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. 2018 Jan 16;128(2):816–825. doi: 10.1172/JCI96160

Figure 3. Inhibition of OATP1B-type transporters by nilotinib.

Figure 3

Inhibition of OATP1B1 function by tyrosine kinase inhibitors (TKIs) in vitro (10 μM; 15-minute preincubation), using 8-(2-[fluoresceinyl]-aminoethylthio)-adenosine-3′,5′-cyclic monophosphate (8Fc-A) (A) and estradiol-17β-D-glucuronide (E2G) (B) as OATP1B1 substrates in transfected HEK293 cells. (C) Concentration-dependent inhibition of OATP1B1 function by nilotinib using 8Fc-A (2 μM; 15-minute uptake) as a substrate. Inhibition of OATP1B3 (D) and OATP1B2 (E) by nilotinib using 2 different substrates (2 μM; 15-minute uptake). Data (n = 6–9 per group) were normalized to substrate uptake in the absence of nilotinib, and corrected for nonspecific uptake in cells transfected with an empty vector. (F) Plasma concentration-time curves of paclitaxel after paclitaxel administration (10 mg/kg) pretreated with nilotinib (100 mg/kg; p.o.) or vehicle (n = 5 per group). All data represent mean values (bars or symbols) and SD (error bars). *Indicates significant differences from the corresponding vehicle control group (P < 0.05), as evaluated with an unpaired 2-sided Student’s t test with Welch’s correction.