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V Nagaraju - One of the best experts on this subject based on the ideXlab platform.
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Separation and determination of synthetic impurities of Difloxacin by reversed-phase high-performance liquid chromatography.
Journal of pharmaceutical and biomedical analysis, 2004Co-Authors: R. Nageswara Rao, V NagarajuAbstract:A simple and rapid reversed-phase high-performance liquid chromatographic method for separation and determination of process-related impurities of Difloxacin (DFL) was developed. The separation was achieved on a reversed-phase C(18) column using methanol-water-acetic acid (78:21.9:0.1, v/v/v) as a mobile solvent at a flow rate of 1.0 ml/min at 28 degrees C using UV detection at 230 nm. It was linear over a range of 0.03 x 10(-6) to 1.60 x 10(-6)g for process related impurities and 0.05 x 10(-6) to 2.40 x 10(-6)g for Difloxacin. The detection limits were 0.009 x 10(-6) to 0.024 x 10(-6)g for all the compounds examined. The recoveries were found to be in the range of 97.6-102.0% for impurities as well as Difloxacin. The precision and robustness of the method were evaluated. It was used for not only quality assurance, but also monitoring the synthetic reactions involved in the process development work of Difloxacin. The method was found to be specific, precise and reliable for the determination of unreacted levels of raw materials, intermediates in the reaction mixtures and the finished products of Difloxacin.
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Separation and determination of synthetic impurities of norfloxacin by reversed-phase high performance liquid chromatography.
Journal of Pharmaceutical and Biomedical Analysis, 2004Co-Authors: R. Nageswara Rao, V NagarajuAbstract:Abstract A simple and rapid reversed-phase high-performance liquid chromatographic method for separation and determination of process-related impurities of Difloxacin (DFL) was developed. The separation was achieved on a reversed-phase C 18 column using methanol–water–acetic acid (78:21.9:0.1, v/v/v) as a mobile solvent at a flow rate of 1.0 ml/min at 28 °C using UV detection at 230 nm. It was linear over a range of 0.03 × 10 −6 to 1.60 × 10 −6 g for process related impurities and 0.05 × 10 −6 to 2.40 × 10 −6 g for Difloxacin. The detection limits were 0.009 × 10 −6 to 0.024 × 10 −6 g for all the compounds examined. The recoveries were found to be in the range of 97.6–102.0% for impurities as well as Difloxacin. The precision and robustness of the method were evaluated. It was used for not only quality assurance, but also monitoring the synthetic reactions involved in the process development work of Difloxacin. The method was found to be specific, precise and reliable for the determination of unreacted levels of raw materials, intermediates in the reaction mixtures and the finished products of Difloxacin.
Gupta S - One of the best experts on this subject based on the ideXlab platform.
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Difloxacin reverses multidrug-resistance in p388 adr cells via a mechanism independent of p-glycoprotein and without correcting drug transport or subcellular drug distribution.
International journal of oncology, 1995Co-Authors: Gupta S, F Thadepalli, Gollapudi SAbstract:In this study, we have examined in vitro chemosensitizing activity of Difloxacin, a quinolone antimicrobial agent, in multidrug resistant murine leukemia P388/ADR cell line that overexpresses P-glycoprotein and exhibits decreased accumulation of anthracyclines and vincristine. Difloxacin, in a concentration-dependent manner, increased the sensitivity of P388/ADR cells to daunorubicin, adriamycin and vincristine without correcting the altered drug accumulation and subcellular distribution of daunorubicin. Furthermore, Difloxacin had no significant effect on intracellular accumulation of rhodamine 123 dye, a substrate for P-glycoprotein. In addition, Difloxacin increased the sensitivity of drug sensitive parental P388 cells to vincristine. Taken together these data suggest that Difloxacin reverses MDR by a mechanism independent of P-glycoprotein. The chemosensitizing effect of Difloxacin was observed at clinically achievable plasma concentrations. These data suggest that Difloxacin is an effective chemosensitizer of multidrug resistant tumor cells and is a potential candidate for clinical use to reverse MDR.
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Difloxacin reverses multidrug resistance in HL-60/AR cells that overexpress the multidrug resistance-related protein (MRP) gene.
Oncology research, 1995Co-Authors: Gollapudi S, F Thadepalli, C. H. Kim, Gupta SAbstract:In this study, we have examined the in vitro chemosensitizing activity of Difloxacin, a quinolone antimicrobial agent, in the multidrug-resistant human myeloid leukemia HL-60/AR cell line. HL-60/AR cells were found to overexpress multidrug resistance-associated protein (MRP) mRNA as compared to HL-60 cells. Difloxacin, in a concentration-dependent manner, increased the sensitivity of HL-60/AR cells to daunorubicin, adriamycin, and vincristine, and partially corrected the altered drug transport. In addition, Difloxacin corrected subcellular distribution of adriamycin by inducing redistribution of the drug from the perinuclear region to the nucleus in HL-60/AR cells. The chemosensitizing effect of Difloxacin was observed at clinically achievable concentrations. We conclude that Difloxacin is an effective chemosensitizer of MRP-associated multidrug-resistant tumor cells and is a potential candidate for clinical use to reverse multidrug resistance.
S Gupta - One of the best experts on this subject based on the ideXlab platform.
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Difloxacin reverses multidrug resistance in hl 60 ar cells that overexpress the multidrug resistance related protein mrp gene
Oncology Research, 1995Co-Authors: S Gollapudi, F Thadepalli, C. H. Kim, S GuptaAbstract:In this study, we have examined the in vitro chemosensitizing activity of Difloxacin, a quinolone antimicrobial agent, in the multidrug-resistant human myeloid leukemia HL-60/AR cell line. HL-60/AR cells were found to overexpress multidrug resistance-associated protein (MRP) mRNA as compared to HL-60 cells. Difloxacin, in a concentration-dependent manner, increased the sensitivity of HL-60/AR cells to daunorubicin, adriamycin, and vincristine, and partially corrected the altered drug transport. In addition, Difloxacin corrected subcellular distribution of adriamycin by inducing redistribution of the drug from the perinuclear region to the nucleus in HL-60/AR cells. The chemosensitizing effect of Difloxacin was observed at clinically achievable concentrations. We conclude that Difloxacin is an effective chemosensitizer of MRP-associated multidrug-resistant tumor cells and is a potential candidate for clinical use to reverse multidrug resistance.
F Thadepalli - One of the best experts on this subject based on the ideXlab platform.
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Difloxacin reverses multidrug-resistance in p388 adr cells via a mechanism independent of p-glycoprotein and without correcting drug transport or subcellular drug distribution.
International journal of oncology, 1995Co-Authors: Gupta S, F Thadepalli, Gollapudi SAbstract:In this study, we have examined in vitro chemosensitizing activity of Difloxacin, a quinolone antimicrobial agent, in multidrug resistant murine leukemia P388/ADR cell line that overexpresses P-glycoprotein and exhibits decreased accumulation of anthracyclines and vincristine. Difloxacin, in a concentration-dependent manner, increased the sensitivity of P388/ADR cells to daunorubicin, adriamycin and vincristine without correcting the altered drug accumulation and subcellular distribution of daunorubicin. Furthermore, Difloxacin had no significant effect on intracellular accumulation of rhodamine 123 dye, a substrate for P-glycoprotein. In addition, Difloxacin increased the sensitivity of drug sensitive parental P388 cells to vincristine. Taken together these data suggest that Difloxacin reverses MDR by a mechanism independent of P-glycoprotein. The chemosensitizing effect of Difloxacin was observed at clinically achievable plasma concentrations. These data suggest that Difloxacin is an effective chemosensitizer of multidrug resistant tumor cells and is a potential candidate for clinical use to reverse MDR.
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Difloxacin reverses multidrug resistance in HL-60/AR cells that overexpress the multidrug resistance-related protein (MRP) gene.
Oncology research, 1995Co-Authors: Gollapudi S, F Thadepalli, C. H. Kim, Gupta SAbstract:In this study, we have examined the in vitro chemosensitizing activity of Difloxacin, a quinolone antimicrobial agent, in the multidrug-resistant human myeloid leukemia HL-60/AR cell line. HL-60/AR cells were found to overexpress multidrug resistance-associated protein (MRP) mRNA as compared to HL-60 cells. Difloxacin, in a concentration-dependent manner, increased the sensitivity of HL-60/AR cells to daunorubicin, adriamycin, and vincristine, and partially corrected the altered drug transport. In addition, Difloxacin corrected subcellular distribution of adriamycin by inducing redistribution of the drug from the perinuclear region to the nucleus in HL-60/AR cells. The chemosensitizing effect of Difloxacin was observed at clinically achievable concentrations. We conclude that Difloxacin is an effective chemosensitizer of MRP-associated multidrug-resistant tumor cells and is a potential candidate for clinical use to reverse multidrug resistance.
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Difloxacin reverses multidrug resistance in hl 60 ar cells that overexpress the multidrug resistance related protein mrp gene
Oncology Research, 1995Co-Authors: S Gollapudi, F Thadepalli, C. H. Kim, S GuptaAbstract:In this study, we have examined the in vitro chemosensitizing activity of Difloxacin, a quinolone antimicrobial agent, in the multidrug-resistant human myeloid leukemia HL-60/AR cell line. HL-60/AR cells were found to overexpress multidrug resistance-associated protein (MRP) mRNA as compared to HL-60 cells. Difloxacin, in a concentration-dependent manner, increased the sensitivity of HL-60/AR cells to daunorubicin, adriamycin, and vincristine, and partially corrected the altered drug transport. In addition, Difloxacin corrected subcellular distribution of adriamycin by inducing redistribution of the drug from the perinuclear region to the nucleus in HL-60/AR cells. The chemosensitizing effect of Difloxacin was observed at clinically achievable concentrations. We conclude that Difloxacin is an effective chemosensitizer of MRP-associated multidrug-resistant tumor cells and is a potential candidate for clinical use to reverse multidrug resistance.
C. H. Kim - One of the best experts on this subject based on the ideXlab platform.
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Difloxacin reverses multidrug resistance in HL-60/AR cells that overexpress the multidrug resistance-related protein (MRP) gene.
Oncology research, 1995Co-Authors: Gollapudi S, F Thadepalli, C. H. Kim, Gupta SAbstract:In this study, we have examined the in vitro chemosensitizing activity of Difloxacin, a quinolone antimicrobial agent, in the multidrug-resistant human myeloid leukemia HL-60/AR cell line. HL-60/AR cells were found to overexpress multidrug resistance-associated protein (MRP) mRNA as compared to HL-60 cells. Difloxacin, in a concentration-dependent manner, increased the sensitivity of HL-60/AR cells to daunorubicin, adriamycin, and vincristine, and partially corrected the altered drug transport. In addition, Difloxacin corrected subcellular distribution of adriamycin by inducing redistribution of the drug from the perinuclear region to the nucleus in HL-60/AR cells. The chemosensitizing effect of Difloxacin was observed at clinically achievable concentrations. We conclude that Difloxacin is an effective chemosensitizer of MRP-associated multidrug-resistant tumor cells and is a potential candidate for clinical use to reverse multidrug resistance.
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Difloxacin reverses multidrug resistance in hl 60 ar cells that overexpress the multidrug resistance related protein mrp gene
Oncology Research, 1995Co-Authors: S Gollapudi, F Thadepalli, C. H. Kim, S GuptaAbstract:In this study, we have examined the in vitro chemosensitizing activity of Difloxacin, a quinolone antimicrobial agent, in the multidrug-resistant human myeloid leukemia HL-60/AR cell line. HL-60/AR cells were found to overexpress multidrug resistance-associated protein (MRP) mRNA as compared to HL-60 cells. Difloxacin, in a concentration-dependent manner, increased the sensitivity of HL-60/AR cells to daunorubicin, adriamycin, and vincristine, and partially corrected the altered drug transport. In addition, Difloxacin corrected subcellular distribution of adriamycin by inducing redistribution of the drug from the perinuclear region to the nucleus in HL-60/AR cells. The chemosensitizing effect of Difloxacin was observed at clinically achievable concentrations. We conclude that Difloxacin is an effective chemosensitizer of MRP-associated multidrug-resistant tumor cells and is a potential candidate for clinical use to reverse multidrug resistance.