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  • Bioactive Products
    Catalog No. Information
    CFN99581 Neferine

    1. Neferine has anti-tumor activities , Metabolic activation mediated by CYP3A4 and GSH depletion enhanced Neferine-induced cytotoxicity.
    2. Neferine can be helpful to increase the efficacy of DOX and to achieve anticancer synergism by curbing the toxicity.
    3. Neferine inhibited high glucose-induced endothelial apoptosis via blocking ROS/Akt/NF-κB pathway, which provides the evidence for using Neferine to treat diabetic vasculopathy.
    4. Neferine induced apoptosis in a dose-dependent manner with the hypergeneration of reactive oxygen species, activation of MAPKs, lipid peroxidation, depletion of cellular antioxidant pool, loss of mitochondrial membrane potential, and intracellular calcium accumulation.
    CFN99989 Saikosaponin D

    1. Saikosaponin is a novel SERCA inhibitor by inhibiting NF-κB and STAT3 signaling to protect against acetaminophen-induced hepatotoxicity.
    2. Saikosaponin is a potent inhibitory on acute hepatic injury by CCl4 and a potent cytotoxicity agent for human hepatocellular carcinoma cells.
    3. Saikosaponin has the antiproliferative effect in A549 cells that may be the induction of p53 and activity of the Fas/FasL apoptotic system.
    CFN92097 Gambogenic acid

    1. Gambogenic acid induces mitochondria-dependent apoptosis and increases P53 expression in human gastric carcinoma cell line.
    2. Gambogenic acid suppresses breast cancer MDA-MB-231 cell growth by mediating apoptosis through death receptor and mitochondrial pathways in vivo and in vitro.
    3. Gambogenic acid can cause aberrant autophagy to induce cell death and may suggest the potential application of Gambogenic acid as a tool or viable drug in anticancer therapies.
    4. Gambogenic acid could inhibit the proliferation of melanoma B16 cells and induce their apoptosis within certain time and concentration ranges. Its mechanism in inducing the cell apoptosis may be related to PI3K/Akt/mTOR signaling pathways.
    CFN92406 Alisol B

    1. Alisol B can suppress C3a induced epithelial-mesenchymal transition .
    2. Alisol B may be a potential novel therapeutic molecule for bone disorders through targeting the differentiation of osteoclasts as well as their functions.
    3. Alisol B also inhibited RANKL-induced expression of NFATc1 and c-Fos, which are key transcription factors for osteoclastogenesis.
    4. The molecular target of Alisol B is the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase, it provides detailed insights into the cytotoxic mechanism of a novel antitumor compound.