rifampin and Leukemia-P388

rifampin has been researched along with Leukemia-P388* in 2 studies

Other Studies

2 other study(ies) available for rifampin and Leukemia-P388

ArticleYear
Isolation and biological evaluation of filiformin, plakortide F, and plakortone G from the Caribbean sponge Plakortis sp.
    Journal of natural products, 2001, Volume: 64, Issue:11

    The bioassay- and spectroscopic-guided fractionation of the antimalarial extract from a Jamaican sponge, Plakortis sp., resulted in the isolation of three metabolites. The previously reported bromoaromatic filiformin (1) was obtained from our sample of Plakortis sp., and the potential origins of this compound are discussed. The peroxide-containing metabolite, plakortide F (2), is a more typical Plakortis metabolite and was shown to exhibit significant activity against Plasmodium falciparum in vitro. The isolation, structure, and bioactivity of a new lactone, plakortone G (3), are also reported.

    Topics: Animals; Antimalarials; Bromobenzenes; Chromatography, High Pressure Liquid; Colonic Neoplasms; Dioxanes; Gas Chromatography-Mass Spectrometry; Hepatitis B; HIV; Humans; Jamaica; Lactones; Leukemia P388; Lung Neoplasms; Mice; Molecular Structure; Mycobacterium tuberculosis; Neoplasms, Unknown Primary; Nuclear Magnetic Resonance, Biomolecular; Plasmodium berghei; Plasmodium falciparum; Porifera; Spectrometry, Mass, Electrospray Ionization; Tumor Cells, Cultured

2001
Potentiation of pirarubicin activity in multidrug resistant cells by rifampicin.
    Biological & pharmaceutical bulletin, 1997, Volume: 20, Issue:12

    The effect of the anti-tuberculosis drug rifampicin on pirarubicin activity was investigated in multidrug-resistant cells overexpressing P-glycoprotein. Rifampicin increased the sensitivity of pirarubicin to anthracycline-resistant mouse leukemic P388 cells and significantly enhanced the cytotoxicity and intracellular accumulation of pirarubicin in resistant cells, but had no effect in parent cells. By contrast, two other rifamycins, rifamycin B and SV, had no effect on pirarubicin accumulation in resistant cells. Rifampicin also enhanced pirarubicin-induced apoptosis and G2/M blockade on the cell cycle in resistant cells. These results show that rifampicin enhances the cytotoxic action of pirarubicin in resistant cells, at least partly via the inhibition of cellular pirarubicin efflux.

    Topics: Animals; Antibiotics, Antineoplastic; Antibiotics, Antitubercular; Apoptosis; Cell Cycle; Doxorubicin; Drug Resistance, Multiple; Drug Synergism; Gene Expression Regulation, Neoplastic; Genes, MDR; Leukemia P388; Mice; Rifampin; Tetrazolium Salts; Thiazoles

1997