OATP1B1 (a.k.a. OATP-C, OATP2, LST-1, or SLC21A6) is a liver-specific organic 
anion uptake transporter and has been shown to be a higher affinity bilirubin 
uptake transporter than OATP1B3. Using human embryonic kidney (HEK 293) cells 
stably transfected with OATP1B1, we have studied the effects of indinavir, 
saquinavir, cyclosporin A, and rifamycin SV on human OATP1B1 transport function. 
These drugs are potent inhibitors of OATP1B1 transport activity in vitro. We 
further provide evidence that the calculated fraction of OATP1B1 inhibited at 
the clinical exposure level correlated very well with the observed 
hyperbilirubinemia outcome for these drugs in humans. Our data support the 
hypothesis that inhibition of OATP1B1 is an important mechanism for drug-induced 
unconjugated hyperbilirubinemia. Inhibition of OATPs may be an important 
mechanism in drug-drug and drug-endogenous substance interactions.