1. Cell Cycle/DNA Damage
    Metabolic Enzyme/Protease
    Immunology/Inflammation
    NF-κB
    Stem Cell/Wnt
    JAK/STAT Signaling
    Apoptosis
  2. PPAR
    Reactive Oxygen Species
    STAT
    NF-κB
    Apoptosis
  3. Astaxanthin

Astaxanthin 

Cat. No.: HY-B2163 Purity: ≥98.0%
Handling Instructions

Astaxanthin, the red dietary carotenoid, is an orally effective and potent antioxidant. Astaxanthin inhibits NF-κB and down-regulates VEGF in blood glucose. Astaxanthin exerts anti-cancer cell proliferation, increases apoptosis, impairs migration and invasion by activating PPARγ and reducing the expression of STAT3. Astaxanthin also has neuroprotective and anti-inflammatory activity and can be used in studies of cancer, diabetic retinopathy, cardiovascular disease, and in the coloring of animal feed.

For research use only. We do not sell to patients.

Astaxanthin Chemical Structure

Astaxanthin Chemical Structure

CAS No. : 472-61-7

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Based on 1 publication(s) in Google Scholar

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1 Publications Citing Use of MCE Astaxanthin

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  • Biological Activity

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  • References

  • Customer Review

Description

Astaxanthin, the red dietary carotenoid, is an orally effective and potent antioxidant. Astaxanthin inhibits NF-κB and down-regulates VEGF in blood glucose. Astaxanthin exerts anti-cancer cell proliferation, increases apoptosis, impairs migration and invasion by activating PPARγ and reducing the expression of STAT3. Astaxanthin also has neuroprotective and anti-inflammatory activity and can be used in studies of cancer, diabetic retinopathy, cardiovascular disease, and in the coloring of animal feed[1][2][3][4][5].

IC50 & Target[1]

PPARγ

 

STAT3

 

In Vitro

Astaxanthin (50, 100, 150, 200 µM; 48 h) inhibits the proliferation of DU145 cells (IC50<200 µM)[1].
Astaxanthin (200 µM; 24 h) reduces the expression of STAT3 and the related pathway proteins (at both protein and mRNA levels) by inhibiting proliferation, increasing apoptosis and weakening migration and invasion[1]
Astaxanthin protects RPE cells from abnormal activation and oxidative stress (induced by high glucose) by down-regulating VEGF in high glucose at protein levels[2].
Astaxanthin (1-50 µM; 72 h) upregulates protein expression of PPARγ in time- and dose-dependent manners in K562 cells[3].

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

Apoptosis Analysis[1]

Cell Line: DU145 cells
Concentration: 200 µM (pre-incubation)
Incubation Time: 24 h
Result: Increased the percentage of apoptotic cells from 8.5% to 13.1% (compared to blank control).

Cell Migration Assay [1]

Cell Line: DU145 cells
Concentration: 200 µM
Incubation Time: 24 h
Result: Decreased the migration and invasion of DU145 cells (about 41% of cells could not pass from one chamber to another, and 36% cells could not pass through the transwell membrane as compared to the control group).

Cell Proliferation Assay[2]

Cell Line: ARPE-19 cells
Concentration: 50 µM (pre-incubation)
Incubation Time: 7 days
Result: Significantly decreased cell proliferation exposed to high glucose.

Western Blot Analysis[1]

Cell Line: DU145 cells
Concentration: 200 µM
Incubation Time: 24 h
Result: Reduced the expression of STAT3 at both protein and mRNA levels (downregulated the protein expression of JAK2, BCL-2 and NF-κB and upregulated the protein expression of BAX, Caspase3 and Caspase9).

Western Blot Analysis[3]

Cell Line: K562 cells
Concentration: 1-50 µM
Incubation Time: 72 h
Result: Significantly promoted PPARγ protein expression in time- and dose-dependent manners.
In Vivo

Astaxanthin (200 mg/kg; intragastric administration; once daily for 3 weeks) inhibits the growth of DU145 tumor xenografts in nude mice[1].
Astaxanthin (125 or 500 mg/kg; in animal feedings; 7 days) provides significant cardioprotection and reduces oxidative stress in rats[4].

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

Animal Model: Nude mice (approximately 20 g; DU145 tumor xenografts model)[1].
Dosage: 200 mg/kg
Administration: Intragastric administration; once daily for 3 weeks.
Result: Exerted a significant inhibitory effect on tumor growth.
Animal Model: Female C57BL/6 mice (7 weeks old)[4].
Dosage: 125 or 500 mg/kg
Administration: In animal feedings; 7 days.
Result: Significantly reduced mean infarct size in the two treated groups (125 and 500 mg/kg) to 45.1% and 39.1%, respectively.
Exhibited myocardial salvage of 26 and 36% for 125 and 500 mg/kg groups, respectively.
Significantl reduced level of 9-HETE in a dose-dependent manner. 9-HETE is a regioisomer oxidation product of arachidonic acid believed to be a product of free radical-mediated oxidation.
Clinical Trial
Molecular Weight

596.84

Formula

C40H52O4

CAS No.
SMILES

CC(/C=C/C(C(C)(C[[email protected]](O)C1=O)C)=C1C)=C\C=C\C(C)=C\C=C\C=C(C)\C=C\C=C(C)\C=C\C(C(C)(C[[email protected]](O)C2=O)C)=C2C

Structure Classification
Source

Haematococcus pluvialis

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

-20°C, protect from light, stored under nitrogen

*The compound is unstable in solutions, freshly prepared is recommended.

Solvent & Solubility
In Vitro: 

DMSO : 2 mg/mL (3.35 mM; Need ultrasonic)

Acetone : < 1 mg/mL (insoluble)

*Astaxanthin is usually formulated as a suspension.

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.6755 mL 8.3775 mL 16.7549 mL
5 mM --- --- ---
10 mM --- --- ---
*Please refer to the solubility information to select the appropriate solvent.
Purity & Documentation

Purity: ≥98.0%

References
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Astaxanthin
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