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Discovery and development of sorafenib: a multikinase inhibitor for treating cancer

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Wilhelm, Scott, Carter, Christopher, Lynch, Mark, Lowinger, Timothy, Dumas, Jacques, Smith, Roger A., Schwartz, Brian, Simantov, Ronit, Kelley, Susan·2006·Nature Reviews Drug Discovery
DOI 10.1038/nrd2130
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Abstract

In December 2005, sorafenib became the first new treatment to be approved for advanced renal cancer in more than a decade. Wilhelm and colleagues provide the history of this drug, which inhibits several kinases involved in tumour signalling and angiogenesis. Since the molecular revolution of the 1980s, knowledge of the aetiology of cancer has increased considerably, which has led to the discovery and development of targeted therapies tailored to inhibit cancer-specific pathways. The introduction and refinement of rapid, high-throughput screening technologies over the past decade has greatly facilitated this targeted discovery and development process. Here, we describe the discovery and continuing development of sorafenib (previously known as BAY 43-9006), the first oral multikinase inhibitor that targets Raf and affects tumour signalling and the tumour vasculature. The discovery cycle of sorafenib (Nexavar; Bayer Pharmaceuticals) — from initial screening for a lead compound to FDA approval for the treatment of advanced renal cell carcinoma in December 2005 — was completed in just 11 years, with approval being received ∼5 years after the initiation of the first Phase I trial.

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  1. Parada, L. F., Tabin, C. J., Shih, C. & Weinberg, R. A. Human EJ bladder carcinoma oncogene is homologue of Harvey sarcoma virus ras gene. Nature 297, 474–478 (1982). · DOI · Paper page
  2. Weinberg, R. A. Tumor suppressor genes. Science 254, 1138–1146 (1991). · DOI · Paper page
  3. Gallo, R. C. & Wong-Staal, F. Retroviruses as etiologic agents of some animal and human leukemias and lymphomas and as tools for elucidating the molecular mechanism of leukemogenesis. Blood 60, 545–557 (1982). · DOI · Paper page
  4. Varmus, H. Retroviruses. Science 240, 1427–1435 (1988). · DOI · Paper page
  5. Spector, D. H. et al. Uninfected avian cells contain RNA related to the transforming gene of avian sarcoma viruses. Cell 13, 371–379 (1978). · DOI
  6. Bishop, J. M. Cellular oncogenes and retroviruses. Annu. Rev. Biochem. 52, 301–354 (1983). · DOI · Paper page
  7. Frost, P. & Kerbel, R. S. On a possible epigenetic mechanism(s) of tumor cell heterogeneity. The role of DNA methylation. Cancer Metastasis Rev. 2, 375–378 (1983). · DOI
  8. Weinberg, R. A. The molecular basis of oncogenes and tumor suppressor genes. Ann. NY Acad. Sci. 758, 331–338 (1995). · DOI
  9. Niman, H. L. Antisera to a synthetic peptide of the sis viral oncogene product recognize human platelet-derived growth factor. Nature 307, 180–183 (1984). · doi:10.1038/307180a0
  10. Coussens, L. et al. Structural alteration of viral homologue of receptor proto-oncogene fms at carboxyl terminus. Nature 320, 277–280 (1986). · DOI · Paper page
  11. Schechter, A. L. et al. The neu oncogene: an erb-B-related gene encoding a 185, 000-Mr tumour antigen. Nature 312, 513–516 (1984). · DOI · Paper page
  12. Gill, G. N., Bertics, P. J. & Santon, J. B. Epidermal growth factor and its receptor. Mol. Cell Endocrinol. 51, 169–186 (1987). · DOI
  13. Kranenburg, O. The KRAS oncogene: past, present, and future. Biochim. Biophys. Acta 1756, 81–82 (2005).
  14. Bos, J. L. Ras oncogenes in human cancer: a review. Cancer Res. 49, 4682–4689 (1989).
  15. Ponzielli, R., Katz, S., Barsyte-Lovejoy, D. & Penn, L. Z. Cancer therapeutics: targeting the dark side of Myc. Eur. J. Cancer 41, 2485–2501 (2005). · DOI · Paper page
  16. Weiss, C. & Bohmann, D. Deregulated repression of c-Jun provides a potential link to its role in tumorigenesis. Cell Cycle 3, 111–113 (2004). · DOI
  17. Kolch, W., Kotwaliwale, A., Vass, K. & Janosch, P. The role of Raf kinases in malignant transformation. Expert. Rev. Mol. Med. 2002, 1–18 (2002). Review on the importance of Raf kinase signalling in tumour cells. · DOI
  18. O'Neill, E., Rushworth, L., Baccarini, M. & Kolch, W. Role of the kinase MST2 in suppression of apoptosis by the proto-oncogene product Raf-1. Science 306, 2267–2270 (2004). · DOI · Paper page
  19. Brose, M. S. et al. BRAF and RAS mutations in human lung cancer and melanoma. Cancer Res. 62, 6997–7000 (2002).
  20. Salvatore, G. et al. Analysis of BRAF point mutation and RET/PTC rearrangement refines the fine-needle aspiration diagnosis of papillary thyroid carcinoma. J. Clin. Endocrinol. Metab. 89, 5175–5180 (2004). · DOI · Paper page
  21. Melillo, R. M. et al. The RET/PTC-RAS-BRAF linear signaling cascade mediates the motile and mitogenic phenotype of thyroid cancer cells. J. Clin. Invest. 115, 1068–1081 (2005). · DOI · Paper page
  22. Downward, J. Targeting RAS signalling pathways in cancer therapy. Nature Rev. Cancer 3, 11–22 (2003). · DOI · Paper page
  23. Oka, H. et al. Constitutive activation of mitogen-activated protein (MAP) kinases in human renal cell carcinoma. Cancer Res. 55, 4182–4187 (1995).
  24. Hwang, Y. H. et al. Over-expression of c-raf-1 proto-oncogene in liver cirrhosis and hepatocellular carcinoma. Hepatol. Res. 29, 113–121 (2004). · DOI
  25. McPhillips, F. et al. Association of c-Raf expression with survival and its targeting with antisense oligonucleotides in ovarian cancer. Br. J. Cancer 85, 1753–1758 (2001). · doi:10.1054/bjoc.2001.2139
  26. Mukherjee, R., Bartlett, J. M., Krishna, N. S., Underwood, M. A. & Edwards, J. Raf-1 expression may influence progression to androgen insensitive prostate cancer. Prostate 64, 101–107 (2005). · DOI
  27. Kasid, U. & Dritschilo, A. RAF antisense oligonucleotide as a tumor radiosensitizer. Oncogene 22, 5876–5884 (2003). · DOI
  28. Lyons, J. F., Wilhelm, S., Hibner, B. & Bollag, G. Discovery of a novel Raf kinase inhibitor. Endocrine-Related Cancer 8, 219–225 (2001). · DOI · Paper page
  29. McDonald, O. B. et al. A scintillation proximity assay for the Raf/MEK/ERK kinase cascade: high-throughput screening and identification of selective enzyme inhibitors. Anal. Biochem. 268, 318–329 (1999). · DOI
  30. Capdeville, R., Buchdunger, E., Zimmermann, J. & Matter, A. Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug. Nature Rev. Drug Discov. 1, 493–502 (2002). · DOI · Paper page
  31. Dowell, J., Minna, J. D. & Kirkpatrick, P. Erlotinib hydrochloride. Nature Rev. Drug Discov. 4, 13–14 (2005). · DOI · Paper page
  32. Zhang, Z. et al. Oncogenes as novel targets for cancer therapy (part I): growth factors and protein tyrosine kinases. Am. J. Pharmacogenomics 5, 173–190 (2005). · DOI
  33. Aherne, G. W., McDonald, E. & Workman, P. Finding the needle in the haystack: why high-throughput screening is good for your health. Breast Cancer Res. 4, 148–154 (2002). · DOI
  34. Riedl, B. et al. Potent Raf kinase inhibitors from the diphenylurea class: structure activity relationships. Clin. Cancer Res. 20, 83a (2001).
  35. Smith, R. A. et al. Discovery of heterocyclic ureas as a new class of raf kinase inhibitors: identification of a second generation lead by a combinatorial chemistry approach. Bioorg. Med. Chem. Lett. 11, 2775–2778 (2001). · doi:10.1016/s0960-894x(01)00571-6
  36. 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). · DOI
  37. Wilhelm, S. et al. BAY 43-9006, a novel Raf-1 kinase inhibitor (RKI) blocks the Raf/MEK/ERK pathway in tumor cells. Proc. Am. Assoc. Cancer Res. 42, 923 (2001).
  38. Wilhelm, S. M. et al. BAY 43-9006 exhibits broad spectrum oral anti-tumor activity and targets the Raf/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis. Cancer Res. 64, 7099–7109 (2004). Preclinical data describing sorafenib pharmacological target profile and effects on MAPK signalling and anti-angiogenic activity in preclinical human tumour xenograft models in rodents. · DOI · Paper page
  39. Carlomagno, F. et al. BAY 43-9006 inhibition of oncogenic RET mutants. J. Natl. Cancer Inst. 98, 326–334 (2006). · DOI · Paper page
  40. Wan, P. T. et al. Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF. Cell 116, 855–867 (2004). Pivotal paper describing how sorafenib induces inhibition of Raf1, wild-type B-Raf and b-raf V600E , by binding to and stabilizing the conserved kinase domain. This paper confirmed the SAR observations. · DOI · Paper page
  41. Nagar, B. et al. Crystal structures of the kinase domain of c-Abl in complex with the small molecule inhibitors PD173955 and imatinib (STI-571). Cancer Res. 62, 4236–4243 (2002).
  42. Sharma, A. et al. Mutant V599EB-Raf regulates growth and vascular development of malignant melanoma tumors. Cancer Res. 65, 2412–2421 (2005). · DOI · Paper page
  43. Chang, Y. S. et al. BAY 43-9006 (Sorafenib) inhibits ectopic and orthotopic growth of a murine model of renal adenocarcinoma (Renca) predominantly through inhibition of tumor angiogenesis. Clin. Cancer Res. 46, 5831 (2005).
  44. Liu, L. et al. Sorafenib (BAY 43-9006) inhibits the Raf/MEK/ERK pathway in hepatocellular carcinoma (HCC) cells and produces robust efficacy against PLC/PRF/5 HCC tumors in mice. Poster presentation Am. Assoc. Cancer Res.–Natl Cancer Inst.–Eur. Organiz. Res. Treat. Cancer. Philadelphia, Pennsylvania (2005).
  45. Yu, C. et al. The role of Mcl-1 downregulation in the proapoptotic activity of the multikinase inhibitor BAY 43-9006. Oncogene 24, 6861–6869 (2005). Preclinical data describing the downregulation of the prosurvival protein MCL1 and pro-apoptotic activity of sorafenib in tumour cells. · DOI · Paper page
  46. Rahmani, M., Maynard Davis, E., Bauer, C., Dent, P. & Grant, S. Apoptosis induced by the kinase inhibitor BAY 43-9006 in human leukemia cells involves down-regulation of mcl-1 through inhibition of translation. J. Biol. Chem. 280, 35217–35227 (2005). · DOI · Paper page
  47. Panka, D. J., Wang, W., Atkins, M. B. & Mier, J. W. The Raf inhibitor BAY 43-9006 (Sorafenib) induces caspase-independent apoptosis in melanoma cells. Cancer Res. 66, 1611–1619 (2006). · DOI
  48. Strumberg, D. et al. Phase I clinical and pharmacokinetic study of the novel Raf kinase and vascular endothelial growth factor receptor inhibitor BAY 43-9006 in patients with advanced refractory solid tumors. J. Clin. Oncol. 23, 965–972 (2005). · DOI · Paper page
  49. Clark, J. W., Eder, J. P., Ryan, D., Lee, R. & Lenz, H.-J. The safety and pharmacokinetics of the multi-targeted tyrosine kinase inhibitor (including Raf kinase and VEGF kinase), BAY 43-9006, in patients with advanced, refractory solid tumors. Clin. Cancer Res. 11, 5472–5480 (2005). · DOI · Paper page
  50. Awada, A. et al. Phase I safety and pharmacokinetics of BAY 43-9006 administered for 21 days on/7 days off in patients with advanced, refractory solid tumours. Br. J. Cancer 92, 1855–1861 (2005). · DOI · Paper page
  51. Moore, M. et al. Phase I study to determine the safety and pharmacokinetics of the novel Raf kinase and VEGFR inhibitor BAY 43-9006, administered for 28 days on/7 days off in patients with advanced, refractory solid tumors. Ann. Oncol. 16, 1688–1694 (2005). · DOI · Paper page
  52. Strumberg, D. et al. Pooled safety analysis of BAY 43-9006 (sorafenib) monotherapy in patients with advanced solid tumours: Is rash associated with treatment outcome? Eur. J. Cancer 42, 548–556 (2006). · DOI
  53. Kupsch, P. et al. Results of a Phase I trial of sorafenib (BAY 43-9006) in combination with oxaliplatin in patients with refractory solid tumors, including colorectal cancer. Clin. Colorectal Cancer 5, 188–196 (2005). · doi:10.3816/ccc.2005.n.030
  54. Flaherty, K. T. et al. Sorafenib combined with carboplatin and paclitaxel for metastatic melanoma: PFS and response versus B-Raf status. Proc. 4th Intl. Symp. Targeted Anticancer Ther. Amsterdam, The Netherlands [online] , (2006).
  55. Siu, L. L. et al. Phase I/II trial of sorafenib and gemcitabine in advanced solid tumors and in advanced pancreatic cancer. Clin. Cancer Res. 12, 144–151 (2006). · DOI · Paper page
  56. Richly, H. et al. Results of a Phase I trial of sorafenib (BAY 43-9006) in combination with doxorubicin in patients with refractory solid tumors. Ann. Oncol. 17, 866–873 (2006). · DOI
  57. Awada, A. et al. A Phase I study of BAY 43-9006, a novel Raf kinase and VEGFR inhibitor, in combination with Taxotere in patients with advanced solid tumors. Poster presentation Am. Assoc. Cancer Res.–Natl Cancer Inst.–Eur. Organiz. Res. Treat. Cancer. Geneva, Switzerland (2004).
  58. Steinbild, S. et al. Phase I study of BAY 43-9006 (sorafenib), a Raf kinase and VEGFR inhibitor, combined with irinotecan (CPT-11) in advanced solid tumors. J. Clin. Oncol. 23, 3115 (2005). · doi:10.1200/jco.2005.23.16_suppl.3115
  59. Eisen, T. et al. Phase I trial of BAY 43-9006 (sorafenib) combined with dacarbazine (DTIC) in metastatic melanoma patients. J. Clin. Oncol. 23, 7508 (2005). · doi:10.1200/jco.2005.23.16_suppl.7508
  60. Gollob, J. et al. Phase II trial of sorafenib (BAY 43-9006) in combination with interferon alpha 2b in patients with metastatic renal cell carcinoma. Eur. J. Cancer Supplements 3, 226 (2005).
  61. Robert, C. et al. Phase I trial of sorafenib (BAY 43-9006) in combination with interferon alpha 2a in patients with unresectable and/or metastatic renal cell carcinoma and malignant melanoma. Eur. J. Cancer Supplements 3, 254 (2005).
  62. Hainsworth, J. D. et al. Treatment of metastatic renal cell carcinoma with a combination of bevacizumab and erlotinib. J. Clin. Oncol. 23, 7889–7896 (2005). · DOI · Paper page
  63. Takahashi, A. et al. Markedly increased amounts of messenger RNAs for vascular endothelial growth factor and placenta growth factor in renal cell carcinoma associated with angiogenesis. Cancer Res. 54, 4233–4237 (1994).
  64. Smith, K. et al. Silencing of epidermal growth factor receptor suppresses hypoxia-inducible factor-2-driven VHL-/- renal cancer. Cancer Res. 65, 5221–5230 (2005). · DOI · Paper page
  65. Gunaratnam, L. et al. Hypoxia inducible factor activates the transforming growth factor-alpha/epidermal growth factor receptor growth stimulatory pathway in VHL(-/-) renal cell carcinoma cells. J. Biol. Chem. 278, 44966–44974 (2003). · DOI · Paper page
  66. Ratain, M. J. et al. Phase II placebo-controlled randomized discontinuation trial of sorafenib in patients with metastatic renal cell carcinoma. J. Clin. Oncol. 24, 2505–2512 (2006). Pivotal Phase II trial demonstrating sorafenib's significant PFS benefit over placebo and its acceptable tolerability in patients with advanced refractory RCC. These findings formed the basis of sorafenib's recent FDA approval for this indication. · DOI · Paper page
  67. Escudier, B. et al. Randomized phase III trial of the multi-kinase inhibitor sorafenib (BAY 43-9006) in patients with advanced renal cell carcinoma (RCC). Eur. J. Cancer Supplements 3, 226 (2005). Pivotal Phase III trial confirming sorafenib's significant PFS benefit and acceptable tolerability in patients with advanced refractory RCC. These findings formed the basis of sorafenib's recent FDA approval for this indication.
  68. Motzer, R. J. et al. Prognostic factors for survival in previously treated patients with metastatic renal cell carcinoma. J. Clin. Oncol. 22, 454–463 (2004). · DOI · Paper page
  69. Abou-Alfa, G. K. et al. Phase II biomarker analysis of sorafenib (BAY 43-9006) in patients with advanced hepatocellular carcinoma. Poster presentation Am. Assoc. Cancer Res.–Natl Cancer Inst.–Eur. Organiz. Res. Treat. Cancer. Philadelphia, Pennsylvania (2005).
  70. Gatzemeier, U. et al. Phase II trial of single-agent sorafenib in patients with advanced non-small-cell lung carcinoma. J. Clin. Oncol. 24, 364s (2006). · doi:10.1200/jco.2006.24.18_suppl.7002
  71. Kloos, R. et al. Significant clinical and biologic activity of RAF/VEGF-R kinase inhibitor BAY 43-9006 in patients with metastatic papillary thyroid carcinoma (PTC): Updated results of a phase II study. J. Clin. Oncol. 24, 288s (2006). · DOI
  72. Steinbild, S. et al. Phase II study of sorafenib (BAY43-9006) in hormone-refractory patients with prostate cancer: a study of the Central European Society for Anticancer Drug Research — EWIV (CESAR). J. Clin. Oncol. 24, 144s (2006). · doi:10.1200/jco.2006.24.18_suppl.3094
  73. Dahut, W. L. et al. Bony metastatic disease responses to sorafenib (BAY 43-9006) independent of PSA in patients with metastatic androgen independent prostate cancer. J. Clin. Oncol. 24, 218s (2006). · doi:10.1200/jco.2006.24.18_suppl.4506
  74. Moreno-Aspitia, A. et al. BAY 43-9006 as single oral agent in patients with metastatic breast cancer previously exposed to anthracycline and/or taxane. J. Clin. Oncol. 24, 577 (2006). · doi:10.1200/jco.2006.24.18_suppl.577
  75. Wright, J. J., Zerivitz, K. & Gravell, A. Clinical trials referral resource. Current clinical trials of BAY 43-9006, Part 1. Oncology (Williston Park) 19, 499–502 (2005).
  76. Lorigan, P. et al. Phase II trial of sorafenib combined with dacarbazine in metastatic melanoma patients. J. Clin. Oncol. 24, 8012 (2006). · doi:10.1200/jco.2006.24.18_suppl.8012
  77. Sosman, J. et al. A phase I/II trial of sorafenib (S) with bevacizumab (B) in metastatic renal cell cancer (mRCC) patients (Pts). J. Clin. Oncol. 24, 128s (2006). · doi:10.1200/jco.2006.24.18_suppl.3031
  78. Azad, N. S. et al. Increased efficacy and toxicity with combination anti-VEGF therapy using sorafenib and bevacizumab. J. Clin. Oncol. 24, 121s (2006).
  79. Elting, J. et al. Biomarkers associated with clinical outcomes in TARGETs, a Phase III single-agent, placebo-controlled study of sorafenib in advanced renal cell carcinoma. Proc. Am. Assoc. Cancer Res. 47, A2909 (2006).
  80. Advani, A. S. C-kit as a target in the treatment of acute myelogenous leukemia. Curr. Hematol. Rep. 4, 51–58 (2005).
  81. Markovic, A., MacKenzie, K. L. & Lock, R. B. FLT-3: a new focus in the understanding of acute leukemia. Int. J. Biochem. Cell Biol. 37, 1168–1172 (2005). · DOI
  82. Chen, L. L. et al. Imatinib resistance in gastrointestinal stromal tumors. Curr. Oncol. Rep. 7, 293–299 (2005). · doi:10.1007/s11912-005-0053-6
  83. Kodama, Y. et al. The RET proto-oncogene: a molecular therapeutic target in thyroid cancer. Cancer Sci. 96, 143–148 (2005). · DOI
  84. Flaherty, K. T. et al. Phase I/II, pharmacokinetic and pharmacodynamic trial of BAY 43-9006 alone in patients with metastatic melanoma. Proc. Am. Soc. Clin. Oncol. 23, 201s (2005).
  85. Blumenschein, G. R. et al. Phase II multicenter uncontrolled trial of single agent sorafenib (BAY 43-9006) in relapsed or refractory advanced non-small cell lung cancer. Poster presentation Am. Assoc. Cancer Res.–Natl Cancer Inst.–Eur. Organiz. Res. Treat. Cancer. Philadelphia, Pennsylvania (2005).
  86. Salvatore, G. et al. B-RAF is a therapeutic target in aggressive thyroid carcinoma. Clin. Cancer Res. 12, 1623–1629 (2006). · DOI · Paper page
  87. Levy, J. et al. Analysis of transcription and protein expression changes in the 786-O human renal cell carcinoma tumor xenograft model in response to treatment with the multi-kinase inhibitor sorafenib (BAY 43-9006). Proc. Am. Assoc. Cancer Res. 47, 213–214 (2006).

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Metadata

Authors
Wilhelm, S., Carter, C., Lynch, M., Lowinger, T., Dumas, J., Smith, R. A., Schwartz, B., Simantov, R., & Kelley, S.
Venue
Nature Reviews Drug Discovery
Publisher
Springer Science and Business Media LLC
Published
2006-10-01
Volume
5
Issue
10
Pages
835-844
ISSN
  • 1474-1776 (ISSN-L)
  • 1474-1784
DOI
10.1038/nrd2130
OpenAlex
W2061345986
Cited by
1,829
References
4
FWCI
9.96
Type
journal article
Language
en
Open access
hybrid
Licence

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Wilhelm, S., Carter, C., Lynch, M., Lowinger, T., Dumas, J., Smith, R. A., Schwartz, B., Simantov, R., & Kelley, S. (2006). Discovery and development of sorafenib: a multikinase inhibitor for treating cancer. Nature Reviews Drug Discovery. https://doi.org/10.1038/nrd2130

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