Norbixin
Norbixin is an orally active natural product with multiple activities such as retinal protection and oxidative stress regulation. Norbixin scavenges ROS, chelates metal ions, regulates plasmid and genomic DNA breakage, inhibits H2O2-induced mutagenesis, activates PPAR-α, modulates lipid levels, restores or regulates antioxidant enzyme activity, and alters NO levels. Norbixin prevents A2E accumulation and protects photoreceptor cells and retinal pigment epithelial cells. Norbixin is a derivative of Bixin (HY-N6884). Norbixin can be used in research related to diseases such as macular degeneration and diabetes, and also serves as a natural textile dye.
Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.
- CAS No.: 542-40-5
- Formule: C24H28O4
- Masse moléculaire:380.48
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Stockage:
-80°C, protect from light
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Activité biologique
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Chemical Information
- Pureté et documentation
- Références
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Activité biologique
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PPARα |
Norbixin (5-50 μM; administered 48 h prior to illumination) potently protects primary porcine retinal pigment epithelial (RPE) cells against A2E-mediated blue light phototoxic damage[1].
Norbixin (5-20 μM; administered 48 h prior to A2E addition) reduces A2E accumulation in primary porcine retinal pigment epithelial (RPE) cells in a dose-dependent manner[1].
Norbixin delivers the maximum color strength when dyeing ferrous sulfate pre-mordanted cotton fabrics[2].
Norbixin protects plasmid pZEM3-EJ-Ras DNA against oxidative breakage induced by Sn2+ and Fe2+, but acts as a pro-oxidant to enhance Sn2+-induced DNA damage at concentrations below 100 μM[3].
Norbixin (1-5 mg/plate; 30 min) exhibits antimutagenic activity against H2O2-induced mutagenicity in Salmonella typhimurium TA102[3].
Norbixin (10-450 μM; 2 h) protects Balb/c 3T3 fibroblasts against H2O2-induced DNA damage under low-serum conditions; however, at concentrations above 50 μM, it exacerbates DNA damage under low-serum conditions, exerts no protective effect under high-serum conditions, and shows no inherent genotoxicity itself[3].
Norbixin (10-250 μM; 0-120 h) exerts cytostatic effects on Balb/c 3T3 fibroblasts, with an IC50 of 150 μM for inhibiting DNA synthesis, and shows no lethal cytotoxicity at the highest concentration of 250 μM[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:primary porcine RPE cells
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Concentration:5, 10, 20, 50 μM
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Incubation Time:48 h
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Result:Protected primary porcine RPE cells against A2E-mediated blue-light phototoxicity, with 72.5% cell survival observed at 5 μM and peak protection of 83% at 20 μM.
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Cell Line:Balb/c 3T3 fibroblasts (clone A31)
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Concentration:10, 25, 50, 100, 250 μM
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Incubation Time:0, 24, 48, 72, 120 h
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Result:Exerted a cytostatic effect on fibroblasts, with an IC50 of 150 μM for inhibition of DNA synthesis.
Showed no lethal cytotoxic effects across tested concentrations.
Norbixin (10-100 mg/kg; i.p.; administered 4 times) dose-dependently protects rats against blue light-induced retinal injury[1].
Norbixin (2.5 mg/day; oral administration; continuous dosing; 3 months) reduces retinal A2E accumulation in Abca4-/- Rdh8-/- mice[1].
Norbixin (10-100 mg/kg; p.o.; daily; for 30 consecutive days) reduces NOx levels and normalizes catalase activity at the dose of 10 mg/kg, but fails to improve blood glucose, dyslipidemia or protein oxidation in streptozotocin (HY-13753)-induced diabetic rats; in contrast, the 100 mg/kg dose exacerbates dyslipidemia and oxidative stress markers including protein oxidation and NOx levels[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Abca4-/- Rdh8-/- (carrying Rpe65-Leu450 and rd8 mutations; 7 weeks old)[1]
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Dosage:130 μM (final intravitreal concentration)
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Administration:i.vit.; once; 24 hours before light exposure
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Result:Maintained significantly higher a- and b-wave amplitudes compared to non-injected or vehicle-injected eyes.
Preserved 4 to 6 rows of photoreceptors in the central retina 1 week after light exposure, compared to 0 to 2 rows in non-injected or vehicle-injected eyes.
Partially preserved outer segments.
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Animal Model:Sprague-Dawley (male; 240-320 g)[1]
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Dosage:10, 50, 100 mg/kg
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Administration:i.p.; 4 times (30 minutes pre-exposure, 2, 4, 6 hours post-exposure start)
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Result:Dose-dependently alleviated a-wave amplitude loss and diminished b-wave loss by 57% at 100 mg/kg versus vehicle rats.
100 mg/kg preserved 95% retinal photoreceptors; 10 mg/kg and 50 mg/kg afforded partial photoreceptor protection matching the positive control.
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Animal Model:Abca4-/- Rdh8-/- (2 months old at treatment start)[1]
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Dosage:2.5 mg per day
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Administration:p.o.; continuously; 3 months
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Result:Reduced retinal A2E levels to 55% of vehicle-treated control levels (67 pmol/eye vs 122 pmol/eye).
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Animal Model:Wistar rats (adult male, 70-90 days, 200-350 g, Streptozotocin-induced diabetic)[4]
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Dosage:10 mg/kg; 100 mg/kg
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Administration:p.o.; daily; 30 days
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Result:Retained unchanged blood glucose, fructosamine, triglyceride, LDL cholesterol and AOPP levels relative to diabetic vehicle controls; meanwhile reduced HDL cholesterol and TrxR activity against both non-diabetic and diabetic vehicle groups, and lowered NOx content compared with diabetic vehicle controls.
Doubled SOD activity relative to non-diabetic controls and normalized catalase activity in diabetic vehicle groups.
Elevated total cholesterol, LDL cholesterol, triglycerides, AOPP and NOx levels simultaneously versus diabetic vehicle controls, increased SOD activity with stable catalase activity, and upregulated GPx activity against both control groups.
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS No. 542-40-5
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Appearance Solid
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Masse moléculaire 380.48
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Formule C24H28O4
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Color Red to reddish brown
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SMILES
O=C(O)/C=C/C(C)=C/C=C/C(C)=C/C=C/C=C(C)/C=C/C=C(C)/C=C/C(O)=O
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Structure Classification
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Initial Source
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Livraison
Shipping with dry ice.
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Stockage
-80°C, protect from light
Pureté et documentation
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Fiche technique (275 KB)
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SDS (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. Fontaine V, et al. Norbixin Protects Retinal Pigmented Epithelium Cells and Photoreceptors against A2E-Mediated Phototoxicity In Vitro and In Vivo. PloS one. 2016;11(12):e0167793. [Content Brief]
[3]. Kovary K, et al. Biochemical behaviour of norbixin during in vitro DNA damage induced by reactive oxygen species. The British journal of nutrition. 2001 Apr;85(4):431-40. [Content Brief]
[4]. Roehrs M, et al. Bixin and norbixin have opposite effects on glycemia, lipidemia, and oxidative stress in streptozotocin-induced diabetic rats. International journal of endocrinology. 2014;2014:839095. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Norbixin Related Classifications
HY-W587784 Related Classifications
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- Norbixin
- 542-40-5
- PPAR
- Reactive Oxygen Species (ROS)
- NO Synthase
- DNA/RNA Synthesis
- Balb/c 3T3 fibroblasts
- peroxisome proliferator-activated receptor alpha (PPAR-α)
- primary porcine RPE cells
- Salmonella typhimurium TA102
- retinal pigment epithelium cells
- dry age-related macular degeneration
- reactive oxygen species
- fibroblasts
- Abca4-/- Rdh8-/- mice
- diabetes mellitus
- Inhibitor
- inhibitor
- inhibit