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    CAS No. 23696-28-8 Price $100 / 20mg
    Catalog No.CFN90395Purity>=98%
    Molecular Weight263.25Type of CompoundAlkaloids
    FormulaC12H13N3O4Physical DescriptionPowder
    Download     COA    MSDS    SDFSimilar structuralComparison (Web)
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    Olaquindox Description
    Source: From Cyprinus carpio var. Jian
    Biological Activity or Inhibitors: 1. Olaquindox induces apoptosis of HepG2 cells through a caspase-9 dependent mitochondrial pathway, might be suppressed through p38 MAPK and ROS-JNK pathways.
    2. Olaquindox induces autophagy in HepG2 cells is upregulated by Beclin 1 but downregulated by ROS-dependent JNK.
    3. Olaquindox, as one of the antimicrobial growth accelerants, is usually used in livestock production to improve feed efficiency.
    4. Olaquindox has genotoxic activity.
    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.
    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.

    PMID: 29328914

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.

    PMID: 29149595

    Scientific Reports 2017 Dec 11;7(1):17332.
    doi: 10.1038/s41598-017-17427-6.

    PMID: 29230013

    Molecules. 2017 Oct 27;22(11). pii: E1829.
    doi: 10.3390/molecules22111829.

    PMID: 29077044

    J Cell Biochem. 2018 Feb;119(2):2231-2239.
    doi: 10.1002/jcb.26385.

    PMID: 28857247

    Phytomedicine. 2018 Feb 1;40:37-47.

    PMID: 29496173
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.7987 mL 18.9934 mL 37.9867 mL 75.9734 mL 94.9668 mL
    5 mM 0.7597 mL 3.7987 mL 7.5973 mL 15.1947 mL 18.9934 mL
    10 mM 0.3799 mL 1.8993 mL 3.7987 mL 7.5973 mL 9.4967 mL
    50 mM 0.076 mL 0.3799 mL 0.7597 mL 1.5195 mL 1.8993 mL
    100 mM 0.038 mL 0.1899 mL 0.3799 mL 0.7597 mL 0.9497 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.
    Olaquindox References Information
    Citation [1]

    J Appl Toxicol. 2015 Jul;35(7):709-16.

    Reactive oxygen species-dependent JNK downregulated olaquindox-induced autophagy in HepG2 cells.[Pubmed: 25042557]
    Autophagy plays an important role in response to intracellular and extracellular stress to sustain cell survival. However, dysregulated or excessive autophagy may lead to cell death, known as "type II programmed cell death," and it is closely associated with apoptosis. In our previous study, we proposed that Olaquindox induced apoptosis of HepG2 cells through a caspase-9 dependent mitochondrial pathway. In this study, we investigated autophagy induced by Olaquindox and explored the crosstalk between apoptosis and autophagy in Olaquindox-treated HepG2 cells. Olaquindox-induced autophagy was demonstrated by the accumulation of monodansylcadervarine, as well as elevated expression of autophagy-related MAP-LC3 and Beclin 1 proteins. The autophagy inhibitor 3-methyladenine significantly increased the apoptotic rate induced by Olaquindox, which was correlated with increased ratio of Bax/Bcl-2. The further studies showed that Olaquindox increased the levels of reactive oxygen species (ROS), and antioxidant N-acetyl-L-cysteine (NAC) effectively blocked the accumulation of ROS but failed to block autophagy. Moreover, Olaquindox induced the activation of c-Jun N-terminal protein kinase (JNK), and JNK inhibitor SP600125 failed to block autophagy. Instead, Olaquindox-induced autophagy was enhanced by NAC or SP600125. Meanwhile, JNK activation was remarkably blocked by NAC, indicating that ROS may be the upstream signaling molecules of JNK activation and involved in the negative regulation of Olaquindox-induced autophagy. These results suggest that Olaquindox induces autophagy in HepG2 cells and that Olaquindox-induced apoptosis can be enhanced by 3-methyladenine. Olaquindox-induced autophagy in HepG2 cells is upregulated by Beclin 1 but downregulated by ROS-dependent JNK.
    Citation [2]

    Cell Biol Toxicol. 2013 Aug;29(4):229-38.

    Olaquindox-induced apoptosis is suppressed through p38 MAPK and ROS-mediated JNK pathways in HepG2 cells.[Pubmed: 23812630]
    We investigated mitogen-activated protein kinase (MAPK) pathways as well as reactive oxygen species (ROS) in Olaquindox-induced apoptosis. Exposure of HepG2 cells to Olaquindox resulted in the phosphorylation of p38 MAPK and c-Jun N-terminal kinases (JNK). To confirm the role of p38 MAPK and JNK, HepG2 cells were pretreated with MAPKs-specific inhibitors prior to Olaquindox treatment. Olaquindox-induced apoptosis was significantly potentiated by the JNK inhibitor (SP600125) or the p38 MAPK inhibitor (SB203580). Furthermore, we observed that Olaquindox treatment led to ROS generation and that Olaquindox-induced apoptosis and ROS generation were both significantly reduced by the antioxidants, superoxide dismutase and catalase. In addition, the levels of phosphorylation of JNK, but not p38 MAPK, were significantly suppressed after pretreatment of the antioxidants, while inhibition of the activations of JNK or p38 MAPK had no effect on ROS generation. This result suggested that ROS may be the upstream mediator for the activation of JNK. Conclusively, our results suggested that apoptosis in response to Olaquindox treatment in HepG2 cells might be suppressed through p38 MAPK and ROS-JNK pathways.
    Citation [3]

    J Sci Food Agric. 2012 Oct;92(13):2696-702.

    Development of an on-line molecularly imprinted chemiluminescence sensor for determination of trace olaquindox in chick feeds.[Pubmed: 22505192]
    BACKGROUND: Olaquindox, as one of the antimicrobial growth accelerants, is usually used in livestock production to improve feed efficiency. Due to health concerns over possible carcinogenic, mutagenic and photoallergenic effects of Olaquindox on animals, the development of simple, rapid and sensitive analytical method for determination of Olaquindox is crucial and necessary. RESULTS: In this study, a surface molecularly imprinted polymer was prepared by a molecular imprinting technique in combination with a sol-gel process using activated silica gel as a support material. This imprinted material exhibited with good recognition and selective ability, and fast adsorption-desorption dynamics toward Olaquindox. Using it as the recognition element, a new on-line molecularly imprinted solid phase extraction coupled with chemiluminescence sensor for the determination of Olaquindox was developed. The factors affecting preconcentration of the analytes and sensitivity of the method were all investigated. Under the optimal condition, the linear range of the calibration graph was between 2 × 10(-8) and 1 × 10(-6) g mL(-1) , and the detection limit of this method was 7 × 10(-9) g mL(-1) . The blank chick feed samples spiked with Olaquindox at 0.3, 0.9 and 1.5 µg g(-1) levels were extracted and determined by this presented method with recoveries ranging from 87% to 94%. This method was validated by high-performance liquid chromatography and the results correlated well with those obtained by both methods. Moreover, this method was quantitatively analysed with two contaminated chick feed samples. CONCLUSION: This study will provide a sensitive and fast method for the monitoring of Olaquindox residues in foods.
    Citation [4]

    Food Chem Toxicol. 2013 Sep;59:207-14.

    Genotoxicity of quinocetone, cyadox and olaquindox in vitro and in vivo.[Pubmed: 23774262]
    Quinocetone (QCT) and Cyadox (CYA) are important derivative of heterocyclic N-oxide quinoxaline (QdNO), used actively as antimicrobial feed additives in China. Here, we tested and compared the genotoxic potential of QCT and CYA with Olaquindox (OLA) in Ames test, HGPRT gene mutation (HGM) test in V79 cells, unscheduled DNA synthesis (UDS) assay in human peripheral lymphocytes, chromosome aberration (CA) test, and micronucleus (MN) test in mice bone marrow. Olaquindox was found genotoxic in all 5 assays. In Ames test, QCT produced His(+) mutants at 6.9 μg/plate in Salmonella typhimurium TA 97, at 18.2 μg/plate in TA 100, TA 1535, TA 1537, and at 50 μg/plate in TA 98. CYA produced His(+) mutants at 18.2 μg/plate in TA 97, TA 1535, and at 50 μg/plate in TA 98, TA 100 and TA 1537. QCT was found positive in HGM and UDS assay at concentrations ≥10 μg/ml while negative results were reported in CA test and MN test. Collectively, we found that Olaquindox was more genotoxic than QCT and CYA. Genotoxicity of QCT was found at higher concentration levels in Ames test, HGM and UDS assays while CYA showed weak mutagenic potential to bacterial cells in Ames test.