Metabolism, excretion and pharmacokinetics of [¹⁴C]crizotinib following oral administration to healthy subjects

References

• Beumer JH, Beijnen JH, Schellens JHM. (2006). Mass balance studies, with a focus on anticancer drugs. Clin Pharmacokinet 45:33–58
   PubMed Web of Science ®Google Scholar
• Cui JJ, Botrous I, Shen H, et al. (2008). Structure based drug design for the discovery of clinical candidate PF-2341066 as potent and highly selective c-Met inhibitor. Abstracts of Papers, 235th ACS National Meeting 2008 April 6–10; New Orleans, LA. Washington, DC: American Chemical Society, Abstract MEDI 177
   Google Scholar
• Cui JJ, Tran-Dube M, Shen H, et al. (2011). Structure based drug design of crizotinib (PF-02341066), a potent and selective dual inhibitor of mesenchymal-epithelial transition factor (c-MET) kinase and anaplastic lymphoma kinase (ALK). J Med Chem 54:6342–63
   PubMed Web of Science ®Google Scholar
• Gandhi L, Janne PA. (2012). Crizotinib for ALK-rearranged non-small cell lung cancer: a new targeted therapy for a new target. Clin Cancer Res 18:3737–42
   PubMed Web of Science ®Google Scholar
• Hamilton RA, Garnett WR, Kline BJ. (1981). Determination of mean valproic acid serum level by assay of a single pooled sample. Clin Pharmacol Ther 29:408–13
   PubMed Web of Science ®Google Scholar
• Herbst RS, Heymach JV, Lippman SM. (2008). Lung cancer. N Engl J Med 359:1367–80
   PubMed Web of Science ®Google Scholar
• Ito K, Iwatsubo T, Kanamitsu S, et al. (1998). Prediction of pharmacokinetic alterations caused by drug-drug interactions: metabolic interaction in the liver. Pharmacol Rev 50:387–411
   PubMed Web of Science ®Google Scholar
• Janku F, Stewart DJ, Kurzrock R. (2010). Targeted therapy in non-small-cell lung cancer – is it becoming a reality? Nat Rev Clin Oncol 7:401–14
   PubMed Web of Science ®Google Scholar
• Johnson T, Zhou S, Lee C, et al. (2011). Identification of the human enzymes involved in the oxidative metabolism of crizotinib. Drug Metab Rev 43:160
   Google Scholar
• Koivunen JP, Mermel C, Zejnullahu K, et al. (2008). EML4-ALK fusion gene and efficacy of an ALK kinase inhibitor in lung cancer. Clin Cancer Res 14:4275–83
   PubMed Web of Science ®Google Scholar
• Kwak EL, Bang Y-J, Camidge R, et al. (2010). Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer. N Engl J Med 363:1693–703
   PubMed Web of Science ®Google Scholar
• Kwon Y. (2001). Handbook of essential pharmacokinetics, pharmacodynamics, and drug metabolism for industrial scientists. New York: Kluwer Academic/Plenum Publishers
   Google Scholar
• Leclercq L, Cuyckens F, Mannens GSJ, et al. (2009). Which human metabolites have we MIST? Retrospective analysis, practical aspects, and perspectives for metabolite identification and quantification in pharmaceutical development. Chem Res Toxicol 22:280–93
   PubMed Web of Science ®Google Scholar
• Li C, Alvey C, Bello A, et al. (2011). Pharmacokinetics (PK) of crizotinib (PF-02341066) in patients with advanced non-small cell lung cancer (NSCLC) and other solid tumors. J Clin Oncol 29(15 suppl):e13065
   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
• Penner N, Klunk LJ, Prakash C. (2009). Human radiolabeled mass balance studies: objectives, utilities and limitations. Biopharm Drug Dispos 30:185–203
   PubMed Web of Science ®Google Scholar
• Roffey SJ, Obach RS, Gedge JI, Smith DA. (2007). What is the objective of the mass balance study? A retrospective analysis of data in animal and human excretion studies employing radiolabeled drugs. Drug Metab Rev 39:17–43
   PubMed Web of Science ®Google Scholar
• Shaw AT, Kim D-W, Nakagawa K, et al. (2013). Crizotinib versus chemotherapy in advanced ALK-positive lung cancer. N Engl J Med 368:2385–94
   PubMed Web of Science ®Google Scholar
• Shou M, Hayashi M, Pan Y, et al. (2008). Modeling, prediction, and in vitro in vivo correlation of CYP3A4 induction. Drug Metab Dispos 36:2355–70
   PubMed Web of Science ®Google Scholar
• Smith E, Goulet L, Walker G, et al. (2011). Metabolism and excretion of [14C]crizotinib in rats and dogs. Drug Metab Rev 43:76–7
   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 448:561–6
   PubMed Web of Science ®Google Scholar
• Soda M, Takada S, Takeuchi K, et al. (2008). A mouse model for EML4-ALK-positive lung cancer. Proc Natl Acad Sci USA 105:19893–7
   PubMed Web of Science ®Google Scholar
• Tan W, Wilner KD, Bang Y, et al. (2010). Pharmacokinetics (PK) of PF-02341066, a dual ALK/MET inhibitor, after multiple oral doses to advanced cancer patients. J Clin Oncol 28(15 suppl):2596
   Google Scholar
• Trudnowski RJ, Rico RC. (1974). Specific gravity of blood and plasma at 4 and 37 degrees C. Clin Chem 20:615–16
   Google Scholar
• Tyczynski JE, Bray F, Maxwell Parkin D. (2003). Lung cancer in Europe in 2000: epidemiology, prevention, and early detection. Lancet Oncol 4:45–55
   PubMed Web of Science ®Google Scholar
• Xu H, O’Gorman M, Tan W, et al. (2011a). The absolute oral bioavailability of crizotinib, a dual ALK/MET inhibitor, in healthy subjects. Meeting Abstracts, AAPS Annual Meeting and Exposition; 2011 October 23–27; Washington, DC. Arlington, VA: American Association of Pharmaceutical Scientists, Abstract T2370
   Google Scholar
• Xu H, O’Gorman M, Tan W, et al. (2011b). The effect of a potent CYP3A inhibitor ketoconazole on the pharmacokinetics of crizotinib, a dual ALK/MET inhibitor, in healthy subjects. Meeting Abstracts, AAPS Annual Meeting and Exposition; 2011 October 23–27; Washington, DC. Arlington, VA: American Association of Pharmaceutical Scientists, Abstract W5393
   Google Scholar
• Xu H, O’Gorman M, Tan W, et al. (2011c). The effect of a strong CYP3A inducer rifampin on the pharmacokinetics of crizotinib, a dual ALK/MET inhibitor, in healthy subjects. Meeting Abstracts, AAPS Annual Meeting and Exposition; 2011 October 23–27; Washington, DC. Arlington, VA: American Association of Pharmaceutical Scientists, Abstract W5392
   Google Scholar
• Yamazaki S, Skaptason J, Romero D, et al. (2011). Prediction of oral pharmacokinetics of cMet kinase inhibitors in humans: physiologically based pharmacokinetic model versus traditional one-compartment model. Drug Metab Dispos 39:383–93
   PubMed Web of Science ®Google Scholar
• Yamazaki S, Vicini P, Shen Z, et al. (2012). Pharmacokinetic/pharmacodynamic modeling of crizotinib for anaplastic lymphoma kinase inhibition and antitumor efficacy in human tumor xenograft mouse models. J Pharmacol Exp Ther 340:549–57
   PubMed Web of Science ®Google Scholar
• Zhong W-Z, Zhan J, Kang P, Yamazaki S. (2010). Gender specific drug metabolism of PF-02341066 in rats – role of sulfoconjugation. Curr Drug Metab 11:296–306
   Google Scholar
• Zou HY, Li Q, Lee J, et al. (2011). Antitumor efficacy of crizotinib (PF-02341066), a potent and selective ALK and c-Met RTK inhibitor, in EML4-ALK driven NSCLC tumors in vitro and in vivo. Proceedings of the AACR 102nd Annual Meeting; 2011 April 2–6; Orlando, FL. Philadelphia, PA: American Association for Cancer Research, Abstract LB-390
   Google Scholar
• Zou HY, Li Q, Lee JH, et al. (2007). An orally available small-molecule inhibitor of c-Met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanisms. Cancer Res 67:4408–17
   PubMed Web of Science ®Google Scholar