 μg, 390 nmol in 0.1 mL acetone) as the initiator applied topically one week before the first promotion[3]
Dosage: 50 μg (85 nmol) dissolved in 0.1 mL acetone
Administration: Applied topically to the shaved backs of mice 1 h before each Hyptadienic acid (TPA) (HY-N4024) treatment twice a week for 20 weeks
Result: Delayed the formation of papillomas.
Reduced the number of papillomas per mouse in DMBA-initiated and TPA-promoted mouse skin carcinogenesis.
Molecular Weight

582.85

Formula

C40H54O3
CAS No.
SMILES

CC1(C)C(/C=C/C(C)=C/C=C/C(C)=C/C=C/C=C(C)/C=C/C=C(C)/C=C/C(C(C)(C[C@@H]2O)C)=C(C)C2=O)=C(C)C[C@@H](O)C1
Structure Classification
Initial Source

marine bacterium strain SD-212
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Adonixanthin Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Adonixanthin4418-73-9(3S,3′R)-AdonixanthinAktERKp38 MAPKMMPNADPH OxidaseReactive Oxygen Species (ROS)Keap1-Nrf2PKBProtein kinase BExtracellular signal regulated kinasesMatrix metalloproteinasesNOXglioblastomaintracerebral hemorrhageAKTp38,MMPROSInhibitorinhibitorinhibit

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