For subjects with moderate renal impairment, there was no clinically relevant change in the pharmacokinetics of afatinib.

For subjects with severe renal impairment, the mean exposure [maximum plasma concentration (C max) and area under the plasma concentration–time curve from time zero to time of last quantifiable concentration (AUClast)] values of afatinib were increased by 22 and 50 %, respectively. Inter-individual variability was moderate (geometric mean coefficient of variation 34–42 %).

Renal impairment had no effect on the plasma protein binding of afatinib, and urinary excretion of afatinib was minimal.