Allosteric inhibitors of Bcr-abl-dependent cell proliferation

Nature Chemical Biology

Volumn 2, Issue 2, 2006, Pages 95-102

  Adrián, Francisco J ^a   Ding, Qiang ^a   Sim, Taebo ^a   Velentza, Anastasia ^a   Sloan, Christine ^a   Liu, Yi ^a   Zhang, Guobao ^a   Hur, Wooyoung ^a   Ding, Sheng ^b   Manley, Paul ^c   Mestan, Jürgen ^c   Fabbro, Doriano ^c   Gray, Nathanael S ^a  

^a GENOMICS INSTITUTE OF THE NOVARTIS RESEARCH FOUNDATION   (United States)

^b SCRIPPS RESEARCH INSTITUTE   (United States)

^c NOVARTIS PHARMA AG   (Switzerland)

Author keywords

[No Author keywords available]

Indexed keywords

ABELSON KINASE; ADENOSINE TRIPHOSPHATE; ANTILEUKEMIC AGENT; BCR ABL PROTEIN; GNF 2; IMATINIB; PROTEIN INHIBITOR; PROTEIN TYROSINE KINASE; PYRIMIDINE DERIVATIVE; UNCLASSIFIED DRUG; ANTINEOPLASTIC AGENT; GNF 2 COMPOUND; GNF-2 COMPOUND; PIPERAZINE DERIVATIVE; PROTEIN KINASE INHIBITOR;

ALLOSTERISM; ANIMAL CELL; ARTICLE; CELL PROLIFERATION; CHRONIC MYELOID LEUKEMIA; COMBINATORIAL LIBRARY; CONTROLLED STUDY; CYTOTOXICITY; DRUG MECHANISM; DRUG POTENCY; DRUG POTENTIATION; DRUG SCREENING; DRUG STRUCTURE; DRUG TARGETING; ENZYME ACTIVITY; HUMAN; HUMAN CELL; IC 50; MOUSE; MYELOPROLIFERATIVE DISORDER; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; ANIMAL; APOPTOSIS; CELL LINE; CHEMISTRY; DRUG ANTAGONISM; DRUG EFFECT; DRUG RESISTANCE; METABOLISM; PROTEIN BINDING; PROTEIN CONFORMATION;

ANIMALIA;

ANIMALS; ANTINEOPLASTIC AGENTS; APOPTOSIS; CELL LINE; CELL LINE, TRANSFORMED; CELL PROLIFERATION; DRUG RESISTANCE, NEOPLASM; FUSION PROTEINS, BCR-ABL; HUMANS; LEUKEMIA, MYELOID, CHRONIC; MICE; PIPERAZINES; PROTEIN BINDING; PROTEIN CONFORMATION; PROTEIN KINASE INHIBITORS; PROTEIN-TYROSINE KINASES; PYRIMIDINES;

EID: 33644889108     PISSN: 15524450     EISSN: 15524469     Source Type: Journal    
DOI: 10.1038/nchembio760     Document Type: Article

References (35)

1. Schindler, T. et al. Structural mechanism for STI-571 inhibition of Abelson tyrosine kinase. Science 289, 1938-1942 (2000).
2. Gorre, M.E. et al. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science 293, 876-880 (2001).
3. von Bubnoff, N., Schneller, F., Peschel, C. & Duyster, J. BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome- positive leukaemia to STI571: a prospective study. Lancet 359, 487-491 (2002).
4. Cowan-Jacob, S.W. et al. Imatinib (STI571) resistance in chronic myelogenous leukemia: molecular basis of the underlying mechanisms and potential strategies for treatment. Mini Rev. Med. Chem. 4, 285-299 (2004).
5. Weisberg, E. et al. Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. Cancer Cell 7, 129-141 (2005).
6. Shah, N.P. et al. Overriding imatinib resistance with a novel ABL kinase inhibitor. Science 305, 399-401 (2004).
7. Superti-Furga, G. & Courtneidge, S.A. Structure-function relationships in Src family and related protein tyrosine kinases. Bioessays 17, 321-330 (1995).
8. Nagar, B. et al. Structural basis for the autoinhibition of c-Abl tyrosine kinase. Cell 112, 859-871 (2003).
9. Barker, A.J. et al. Studies leading to the identification of ZD1839 (IRESSA): an orally active, selective epidermal growth factor receptor tyrosine kinase inhibitor targeted to the treatment of cancer. Bioorg. Med. Chem. Lett. 11, 1911-1914 (2001).
10. Meijer, L. et al. Biochemical and cellular effects of roscovitine, a potent and selective inhibitor of the cyclin-dependent kinases cdc2, cdk2 and cdk5. Eur. J. Biochem. 243, 527-536 (1997).
11. Buchdunger, E. et al. Inhibition of the Abl protein-tyrosine kinase in vitro and in vivo by a 2-phenylaminopyrimidine derivative. Cancer Res. 56, 100-104 (1996).
12. Regan, J. et al. Pyrazole urea-based inhibitors of p38 MAP kinase: from lead compound to clinical candidate. J. Med. Chem. 45, 2994-3008 (2002).
13. Lyons, J.F., Wilhelm, S., Hibner, B. & Bollag, G. Discovery of a novel Raf kinase inhibitor. Endocr. Relat. Cancer 8, 219-225 (2001).
14. Lowinger, T.B., Riedl, B., Dumas, J. & Smith, R.A. Design and discovery of small molecules targeting raf-1 kinase. Curr. Pharm. Des. 8, 2269-2278 (2002).
15. Ohren, J.F. et al. Structures of human MAP kinase kinase 1 (MEK1) and MEK2 describe novel noncompetitive kinase inhibition. Nat. Struct. Mol. Biol. 11, 1192-1197 (2004).
16. Barnett, S.F. et al. Identification and characterization of pleckstrin-homology-domain-dependent and isoenzyme-specific Akt inhibitors. Biochem. J. 385, 399-408 (2005).
17. Grimsby, J. et al. Allosteric activators of glucokinase: potential role in diabetes therapy. Science 301, 370-373 (2003).
18. Ding, S., Gray, N.S., Wu, X., Ding, Q. & Schultz, P.G. A combinatorial scaffold approach toward kinase-directed heterocycle libraries. J. Am. Chem. Soc. 124, 1594-1596 (2002).
19. Goldman, J.M. & Melo, J.V. Chronic myeloid leukemia-advances in biology and new approaches to treatment. N. Engl. J. Med. 349, 1451-1464 (2003).
20. Druker, B.J. et al. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nat. Med. 2, 561-566 (1996).
21. Carroll, M. et al. CGP 57148, a tyrosine kinase inhibitor, inhibits the growth of cells expressing BCR-ABL, TEL-ABL, and TEL-PDGFR fusion proteins. Blood 90, 4947-4952 (1997).
22. Dorsey, J.F. et al. Interleukin-3 protects Bcr-Abl-transformed hematopoietic progenitor cells from apoptosis induced by Bcr-Abl tyrosine kinase inhibitors. Leukemia 16, 1589-1595 (2002).
23. Hantschel, O. et al. A myristoyl/phosphotyrosine switch regulates c-Abl. Cell 112, 845-857 (2003).
24. Chou, T.C. & Talalay, P. Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors. Adv. Enzyme Regul. 22, 27-55 (1984).
25. von Bubnoff, N. et al. Inhibition of wild-type and mutant Bcr-Abl by pyridopyrimidine-type small molecule kinase inhibitors. Cancer Res. 63, 6395-6404 (2003).
26. Burke, J.R. et al. BMS-345541 is a highly selective inhibitor of IκB kinase that binds at an allosteric site of the enzyme and blocks NF-κB-dependent transcription in mice. J. Biol. Chem. 278, 1450-1456 (2003).
27. Nardi, V., Azam, M. & Daley, G.Q. Mechanisms and implications of imatinib resistance mutations in BCR-ABL. Curr. Opin. Hematol. 11, 35-43 (2004).
28. Huse, M. & Kuriyan, J. The conformational plasticity of protein kinases. Cell 109, 275-282 (2002).
29. Capdeville, R., Buchdunger, E., Zimmermann, J. & Matter, A. Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug. Nat. Rev. Drug Discov. 1, 493-502 (2002).
30. Klejman, A., Rushen, L., Morrione, A., Slupianek, A. & Skorski, T. Phosphatidylinositol-3 kinase inhibitors enhance the anti-leukemia effect of STI571. Oncogene 21, 5868-5876 (2002).
31. Sun, X., Layton, J.E., Elefanty, A. & Lieschke, G.J. Comparison of effects of the tyrosine kinase inhibitors AG957, AG490, and STI571 on BCR-ABL-expressing cells, demonstrating synergy between AG490 and STI571. Blood 97, 2008-2015 (2001).
32. Topaly, J., Zeller, W.J. & Fruehauf, S. Synergistic activity of the new ABL-specific tyrosine kinase inhibitor STI571 and chemotherapeutic drugs on BCR-ABL-positive chronic myelogenous leukemia cells. Leukemia 15, 342-347 (2001).
33. Gumireddy, K. et al. A non-ATP-competitive inhibitor of BCR-ABL overrides imatinib resistance. Proc. Natl. Acad. Sci. USA 102, 1992-1997 (2005).
34. Branford, S. et al. Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis. Blood 102, 276-283 (2003).
35. bcr/abl in myeloid cells. Cancer Res. 56, 3589-3596 (1996).