American Society of Hematology

Figure 2.

$Figure 2. Effect of imatinib as a competitor for BCRP-mediated efflux of mitoxantrone. (A) Effect of imatinib (15 μM) on mitoxantrone steady-state accumulation (3 μM) in MCF7 parental (left panel), MCF7/MR (middle panel), and MCF7/AdVp (right panel). MCF7 sublines were simultaneously incubated for 2 hours with mitoxantrone (3 μM), with or without imatinib as a competitor (1 μM-15 μM). The fluorescence data of at least 20 000 events per time point are shown and fluorescence intensity (peak signal) of mitoxantrone is expressed in arbitrary units (au). (B) Mitoxantrone steady-state accumulation in the presence of 15 μM imatinib in HEK293 cells. Representative results from 3 independent experiments are shown. Relative accumulation data (mean ± SD) are given as a fraction (% control) relative to the accumulation found in HEK293 control cells without imatinib.$

Effect of imatinib as a competitor for BCRP-mediated efflux of mitoxantrone. (A) Effect of imatinib (15 μM) on mitoxantrone steady-state accumulation (3 μM) in MCF7 parental (left panel), MCF7/MR (middle panel), and MCF7/AdVp (right panel). MCF7 sublines were simultaneously incubated for 2 hours with mitoxantrone (3 μM), with or without imatinib as a competitor (1 μM-15 μM). The fluorescence data of at least 20 000 events per time point are shown and fluorescence intensity (peak signal) of mitoxantrone is expressed in arbitrary units (au). (B) Mitoxantrone steady-state accumulation in the presence of 15 μM imatinib in HEK293 cells. Representative results from 3 independent experiments are shown. Relative accumulation data (mean ± SD) are given as a fraction (% control) relative to the accumulation found in HEK293 control cells without imatinib.

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