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  • Bioactive Products
    Antileukaemic Compound Library
    A unique collection of 35 Antileukaemic natural compound library for Antileukaemic screening
    Catalog No: B29 Antileukaemic Compound Library
    Screening Details
    Size: 1mg/well * 35 Compounds
    2mg/well * 35 Compounds
    Catalog No. Information
    CFN99005 Wulignan A1

    1. The extracts and purified compounds of Schisandrae fructus has anti-influenza virus H1N1 and H1N1-TR (a Tamiflu drug resistant virus strain) activities, the extract comprises compounds such as schisandrone, benzoylgomisin P, wulignan A1, epigomisin O, epiwulignan A1, and tigloylgomisin P.
    2. Wulignan A1 exhibits activity against leukemia P-388 in vitro.
    CFN99024 Piceatannol

    1. Piceatannol has antitumor activity.
    2. Piceatannol has the potential to control obesity.
    3. Piceatannol has antioxidant, and anti-inflammatory activities.
    4. Piceatannol inhibits effector T cell functions by suppressing TcR signaling.
    CFN99085 Ganodermanondiol

    1. Ganodermanondiol exhibits potent cytoprotective effects on t-BHP-induced hepatotoxicity in human liver-derived HepG2 cells, presumably through Nrf2-mediated antioxidant enzymes and AMPK.
    2. Ganodermanondiol has an inhibitory effect on the proliferative of HL60 and K562 human tumor cells in a concentration-dependent manner, it can significantly inhibit the proliferation of leukemic cancer cells, and it could be one of the antileukemie active constituents of Ganoderma lucidum.
    3. Ganodermanondiol shows a strong anticomplement activity against the classical pathway (CP) of the complement system with IC(50) values of 41.7 microM.
    4. Ganodermanondiol shows significant anti-human immunodeficiency virus (anti-HIV)-1 protease activity with IC50 values of 20-90 microM.
    CFN99507 Dihydroartemisinin

    1. Dihydroartemisinin is widely used as an intermediate in the preparation of other artemisinin-derived antimalarial drugs, recommended as the first-line anti-malarial drug with low toxicity.
    2. Dihydroartemisinin inhibits endothelial cell proliferation through the suppression of the ERK signaling pathway.
    3. Dihydroartemisinin has anticancer activity, is mediated through apoptotic pathways and inhibiting angiogenesis.
    4. Dihydroartemisinin-induced apoptosis is associated with inhibition of Sarco/Endoplasmic reticulum Calcium ATPase activity in colorectal cancer.
    5. Dihydroartemisinin inhibits cell proliferation via AKT/GSK3β/cyclinD1 pathway and induces apoptosis in A549 lung cancer cells.
    6. Dihydroartemisinin can inhibit tumor growth but not early rounds of papillomavirus replication, indicates that it may be useful for the topical treatment of epithelial papillomavirus lesions, including those that have progressed to the neoplastic state.
    CFN99491 Hispidulin

    1. Hispidulin has anti-oxidative, anti-inflammatory and anti-cancer activities, it can alleviate methamphetamine-induced hyperlocomotion without motor impairment in mice, suggesting a therapeutic potential of Hispidulin in hyper-dopaminergic disorders.
    2. Hispidulin exerts anti-osteoporotic and bone resorption attenuating effects via activating the AMPK signaling pathway.
    3. Hispidulin sensitizes the tumor cells to Gemcitabine and 5-Fluoroucil by down-regulating HIF-1α/P-gp signaling, it appears to be a promising and novel chemosensitizer for gallbladder cancer treatment.
    4. Hispidulin has considerable antiepileptic, neuroprotective, and antiinflammatory effects on kainic acid-induced seizures in rats.
    5. Hispidulin can ameliorate high glucose-mediated endothelial dysfunction via inhibiting PKCβII-associated NLRP3 inflammasome activation and NF-κB signaling, it has potential application in the prevention and treatment of diabetic vascular complications.
    6. Hispidulin targets the VEGF receptor 2-mediated PI3K/Akt/mTOR signaling pathway in endothelial cells, leading to the suppression of pancreatic tumor growth and angiogenesis.
    7. Hispidulin can inhibit platelet aggregation by elevating cAMP levels by a mechanism different from that of theophylline or PGE1.