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National Institutes of Health, Bethesda, MD, and Netherlands Cancer Institute [multidrug-resistance protein 1 (MDR1)-MDCK]; Absorption Systems and AstraZeneca (BCRP-MDCK); ATCC (Caco2). Cells were authenticated during each experiment by monitoring transepithelial electrical resistance, and with positive controls. H1975 cells were obtained from ATCC in 2004, and authenticated by short-tandem repeat analysis in November 2012. PC9 cells (exon 19 deletion) were obtained in November 2011 from Akiko Hiraide at Preclinical Sciences R&D, AstraZeneca, and tested and authenticated by short-tandem repeat analysis in May 2013. Details on cell line maintenance and test compounds are presented as Supplementary Information. Permeability glycoprotein and breast cancer resistance protein substrate assessment. P-gp (also known as MDR1) and BCRP substrate assessments of osimertinib, AZ7550, AZ5104, rociletinib, afatinib, and erlotinib were performed using transfected MDCK cells (MDR1-MDCK; BCRP-MDCK) and the Caco2 (colon carcinoma) cell line. Digoxin, cladribine, and Ko143 10 mmol/L, valspodar 1 mmol/L, and atorvastatin 0. Cell monolayers were grown onto collagen-coated, 12-well, polycarbonate membranes in Costar Transwell plates (1. Test and control compound substrate assessments were carried out in triplicate in each direction (apical [AP]-to-basolateral [BL], and BL-to-AP), co-dosed with 200 ?mol/L Lucifer yellow (LY). Aliquots were taken from the test compound receiver compartment at preselected time points and replaced with an equal volume of fresh transport buffer. Positive control receiver samples were taken at 120 minutes. LC/MS-MS was used for analysis of the test compound, and LY concentration measured using a BMG microplate reader (excitation 485 nm; emission 540 nm). 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