In vitro and in vivo activity of AMG 337, a potent and selective MET kinase inhibitor, in MET-dependent cancer models

Molecular Cancer Therapeutics

Volumn 15, Issue 7, 2016, Pages 1568-1579

  Hughes, Paul E ^a   Rex, Karen ^a   Caenepeel, Sean ^a   Yang, Yajing ^a   Zhang, Yihong ^a   Broome, Martin A ^a   Kha, Hue T ^a   Burgess, Teresa L ^a   Amore, Benny ^a   Kaplan Lefko, Paula J ^a   Moriguchi, Jodi ^a   Werner, Jonathan ^a   Damore, Michael A ^a   Baker, Daniel ^a   Choquette, Deborah M ^a   Harmange, Jean Christophe ^a   Radinsky, Robert ^a   Kendall, Richard ^a   Dussault, Isabelle ^a   Coxon, Angela ^a  

^a AMGEN INC   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADAPTOR PROTEIN; AMG 337; GAB 1 PROTEIN; MITOGEN ACTIVATED PROTEIN KINASE; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN TYROSINE KINASE INHIBITOR; SCATTER FACTOR RECEPTOR; UNCLASSIFIED DRUG; ANTINEOPLASTIC AGENT; PROTEIN KINASE INHIBITOR;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANTINEOPLASTIC ACTIVITY; ARTICLE; CANCER CELL LINE; CELL PROLIFERATION; CELL VIABILITY; CHEMOSENSITIVITY; CONTROLLED STUDY; COPY NUMBER VARIATION; DRUG BLOOD LEVEL; DRUG MECHANISM; FEMALE; GENE AMPLIFICATION; HUMAN; HUMAN CELL; IC50; IN VITRO STUDY; IN VIVO STUDY; MAXIMUM PLASMA CONCENTRATION; MOUSE; NONHUMAN; ONCOGENE; PHARMACODYNAMICS; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION; SINGLE DRUG DOSE; STOMACH TUMOR; TUMOR CELL LINE; TUMOR MODEL; TUMOR VOLUME; TUMOR XENOGRAFT; ANIMAL; ANTAGONISTS AND INHIBITORS; CELL SURVIVAL; CHEMISTRY; DISEASE MODEL; DOSE RESPONSE; DRUG EFFECTS; DRUG SCREENING; GENETICS; METABOLISM; NECROSIS; NEOPLASMS; PATHOLOGY;

ANIMALS; ANTINEOPLASTIC AGENTS; CELL LINE, TUMOR; CELL PROLIFERATION; CELL SURVIVAL; DISEASE MODELS, ANIMAL; DOSE-RESPONSE RELATIONSHIP, DRUG; FEMALE; GENE AMPLIFICATION; HUMANS; MAP KINASE SIGNALING SYSTEM; MICE; NECROSIS; NEOPLASMS; PHOSPHATIDYLINOSITOL 3-KINASES; PROTEIN KINASE INHIBITORS; PROTO-ONCOGENE PROTEINS C-MET; SIGNAL TRANSDUCTION; XENOGRAFT MODEL ANTITUMOR ASSAYS;

EID: 84979500076     PISSN: 15357163     EISSN: 15388514     Source Type: Journal    
DOI: 10.1158/1535-7163.MCT-15-0871     Document Type: Article

References (40)

1. Gherardi E, Birchmeier W, Birchmeier C, Vande Woude G. Targeting MET in cancer: rationale and progress. Nat Rev Cancer 2012;12: 89-103.
2. Jeffers M, Schmidt L, Nakaigawa N, Webb CP, Weirich G, Kishida T, et al. Activating mutations for the met tyrosine kinase receptor in human cancer. Proc Natl Acad Sci U S A 1997;94:11445-50.
3. Schmidt L, Junker K, Nakaigawa N, Kinjerski T, Weirich G, Miller M, et al. Novel mutations of the MET proto-oncogene in papillary renal carcinomas. Oncogene 1999;18:2343-50.
4. Kong-Beltran M, Seshagiri S, Zha J, Zhu W, Bhawe K, Mendoza N, et al. Somatic mutations lead to an oncogenic deletion of met in lung cancer. Cancer Res 2006;66:283-9.
5. National Institutes of Health. The Cancer Genome Atlas. Available from: http://cancergenome.nih.gov/.
6. Memorial Sloan Kettering Cancer Center. cBioPortal for Cancer Genomics. Available from: http://www.cbioportal.org/.
7. Cancer Genome Atlas Research Network. Comprehensive molecular profiling of lung adenocarcinoma. Nature 2014;511:543-50.
8. Cerami E, Gao J, Dogrusoz U, Gross BE, Sumer SO, Aksoy BA, et al. The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data. Cancer Discov 2012;2:401-4.
9. Ahronian LG, Sennott EM, Van Allen EM, Wagle N, Kwak EL, Faris JE, et al. Clinical acquired resistance to RAF inhibitor combinations in BRAFmutant colorectal cancer through MAPK pathway alterations. Cancer Discov 2015;5:358-67.
10. Bardelli A, Corso S, Bertotti A, Hobor S, Valtorta E, Siravegna G, et al. Amplification of the MET receptor drives resistance to anti-EGFR therapies in colorectal cancer. Cancer Discov 2013;3: 658-73.
11. Engelman JA, Zejnullahu K, Mitsudomi T, Song Y, Hyland C, Park JO, et al. MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling. Science 2007;316:1039-43.
12. Turke AB, Zejnullahu K, Wu YL, Song Y, Dias-Santagata D, Lifshits E, et al. Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC. Cancer Cell 2010;17:77-88.
13. Crystal AS, Shaw AT, Sequist LV, Friboulet L, Niederst MJ, Lockerman EL, et al. Patient-derived models of acquired resistance can identify effective drug combinations for cancer. Science 2014;346: 1480-6.
14. Chi AS, Batchelor TT, Kwak EL, Clark JW, Wang DL, Wilner KD, et al. Rapid radiographic and clinical improvement after treatment of a MET-amplified recurrent glioblastoma with a mesenchymal-epithelial transition inhibitor. J Clin Oncol 2012;30:e30-3.
15. Lennerz JK, Kwak EL, Ackerman A, Michael M, Fox SB, Bergethon K, et al. MET amplification identifies a small and aggressive subgroup of esophagogastric adenocarcinoma with evidence of responsiveness to crizotinib. J Clin Oncol 2011;29:4803-10.
16. Frampton GM, Ali SM, Rosenzweig M, Chmielecki J, Lu X, Bauer TM, et al. Activation of MET via diverse exon 14 splicing alterations occurs in multiple tumor types and confers clinical sensitivity to MET inhibitors. Cancer Discov 2015;5:850-9.
17. Paik PK, Drilon A, Fan PD, Yu H, Rekhtman N, Ginsberg MS, et al. Response to MET inhibitors in patients with stage IV lung adenocarcinomas harboring MET mutations causing exon 14 skipping. Cancer Discov 2015;5:842-9.
18. Gonzatti-Haces M, Park M, Dean M, Blair DG, Vande Woude GF. The human met oncogene is a member of the tyrosine kinase family. Princess Takamatsu Symp 1986;17:221-32.
19. Burgess T, Coxon A, Meyer S, Sun J, Rex K, Tsuruda T, et al. Fully human monoclonal antibodies to hepatocyte growth factor with therapeutic potential against hepatocyte growth factor/c-Met-dependent human tumors. Cancer Res 2006;66:1721-9.
20. Boezio AA, Copeland KW, Rex K, K Albrecht B, Bauer D, Bellon SF, et al. Discovery of (R)-6-(1-(8-Fluoro-6-(1-methyl-1H-pyrazol-4-yl)-[1,2,4]triazolo[4,3-a]pyridin-3-y l)ethyl)-3-(2-methoxyethoxy)-1,6-naphthyridin-5(6H)-one (AMG 337), a potent and selective inhibitor of MET with high unbound target coverage and robust in vivo antitumor activity. J Med Chem 2016;59:2328-42.
21. Davis MI, Hunt JP, Herrgard S, Ciceri P, Wodicka LM, Pallares G, et al. Comprehensive analysis of kinase inhibitor selectivity. Nat Biotechnol 2011;29:1046-51.
22. Karaman MW, Herrgard S, Treiber DK, Gallant P, Atteridge CE, Campbell BT, et al. A quantitative analysis of kinase inhibitor selectivity. Nat Biotechnol 2008;26:127-32.
23. Saiki AY, Caenepeel S, Yu D, Lofgren JA, Osgood T, Robertson R, et al. MDM2 antagonists synergize broadly and robustly with compounds targeting fundamental oncogenic signaling pathways. Oncotarget 2014;5:2030-43.
24. Edgar R, Domrachev M, Lash AE. Gene Expression Omnibus: NCBI gene expression and hybridization array data repository. Nucleic Acids Res 2002;30:207-10.
25. National Research Council. Guide For the Care and Use of Laboratory Animals, Eighth Edition. Washington, DC: The National Academies Press; 2011.
26. Tiedt R, Degenkolbe E, Furet P, Appleton BA, Wagner S, Schoepfer J, et al. A drug resistance screen using a selective MET inhibitor reveals a spectrum of mutations that partially overlap with activating mutations found in cancer patients. Cancer Res 2011;71:5255-64.
27. Barretina J, Caponigro G, Stransky N, Venkatesan K, Margolin AA, Kim S, et al. The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity. Nature 2012;483:603-7.
28. Iwai M, Matsuda M, Iwai Y. Cloning of a cancer cell-producing hepatocyte growth factor, vascular endothelial growth factor, and interleukin-8 from gastric cancer cells. In Vitro Cell Dev Biol Anim 2003; 39:288-90.
29. Park M, Dean M, Cooper CS, Schmidt M, O'Brien SJ, Blair DG, et al. Mechanism of met oncogene activation. Cell 1986;45:895-904.
30. Smolen GA, Sordella R, Muir B, Mohapatra G, Barmettler A, Archibald H, et al. Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752. Proc Natl Acad Sci U S A 2006;103:2316-21.
31. Forbes SA, Beare D, Gunasekaran P, Leung K, Bindal N, Boutselakis H, et al. COSMIC: exploring the world's knowledge of somatic mutations in human cancer. Nucleic Acids Res 2015;43:D805-11.
32. Xie Q, Bradley R, Kang L, Koeman J, Ascierto ML, Worschech A, et al. Hepatocyte growth factor (HGF) autocrine activation predicts sensitivity to MET inhibition in glioblastoma. Proc Natl Acad Sci U S A 2012; 109:570-5.
33. Gavine PR, Ren Y, Han L, Lv J, Fan S, Zhang W, et al. Volitinib, a potent and highly selective c-Met inhibitor, effectively blocks c-Met signaling and growth in c-MET amplified gastric cancer patient-derived tumor xenograft models. Mol Oncol 2015;9:323-33.
34. Lee HE, Kim MA, Lee HS, Jung EJ, Yang HK, Lee BL, et al. MET in gastric carcinomas: comparison between protein expression and gene copy number and impact on clinical outcome. Br J Cancer 2012; 107:325-33.
35. Vo TT, Ryan J, Carrasco R, Neuberg D, Rossi DJ, Stone RM, et al. Relative mitochondrial priming of myeloblasts and normal HSCs determines chemotherapeutic success in AML. Cell 2012;151:344-55.
36. Hata AN, Engelman JA, Faber AC. The BCL2 family: key mediators of the apoptotic response to targeted anticancer therapeutics. Cancer Discov 2015;5:475-87.
37. Faber AC, Corcoran RB, Ebi H, Sequist LV, Waltman BA, Chung E, et al. BIM expression in treatment-naive cancers predicts responsiveness to kinase inhibitors. Cancer Discov 2011;1:352-65.
38. Okamoto W, Okamoto I, Arao T, Kuwata K, Hatashita E, Yamaguchi H, et al. Antitumor action of the MET tyrosine kinase inhibitor crizotinib (PF-02341066) in gastric cancer positive for MET amplification. Mol Cancer Ther 2012;11:1557-64.
39. Hong DS, Lo Russo P, Hamid O, Beaupre DM, Janku F, Khan R, et al. Firstin-human study of AMG 337, a highly selective oral inhibitor of MET, in adult patients (pts) with advanced solid tumors. J Clin Oncol 32:5s, 2014 (suppl; abstr 2508).
40. Kwak EL, Lo Russo P, Hamid O, Janku F, Kittaneh M, Catenacci DVT, et al. Clinical activity of AMG 337, an oral MET kinase inhibitor, in adult patients (pts) with MET amplified gastroesophageal junction (GEJ), gastric (G), or esophageal (E) cancer. J Clin Oncol 33, 2015 (suppl 3; abstr 1).