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    alpha-Carotene
    alpha-Carotene
    Information
    CAS No. 7488-99-5 Price
    Catalog No.CFN93610Purity>=98%
    Molecular Weight536.87Type of CompoundMiscellaneous
    FormulaC40H56Physical DescriptionPowder
    Download     COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: alpha-Carotene has anti-metastasis activity, it inhibits metastasis in Lewis lung carcinoma in vitro, and suppresses lung metastasis and tumor growth in combination with taxol in tumor xenografted C57BL/6 mice. alpha-Carotene has inhibitory effects on proliferation of the human neuroblastoma cell line GOTO.
    Targets: FAK | MMP(e.g.TIMP) | MAPK
    In vitro:
    J Nutr Biochem. 2015 Jun;26(6):607-15.
    Alpha-carotene inhibits metastasis in Lewis lung carcinoma in vitro, and suppresses lung metastasis and tumor growth in combination with taxol in tumor xenografted C57BL/6 mice.[Pubmed: 25736483 ]
    This study aimed to investigate the anti-metastatic activity of alpha-Carotene (AC) in Lewis lung carcinoma (LLC) and in combination with taxol in LLC-xenografted C57BL/6 mice.
    METHODS AND RESULTS:
    Cell culture studies reveal that AC significantly inhibited invasion, migration and activities of matrix metalloproteinase (MMP)-2, -9 and urokinase plasminogen activator but increased protein expression of tissue inhibitor of MMP (TIMP)-1, -2 and plasminogen activator inhibitor (PAI)-1. These effects of AC are similar to those of β-carotene at the same concentration (2.5 μM). AC (2.5 μM) also significantly inhibited integrin β1-mediated phosphorylation of focal adhesion kinase (FAK) which then decreased the phosphorylation of MAPK family. Findings from the animal model reveal that AC treatment (5m g/kg) alone significantly decreased lung metastasis without affecting primary tumor growth, whereas taxol treatment (6 mg/kg) alone exhibited significant inhibition on both actions, as compared to tumor control group. AC treatment alone significantly decreased protein expression of integrin β1 but increased protein expression of TIMP-1 and PAI-1 without affecting protein expression of TIMP-2 and phosphorylation of FAK in lung tissues, whereas taxol treatment alone significantly increased protein expression of TIMP-1, PAI-1 and TIMP-2 but decreased protein expression of integrin β1 and phosphorylation of FAK. The combined treatment produced stronger actions on lung metastasis and lung tissues protein expression of TIMP-1, TIMP-2 and PAI-1.
    CONCLUSIONS:
    Overall, we demonstrate that AC effectively inhibits LLC metastasis and suppresses lung metastasis in combination with taxol in LLC-bearing mice, suggesting that AC could be used as an anti-metastatic agent or as an adjuvant for anti-cancer drugs.
    J Natl Cancer Inst. 1989 Nov 1;81(21):1649-52.
    Inhibitory effects of alpha-carotene on proliferation of the human neuroblastoma cell line GOTO.[Pubmed: 2795693]

    METHODS AND RESULTS:
    alpha-Carotene inhibited the proliferation of the human neuroblastoma cell line GOTO in a dose- and time-dependent manner. In addition, it was about 10 times more inhibitory than beta-carotene. Northern blot analysis indicated that alpha-Carotene caused maximum suppression of the level of the N-myc messenger RNA of GOTO cells. This suppression occurred within 18 hours of alpha-Carotene treatment, after which the level of the N-myc messenger RNA gradually recovered to the basal level. Analysis by flow cytometry indicated that when GOTO cells were exposed to alpha-Carotene, they were arrested in the G0-G1 phase of their cell cycle. However, as the level of the N-myc messenger RNA was recovering, these cells resumed normal cycling.
    CONCLUSIONS:
    These results indicate that the reduction in the level of the N-myc messenger RNA caused by alpha-Carotene is closely linked with G0-G1 arrest.
    alpha-Carotene Description
    Source: The roots of Daucus carota
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.8626 mL 9.3132 mL 18.6265 mL 37.253 mL 46.5662 mL
    5 mM 0.3725 mL 1.8626 mL 3.7253 mL 7.4506 mL 9.3132 mL
    10 mM 0.1863 mL 0.9313 mL 1.8626 mL 3.7253 mL 4.6566 mL
    50 mM 0.0373 mL 0.1863 mL 0.3725 mL 0.7451 mL 0.9313 mL
    100 mM 0.0186 mL 0.0931 mL 0.1863 mL 0.3725 mL 0.4657 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Animal Research:
    Cancer Res. 1992 Dec 1;52(23):6583-7.
    Potent preventive action of alpha-carotene against carcinogenesis: spontaneous liver carcinogenesis and promoting stage of lung and skin carcinogenesis in mice are suppressed more effectively by alpha-carotene than by beta-carotene.[Pubmed: 1423303]
    Although beta-carotene has been considered to be a key cancer preventive agent in green and yellow vegetables, other types of carotenoids, such as alpha-Carotene, may also contribute to anticarcinogenic action, since these carotenoids usually coexist with beta-carotene and are detectable in human blood and tissues.
    METHODS AND RESULTS:
    In this study, we compared the inhibitory effect of natural alpha-Carotene, obtained from palm oil, with that of beta-carotene on spontaneous liver carcinogenesis in C3H/He male mice. The mean number of hepatomas per mouse was significantly decreased by alpha-Carotene supplementation (per os administration in drinking water at a concentration of 0.05%, ad libitum) as compared with that in the control group (P < 0.001, Student's t test). On the other hand, beta-carotene, at the same dose as alpha-Carotene, did not show any such significant difference from the control group. Furthermore, we also compared the antitumor-promoting activity of alpha-Carotene with that of beta-carotene against two-stage mouse lung carcinogenesis (initiator, 4-nitroquinoline 1-oxide; promoter, glycerol). alpha-Carotene, but not beta-carotene, reduced the number of lung tumors per mouse to about 30% of that in the control group (P < 0.001, Student's t test). The higher potency of the antitumor-promoting action of alpha-Carotene compared to beta-carotene was confirmed in other experimental systems; e.g., alpha-Carotene was also found to have a stronger effect than beta-carotene in suppressing the promoting activity of 12-O-tetradecanoylphorbol-13-acetate on skin carcinogenesis in 7,12-dimethylbenz[a]anthracene-initiated mice.
    CONCLUSIONS:
    These results suggest that not only beta-carotene, but also other types of carotenoids, such as alpha-Carotene, may play an important role in cancer prevention.