Preclinical evaluation of the potential for cytochrome P450 inhibition and induction of the selective ALK inhibitor, alectinib

References

• Bergethon K, Shaw AT, Ou SI, et al. (2012). ROS1 rearrangements define a unique molecular class of lung cancers. J Clin Oncol 30:863–70.
   PubMed Web of Science ®Google Scholar
• Camidge DR, Doebele RC. (2012). Treating ALK positive lung cancer: early successes and coming challenges. Nat Rev Clin Oncol 9:268–77.
   PubMed Web of Science ®Google Scholar
• Cheng Y, Prusoff WH. (1973). Relationship between the inhibition constant (Ki) and the concentration of inhibitor which causes 50 per cent inhibition (I50) of an enzymatic reaction. Biochem Pharmacol 22:3099–108.
   PubMed Web of Science ®Google Scholar
• Christensen JG, Zou HY, Arango ME, et al. (2007). Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma. Mol Cancer Ther 6:3314–22.
   PubMed Web of Science ®Google Scholar
• Cornish-Bowden A. (1974). A simple graphical method for determining the inhibition constants of mixed, uncompetitive and non-competitive inhibitors. Biochem J 137:143–4.
   PubMed Web of Science ®Google Scholar
• Costa DB, Kobayashi S, Pandya SS, et al. (2011). CSF concentration of the anaplastic lymphoma kinase inhibitor crizotinib. J Clin Oncol 29:e443–5.
   PubMed Web of Science ®Google Scholar
• Doebele RC, Pilling AB, Aisner DL, et al. (2012). Mechanism of resistance to crizotinib in patients with ALK gene rearranged non-small cell lung cancer. Clin Cancer Res 18:1472–82.
   PubMed Web of Science ®Google Scholar
• European Medicines Agency, Committee for Human Medicinal Products (CHMP). (2012). Guideline on the investigation of drug interactions, adopted at 21 June 2012. [Online] Available from: http://www.ema.europa.eu/docs/en_GB/document_library/Scientific_guideline/2012/07/WC500129606.pdf
   Google Scholar
• Gadgeel SM, Gandhi L, Riely G, et al. (2014). Safety and activity of alectinib against systemic disease and brain metastases in patients with crizotinib-resistant ALK-rearranged non-small-cell lung cancer (AF-002JG): results from the dose-finding portion of a phase 1/2 study. Lancet Oncol 15:1119–28.
   PubMed Web of Science ®Google Scholar
• Grimm SW, Einolf HJ, Hall SD, et al. (2009). The conduct of in vitro studies to address time-dependent inhibition of drug-metabolizing enzymes: a perspective of the pharmaceutical research and manufacturers of America. Drug Metab Dispos 37:1355–70.
   PubMed Web of Science ®Google Scholar
• Hsu JC, Carnac R, Henschel V, et al (2016). Population pharmacokinetics (popPK) and exposure-response (ER) analyses to confirm alectinib 600 mg BID dose selection in a crizotinib-progressed or intolerant population. J Clin Oncol 34: Supplement abstract e20598.
   PubMed Web of Science ®Google Scholar
• Katayama R, Shaw AT, Khan TM, et al. (2012). Mechanisms of acquired crizotinib resistance in ALK-rearranged lung cancers. Sci Transl Med 4:120ra17.
   PubMed Web of Science ®Google Scholar
• Katayama R, Sakashita T, Yanagitani N, et al. (2015). P-glycoprotein mediates ceritinib resistance in anaplastic lymphoma kinase-rearranged non-small cell lung cancer. EBioMedicine 3:54–66.
   PubMed Web of Science ®Google Scholar
• Khojasteh SC, Prabhu S, Kenny JR, et al. (2011). Chemical inhibitors of cytochrome P450 isoforms in human liver microsomes: a re-evaluation of P450 isoform selectivity. Eur J Drug Metab Pharmacokinet 36:1–16.
   PubMed Web of Science ®Google Scholar
• Kodama T, Tsukaguchi T, Yoshida M, et al. (2014a). Selective ALK inhibitor alectinib with potent antitumor activity in models of crizotinib resistance. Cancer Lett 351:215–21.
   PubMed Web of Science ®Google Scholar
• Kodama T, Hasegawa M, Takanashi K, et al. (2014b). Antitumor activity of the selective ALK inhibitor alectinib in models of intracranial metastases. Cancer Chemother Pharmacol 74:1023–8.
   PubMed Web of Science ®Google Scholar
• Lee J, Lee S, Oh S, et al. (2012). Assessment of drug-drug interactions caused by metabolism-dependent cytochrome P450 inhibition. Chem Biol Interact 198:49–56.
   PubMed Web of Science ®Google Scholar
• Luo G, Lin J, Fiske WD, et al. (2003). Concurrent induction and mechanism-based inactivation of CYP3A4 by an L-valinamide derivative. Drug Metab Dispos 31:1170–5.
   PubMed Web of Science ®Google Scholar
• Mao J, Johnson TR, Shen Z, Yamazaki S. (2013). Prediction of crizotinib-midazolam interaction using the Simcyp population-based simulator: comparison of CYP3A time-dependent inhibition between human liver microsomes versus hepatocytes. Drug Metab Dispos 41:343–52.
   PubMed Web of Science ®Google Scholar
• Morcos PN, Yu L, Bogman K, et al. (2016a). Absorption, distribution, metabolism and excretion (ADME) of the ALK inhibitor alectinib: results from an absolute bioavailability and mass balance study in healthy subjects. Xenobiotica . [Epub ahead of print]. doi: http://dx.doi.org/10.1080/00498254.2016.1179821.
   PubMed Web of Science ®Google Scholar
• Morcos PN, Cleary Y, Guerini E, et al. (2016b). Clinical drug-drug interactions through cytochrome P450 3A (CYP3A) for the selective ALK inhibitor alectinib. Clin Pharmacol Drug Dev . [Epub ahead of print]. doi: 10.1002/cpdd.298.
   Web of Science ®Google Scholar
• Mullins ME, Horowitz BZ, Linden DH, et al. (1998). Life-threatening interaction of mibefradil and beta-blockers with dihydropyridine calcium channel blockers. J Am Med Assoc 280:157–8.
   PubMed Web of Science ®Google Scholar
• Prueksaritanont T, Ma B, Tang C, et al. (1999). Metabolic interactions between mibefradil and HMG-CoA reductase inhibitors: an in vitro investigation with human liver preparations. Br J Clin Pharmacol 47:291–8.
   PubMed Web of Science ®Google Scholar
• Rikova K, Guo A, Zeng Q, et al. (2007). Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. Cell 131:1190–203.
   PubMed Web of Science ®Google Scholar
• Sakamoto H, Tsukaguchi T, Hiroshima S, et al. (2011). CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell 19:679–90.
   PubMed Web of Science ®Google Scholar
• Salsali M, Holt A, Baker GB. (2004). Inhibitory effects of the monoamine oxidase inhibitor tranylcypromine on the cytochrome P450 enzymes CYP2C19, CYP2C9, and CYP2D6. Cell Mol Neurobiol 24:63–76.
   PubMed Web of Science ®Google Scholar
• Sasaki T, Koivunen J, Ogino A, et al. (2011). A novel ALK secondary mutation and EGFR signaling cause resistance to ALK kinase inhibitors. Cancer Res 71:6051–60.
   PubMed Web of Science ®Google Scholar
• Seto T, Kiura K, Nishio M, et al. (2013). CH5424802 (RO5424802) for patients with ALK-rearranged advanced non-small-cell lung cancer (AF-001JP study): a single-arm, open-label, phase 1-2 study. Lancet Oncol 14:590–8.
   PubMed Web of Science ®Google Scholar
• Silverman RB. (1995). Mechanism-based enzyme inactivators. Meth Enzymol 249:240–83.
   PubMed Web of Science ®Google Scholar
• Soda M, Choi YL, Enomoto M, et al. (2007). Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer. Nature 448:561–7.
   PubMed Web of Science ®Google Scholar
• Solomon BJ, Mok T, Kim D, et al. (2014). First-line crizotinib versus chemotherapy in ALK-positive lung cancer. N Engl J Med 371:2167–77.
   PubMed Web of Science ®Google Scholar
• Stresser DM, Mason AK, Perloff ES, et al. (2009). Differential time- and NADPH-dependent inhibition of CYP2C19 by enantiomers of fluoxetine. Drug Metab Dispos 37:695–8.
   PubMed Web of Science ®Google Scholar
• US Food and Drug Administration, Center for drug evaluation and research. (2006). Guidance for Industry: Drug interaction studies – study design, data analysis, and implications for dosing and labeling, draft guidance. [Online] Available from: http://www.fda.gov/OHRMS/DOCKETS/98fr/06d-0344-gdl0001.pdf.
   Google Scholar
• US Food and Drug Administration, Center for drug evaluation and research. (2011). Clinical Pharmacology and biopharmaceutics reviews, NDA/BLA number: 202570. [Online] Available from: http://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/202570Orig1s000ClinPharmR.pdf.
   Google Scholar
• US Food and Drug Administration, Center for drug evaluation and research. (2014). Clinical Pharmacology and biopharmaceutics reviews, NDA/BLA number: 205755. [Online] Available from: http://www.accessdata.fda.gov/drugsatfda_docs/nda/2014/205755Orig1s000ClinPharmR.pdf.
   Google Scholar
• US Food and Drug Administration, Center for drug evaluation and research. (2015a). US package inserts, Reference ID: 3859407. [Online] Available from: http://www.accessdata.fda.gov/drugsatfda_docs/label/2015/208434s000lbl.pdf.
   Google Scholar
• US Food and Drug Administration, Center for drug evaluation and research. (2015b). Clinical Pharmacology and biopharmaceutics reviews, NDA/BLA number: 208434. [Online] Available from: http://www.accessdata.fda.gov/drugsatfda_docs/nda/2015/208434Orig1s000ClinPharmR.pdf.
   Google Scholar
• Webb TR, Slavish J, George RE, et al. (2009). Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy. Expert Rev Anticancer Ther 9:331–56.
   PubMed Web of Science ®Google Scholar
• Yeo KR, Yeo WW. (2001). Inhibitory effects of verapamil and diltiazem on simvastatin metabolism in human liver microsomes. Br J Clin Pharmacol 51:461–70.
   PubMed Web of Science ®Google Scholar