1. Budzyn K., Marley P. D., Sobey C. G. Targeting Rho and Rho- kinase in the treatment of cardiovascular disease // Trends in pharmacological sciences. 2006. Vol. 27. №. 2. P. 97-104.
2. Sasaki Y., Suzuki M., Hidaka H. The novel and specific Rho- kinase inhibitor (S)-(+)-2-methyl-1-[(4-methyl-5-isoquinoline) sulfonyl]- homopiperazine as a probing molecule for Rho-kinase-involved pathway // Pharmacology & therapeutics. 2002. Vol. 93. №. 2-3. P. 225-232.
3. Rath N., Olson M. F. Rho- associated kinases in tumorigenesis: re- considering ROCK inhibition for cancer therapy // EMBO reports. 2012. Vol. 13. №. 10. P. 900-908.
4. O’Dell KM, Rummel AE. Tofacitinib: A novel oral Janus kinase inhibitor for rheumatoid arthritis // Formulary. 2012. Vol. 47.№.10. P. 353-358.
5. Grant S. K. Therapeutic protein kinase inhibitors // Cellular and molecular life sciences. 2009. Vol. 66. №. 7. P. 1163-1177.
6. Mazzei M. E., Richeldi L., Collard H. R. Nintedanib in the treatment of idiopathic pulmonary fibrosis // Therapeutic advances in respiratory disease. 2015. Vol. 9. №. 3. P. 121-129.
7. Reichert J. M., Wenger J. B. Development trends for new cancer
therapeutics and vaccines // Drug discovery today. 2008. Vol. 13. №. 1-2.
P. 30-37.
8. Walker I, Newell H. Do molecularly targeted agents in oncology have reduced attrition rates // Nat Rev Drug Discov. 2009. Vol. 8. №. 1. P. 15-16.
9. Capdeville R. et al. Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug // Nature reviews Drug discovery. 2002.
Vol. 1. №. 7. P. 493-502.
10. Roth B. L., Sheffler D. J., Kroeze W. K. Magic shotguns versus magic bullets: selectively non-selective drugs for mood disorders and schizophrenia // Nature reviews Drug discovery. 2004. Vol. 3. №. 4. P. 353-359.
11. Goldstein D. M., Gray N. S., Zarrinkar P. P. High-throughput kinase profiling as a platform for drug discovery // Nature reviews Drug discovery. 2008. Vol. 7. №. 5. P. 391-397.
12. Patricelli M. P. et al. Functional interrogation of the kinome using nucleotide acyl phosphates // Biochemistry. 2007. Vol. 46. №. 2. P. 350-358.
13. Shoshan M. C., Linder S. Target specificity and off-target effects as determinants of cancer drug efficacy // Expert opinion on drug metabolism & toxicology. 2008. Vol. 4. №. 3. P. 273-280.
14. Csermely P., Agoston V., Pongor S. The efficiency of multi¬target drugs: the network approach might help drug design // Trends in pharmacological sciences. 2005. Vol. 26. №. 4. P. 178-182.
15. Hopkins A. L., Mason J. S., Overington J. P. Can we rationally design promiscuous drugs? // Current opinion in structural biology. 2006. Vol. 16. №. 1. P. 127-136.
16. Jenwitheesuk E. et al. Novel paradigms for drug discovery: computational multitarget screening // Trends in pharmacological sciences. 2008. Vol. 29. №. 2. P. 62-71.
17. Roskoski Jr R. Classification of small molecule protein kinase inhibitors based upon the structures of their drug-enzyme complexes // Pharmacological research. 2016. Vol. 103. P. 26-48.
18. Zhang J., Yang P. L., Gray N. S. Targeting cancer with small molecule kinase inhibitors // Nature Reviews Cancer. 2009. Vol. 9. №. 1. P.
28-39.
19. Knight Z. A., Shokat K. M. Features of selective kinase inhibitors // Chemistry & biology. 2005. Vol. 12. №. 6. P. 621-637.
20. Yung-Chi C., Prusoff W. H. Relationship between the inhibition constant (Ki) and the concentration of inhibitor which causes 50 per cent inhibition (I50) of an enzymatic reaction // Biochemical pharmacology. 1973. Vol. 22. №. 23. P. 3099-3108.
21. Garuti L., Roberti M., Bottegoni G. Non-ATP competitive protein kinase inhibitors // Current medicinal chemistry. 2010. Vol. 17. №. 25. P. 2804-2821.
22. Tummino P. J., Copeland R. A. Residence time of receptor¬ligand complexes and its effect on biological function // Biochemistry. 2008. Vol. 47. №. 20. P. 5481-5492.
23. Bradshaw J. M. et al. Prolonged and tunable residence time using reversible covalent kinase inhibitors // Nature chemical biology. 2015. Vol.
11. №. 7. P. 525-531.
24. Copeland R. A. The drug-target residence time model: a 10-year
retrospective // Nature Reviews Drug Discovery. 2016. Vol. 15. №. 2. P.
87-95.
25. Arteaga CL. Molecular therapeutics: Is one promiscuous drug against multiple targets better than combinations of molecule-specific drugs // Clin Cancer Res 2003. Vol. 9. №. 4. P. 1231-1232.
26. Faivre S., Djelloul S., Raymond E. New paradigms in anticancer therapy: targeting multiple signaling pathways with kinase inhibitors // Seminars in oncology. Elsevier, 2006. Vol. 33. №. 4. P. 407-420.
27. de Jonge M. J. A., Verweij J. Multiple targeted tyrosine kinase inhibition in the clinic: all for one or one for all? // European Journal of Cancer. 2006. Vol. 42. №. 10. P. 1351-1356.
28. Van Etten R. A. Pathogenesis and treatment of Ph+ leukemia: recent insights from mouse models // Current opinion in hematology. 2001. Vol. 8. №. 4. P. 224-230.
29. Druker B. J. Imatinib: paradigm or anomaly? // Cell Cycle. 2004. Vol. 3. №. 7. P. 833-835.
30. Weinstein I. B., Joe A. K. Mechanisms of disease: oncogene addiction—a rationale for molecular targeting in cancer therapy // Nature Reviews Clinical Oncology. 2006. Vol. 3. №. 8. P. 448-457.
31. Sharma S. V., Settleman J. Oncogene addiction: setting the stage for molecularly targeted cancer therapy // Genes & development. 2007. Vol. 21. №. 24. P. 3214-3231.
32. Comoglio P. M., Giordano S., Trusolino L. Drug development of MET inhibitors: targeting oncogene addiction and expedience // Nature reviews Drug discovery. 2008. Vol. 7. №. 6. P. 504-516.
33. Daub H., Specht K., Ullrich A. Strategies to overcome resistance to targeted protein kinase inhibitors // Nature reviews drug discovery. 2004. Vol. 3. №. 12. P. 1001-1010.
34. Engelman J. A., Janne P. A. Mechanisms of acquired resistanc e to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer // Clinical Cancer Research. 2008. Vol. 14. №. 10. P. 2895¬2899.
35. D’Amato V. et al. Mechanisms of lapatinib resistance in HER2 - driven breast cancer // Cancer treatment reviews. 2015. Vol. 41. №. 10. P. 877-883.
36. Fojo T. Multiple paths to a drug resistance phenotype: mutations, translocations, deletions and amplification of coding genes or promoter regions, epigenetic changes and microRNAs // Drug resistance updates. 2007. Vol. 10. №. 1-2. P. 59-67.
37. Duesberg P., Stindl R., Hehlmann R. Origin of multidrug resistance in cells with and without multidrug resistance genes: chromosome reassortments catalyzed by aneuploidy // Proceedings of the National Academy of Sciences. 2001. Vol. 98. №. 20. P. 11283-11288.
38. Duesberg P. et al. Cancer drug resistance: the central role of the karyotype // Drug Resistance Updates. 2007. Vol. 10. №. 1-2. P. 51-58.
39. Kerkela R. et al. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate // Nature medicine. 2006. Vol. 12. №. 8. P. 908-916.
40. Berman E. et al. Altered bone and mineral metabolism in patients receiving imatinib mesylate // New England Journal of Medicine. 2006. Vol. 354. №. 19. P. 2006-2013.
41. Bianchini D. et al. Epidermal growth factor receptor inhibitor- related skin toxicity: mechanisms, treatment, and its potential role as a predictive marker // Clinical colorectal cancer. 2008. Vol. 7. №. 1. P. 33¬43.
42. Robert C. et al. Dermatologic symptoms associated with the multikinase inhibitor sorafenib // Journal of the American Academy of Dermatology. 2009. Vol. 60. №. 2. P. 299-305.
43. Barrick C. J. et al. Chronic pharmacologic inhibition of EGFR leads to cardiac dysfunction in C57BL/6J mice // Toxicology and applied pharmacology. 2008. Vol. 228. №. 3. P. 315-325.
44. Force T., Krause D. S., Van Etten R. A. Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition // Nature Reviews Cancer. 2007. Vol. 7. №. 5. P. 332-344.
45. Crouthamel M. C. et al. Mechanism and management of AKT inhibitor-induced hyperglycemia // Clinical Cancer Research. 2009. Vol. 15. №. 1. P. 217-225.
46. de Klein A. et al. A cellular oncogene is translocated to the
Philadelphia chromosome in chronic myelocytic leukaemia // Nature. 1982.
Vol. 300. №. 5894. P. 765-767.
47. Kantarjian H. et al. Very long- term follow- up results of
imatinib mesylate therapy in chronic phase chronic myeloid leukemia after failure of interferon alpha therapy // Cancer. 2012. Vol. 118. №. 12. P.
3116-3122.
48. Quintas-Cardama A., Kantarjian H., Cortes J. Flying under the radar: the new wave of BCR-ABL inhibitors // Nature Reviews Drug Discovery. 2007. Vol. 6. №. 10. P. 834-848.
49. Morphy R. Selectively nonselective kinase inhibition: striking the right balance // Journal of medicinal chemistry. 2009. Vol. 53. №. 4. P. 1413-1437.
50. Keller-von Amsberg G., Koschmieder S. Profile of bosutinib and its clinical potential in the treatment of chronic myeloid leukemia // OncoTargets and therapy. 2013. Vol. 6. P. 99-106.
51. Mauro MJ. T315I, more or less, predicts for major molecular response: The devil is in the details // Haematologica. 2013. Vol. 98. №. 5. P. 665-666.
52. Parsons S. J., Parsons J. T. Src family kinases, key regulators of signal transduction // Oncogene. 2004. Vol. 23. №. 48. P. 7906-7909.
53. Nam H. J. et al. Antitumor activity of saracatinib (AZD0530), a c- Src/Abl kinase inhibitor, alone or in combination with chemotherapeutic agents in gastric cancer // Molecular cancer therapeutics. 2013. Vol. 12. №. 1. P. 16-26.
54. Nygaard H. B. et al. A phase Ib multiple ascending dose study of the safety, tolerability, and central nervous system availability of AZD0530 (saracatinib) in Alzheimer’s disease // Alzheimer's research & therapy. 2015. Vol. 7. №. 1. P. 35.
55. Zhang S., Yu D. Targeting Src family kinases in anti-cancer therapies: turning promise into triumph // Trends in pharmacological sciences. 2012. Vol. 33. №. 3. P. 122-128.
56. Noren N. K. et al. The EphB4 receptor suppresses breast cancer cell tumorigenicity through an Abl-Crk pathway // Nature cell biology.
2006. Vol. 8. №. 8. P. 815-825.
57. Fraser C. et al. Rapid discovery and structure-activity
relationships of pyrazolopyrimidines that potently suppress breast cancer cell growth via SRC kinase inhibition with exceptional selectivity over ABL kinase // Journal of medicinal chemistry. 2016. Vol. 59. №. 10. P. 4697¬
4710.
58. Baselga J., Swain S. M. Novel anticancer targets: revisiting ERBB2 and discovering ERBB3 // Nature Reviews Cancer. 2009. Vol. 9. №. 7. P. 463-475.
59. Lynch T. J. et al. Activating mutations in the epidermal growth
factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib // New England Journal of Medicine. 2004. Vol. 350. №. 21. P.
2129-2139.
60. Burotto M. et al. Gefitinib and erlotinib in metastatic non-small cell lung cancer: a meta-analysis of toxicity and efficacy of randomized clinical trials // The oncologist. 2015. Vol. 20. №. 4. P. 400-410.
61. Moy B, Kirkpatrick P, Kar S, Goss P. Lapatinib // Nat Rev Drug Discovery. 2007. Vol. 6. №. 6. P. 431-432.
62. Tan C. S., Gilligan D., Pacey S. Treatment approaches for EGFR- inhibitor-resistant patients with non-small-cell lung cancer // The Lancet Oncology. 2015. Vol. 16. №. 9. P. e447-e459.
63. Krop I. E. Lessons from breast cancer trials of HER2-kinase inhibitors // The Lancet Oncology. 2016. Vol. 17. №. 3. P. 267-268.
64. Nagasawa J. et al. Novel HER2 selective tyrosine kinase inhibitor, TAK- 165, inhibits bladder, kidney and androgen- independent prostate cancer in vitro and in vivo // International journal of urology. 2006. Vol. 13. №. 5. P. 587-592.
65. Cheng H., Nair S. K., Murray B. W. Recent progress on third generation covalent EGFR inhibitors // Bioorganic & medicinal chemistry letters. 2016. Vol. 26. №. 8. P. 1861-1868.
66. Sanderson K. Irreversible kinase inhibitors gain traction // Nat Rev Drug Discov. 2013. Vol. 12. №. 9. P. 649-651.
67 Singh J. et al. The resurgence of covalent drugs // Nature reviews Drug discovery. 2011. Vol. 10. №. 4. P. 307-317.
68. Solca F. et al. Target binding properties and cellular activity of
afatinib (BIBW 2992), an irreversible ErbB family blocker // Journal of Pharmacology and Experimental Therapeutics. 2012. Vol. 343. №. 2. P.
342-350.
69. Hsieh A. C., Moasser M. M. Targeting HER proteins in cancer therapy and the role of the non-target HER3 // British journal of cancer.
2007. Vol. 97. №. 4. P. 453-457.
70. Greig S. L. Osimertinib: first global approval // Drugs. 2016. Vol. 76. №. 2. P. 263-273.
71. Minguet J., Smith K. H., Bramlage P. Targeted therapies for
treatment of non- small cell lung cancer—Recent advances and future perspectives // International journal of cancer. 2016. Vol. 138. №. 11. P.
2549-2561.
72. Jackson A. L. et al. Targeting angiogenesis: vascular endothelial growth factor and related signaling pathways // Translational Cancer Research. 2015. Vol. 4. №. 1. P. 70-83.
73. Heldin C. H. Targeting the PDGF signaling pathway in tumor
treatment // Cell Communication and Signaling. 2013. Vol. 11. №. 1. P.
97.
74. Garcia- Echeverria C., Traxler P., Evans D. B. ATP site- directed competitive and irreversible inhibitors of protein kinases // Medicinal research reviews. 2000. Vol. 20. №. 1. P. 28-57.
75. MacKenzie B. A. et al. Increased FGF1-FGFRc expression in idiopathic pulmonary fibrosis // Respiratory research. 2015. Vol. 16. №. 1. P. 83
76. Paez-Ribes M. et al. Antiangiogenic therapy elicits malignant progression of tumors to increased local invasion and distant metastasis // Cancer cell. 2009. Vol. 15. №. 3. P. 220-231.
77. Ebos J. M. L. et al. Accelerated metastasis after short-term treatment with a potent inhibitor of tumor angiogenesis // Cancer cell. 2009. Vol. 15. №. 3. P. 232-239.
78. Sennino B., McDonald D. M. Controlling escape from angiogenesis inhibitors // Nature Reviews Cancer. 2012. Vol. 12. №. 10. P. 699-709.
79. Small D. FLT3 mutations: biology and treatment // ASH Education Program Book. 2006. Vol. 2006. №. 1. P. 178-184.
80. Zorn J. A. et al. Crystal structure of the FLT3 kinase domain bound to the inhibitor quizartinib (AC220) // PloS one. 2015. Vol. 10. №.
4. P. e0121177.
81. Zarrinkar P. P. et al. AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML) // Blood. 2009. Vol. 114. №. 14. P. 2984-2992.
82. Smith C. C. et al. Crenolanib is a selective type I pan-FLT3 inhibitor // Proceedings of the National Academy of Sciences. 2014. Vol.
111. №. 14. P. 5319-5324.
83. Zhao Z. et al. Exploration of type II binding mode: a privileged approach for kinase inhibitor focused drug discovery? // ACS chemical biology. 2014. Vol. 9. - №. 6. P. 1230-1241.
84. Lennartsson J., Ronnstrand L. Stem cell factor receptor/c-Kit: from basic science to clinical implications // Physiological reviews. 2012. Vol. 92. №. 4. P. 1619-1649.
85. Nishida T., Doi T., Naito Y. Tyrosine kinase inhibitors in the treatment of unresectable or metastatic gastrointestinal stromal tumors // Expert opinion on pharmacotherapy. 2014. Vol. 15. №. 14. P. 1979-1989.
86. Ustun C. et al. Chemotherapy and dasatinib induce long-term hematologic and molecular remission in systemic mastocytosis with acute myeloid leukemia with KITD816V // Leukemia research. 2009. Vol. 33. №. 5. P. 735-741.
87. Zhu Y. et al. CSF1/CSF1R blockade reprograms tumor¬infiltrating macrophages and improves response to T-cell checkpoint immunotherapy in pancreatic cancer models // Cancer research. 2014. Vol. 74. №. 18. P. 5057-5069.
88. Hallinan N. et al. Targeting the fibroblast growth factor receptor family in cancer // Cancer treatment reviews. 2016. Vol. 46. P. 51-62.
89. Sohl C. D. et al. Illuminating the molecular mechanisms of tyrosine kinase inhibitor resistance for the FGFR1 gatekeeper mutation: the Achilles’ heel of targeted therapy // ACS chemical biology. 2015. Vol. 10. №. 5. P. 1319-1329.
90. Bean J. et al. MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib // Proceedings of the National Academy of Sciences. 2007. Vol. 104. №. 52. P. 20932-20937.
91. Di Renzo M. F. et al. Overexpression and amplification of the met/HGF receptor gene during the progression of colorectal cancer //79
Clinical Cancer Research. 1995. Vol. 1. №. 2. P. 147-154.
92. Yakes F. M. et al. Cabozantinib (XL184), a novel MET and
VEGFR2 inhibitor, simultaneously suppresses metastasis, angiogenesis, and tumor growth // Molecular cancer therapeutics. 2011. Vol. 10. №. 12. P.
2298-2308.
93. Peters S., Adjei A. A. MET: a promising anticancer therapeutic target // Nature reviews Clinical oncology. 2012. Vol. 9. №. 6. P. 314-326.
94. Duchemann B, Friboulet L, Besse B. Therapeutic management of ALK+ nonsmall cell lung cancer patients. // Eur Respir J. 2015. Vol. 46. №. 1. P. 230-242.
95. Gambacorti Passerini C. et al. Crizotinib in advanced, chemoresistant anaplastic lymphoma kinase-positive lymphoma patients // JNCI: Journal of the National Cancer Institute. 2014. Vol. 106. №. 2.
96. Choi Y. L. et al. EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors // New England Journal of Medicine. 2010. Vol. 363. №. 18. P. 1734-1739.
97. Fontana D. et al. Activity of second- generation ALK inhibitors against crizotinib- resistant mutants in an NPM- ALK model compared to EML4- ALK // Cancer medicine. 2015. Vol. 4. №. 7. P. 953-965.
98. Zhang I. et al. Targeting brain metastases in ALK-rearranged non-small-cell lung cancer // The Lancet Oncology. 2015. Vol. 16. №. 13. P.
e510-e521.
99. Johnson T. W. et al. Discovery of (10 R)-7-Amino-12-fluoro-2,
10, 16-trimethyl-15-oxo-10, 15, 16, 17-tetrahydro-2H-8, 4-(metheno)
pyrazolo [4, 3-h][2, 5, 11]-benzoxadiazacyclotetradecine-3-carbonitrile (PF- 06463922), a macrocyclic inhibitor of anaplastic lymphoma kinase (ALK) and c-ros oncogene 1 (ROS1) with preclinical brain exposure and broad¬spectrum potency against ALK-resistant mutations // Journal of medicinal chemistry. 2014. Vol. 57. №. 11. P. 4720-4744. 80
100. Ryan P. D., Goss P. E. The emerging role of the insulin-like growth factor pathway as a therapeutic target in cancer // The oncologist.
2008. Vol. 13. №. 1. P. 16-24.
101. Pillai R. N., Ramalingam S. S. Inhibition of insulin-like growth factor receptor: end of a targeted therapy // Translational lung cancer research. 2013. Vol. 2. №. 1. P. 14-22.
102. Gombos A. et al. Clinical development of insulin-like growth factor receptor—1 (IGF-1R) inhibitors: At the crossroad? // Investigational new drugs. 2012. Vol. 30. №. 6. P. 2433-2442.
103. Vaishnavi A., Le A. T., Doebele R. C. TRKing down an old oncogene in a new era of targeted therapy // Cancer discovery. 2015. Vol.
5. №. 1. P. 25-34.
104. Thiele C. J., Li Z., McKee A. E. On Trk—the TrkB signal transduction pathway is an increasingly important target in cancer biology // Clinical cancer research. 2009. Vol. 15. №. 19. P. 5962-5967.
105Ardini E. et al. Entrectinib, a Pan-TRK, ROS1, and ALK Inhibitor with Activity in Multiple Molecularly Defined Cancer Indications // Molecular cancer therapeutics. 2016. Vol. 15. №. 4. P. 628-639.
106. Graham D. K. et al. The TAM family: phosphatidylserine- sensing receptor tyrosine kinases gone awry in cancer // Nature reviews Cancer. 2014. Vol. 14. №. 12. P. 769-785.
107. Myers SH, Brunton VG, Unciti-Broceta A. AXL inhibitors in cancer: A medicinal chemistry perspective. // J Med Chem. 2016. Vol. 59. №. 8. P. 3593-3608.
108. Mori M. et al. ASP2215, a novel FLT3/AXL inhibitor: Preclinical evaluation in acute myeloid leukemia (AML). - 2014. // J Clin Oncol. 2014.Vol. 32
109. Mulligan L. M. RET revisited: expanding the oncogenic
portfolio // Nature Reviews Cancer. 2014. Vol. 14. №. 3. P. 173-186.
110. Drilon A. et al. Response to Cabozantinib in patients with RET fusion-positive lung adenocarcinomas // Cancer discovery. 2013. Vol. 3. №. 6. P. 630-635.
111. Gautschi O. et al. A patient with lung adenocarcinoma and RET fusion treated with vandetanib // Journal of Thoracic Oncology. 2013. Vol. 8. №. 5. P. e43-e44.
112. Krajewska J., Kukulska A., Jarzab B. Efficacy of lenvatinib in treating thyroid cancer // Expert opinion on pharmacotherapy. 2016. Vol. 17. №. 12. P. 1683-1691.
113. Krajewska J., Olczyk T., Jarzab B. Cabozantinib for the treatment of progressive metastatic medullary thyroid cancer // Expert review of clinical pharmacology. 2016. Vol. 9. №. 1. P. 69-79.
114. Hayman S. R. et al. VEGF inhibition, hypertension, and renal toxicity // Current oncology reports. 2012. Vol. 14. №. 4. P. 285-294.
115. Jordan A. M. et al. Anilinoquinazoline inhibitors of the RET kinase domain—Elaboration of the 7-position // Bioorganic & medicinal chemistry letters. 2016. Vol. 26. №. 11. P. 2724-2729.
116. Song M. Progress in discovery of KIF5B-RET kinase inhibitors for the treatment of non-small-cell lung cancer // J. Med. Chem. 2015. Vol. 58. №. 9. P. 3672-3681.
117. Drabsch Y., Ten Dijke P. TGF-0 signalling and its role in cancer progression and metastasis // Cancer and Metastasis Reviews. 2012. Vol. 31. №. 3-4. P. 553-568.
118. Zhou L. et al. Reduced SMAD7 leads to overactivation of TGF- в signaling in MDS that can be reversed by a specific inhibitor of TGF-0 receptor I kinase // Cancer research. 2011. Vol. 71. №. 3. P. 955-963.
119. Akhurst R. J., Hata A. Targeting the TGF0 signalling pathway in
disease // Nature reviews Drug discovery. 2012. Vol. 11. №. 10. P. 790¬
811.
120. Quintas-Cardama A. et al. Janus kinase inhibitors for the treatment of myeloproliferative neoplasias and beyond // Nature reviews Drug discovery. 2011. Vol. 10. №. 2. P. 127-140.
121. Quintas-Cardama A. et al. Preclinical characterization of the
selective JAK1/2 inhibitor INCB018424: therapeutic implications for the treatment of myeloproliferative neoplasms // Blood. 2010. Vol. 115. №.
15. P. 3109-3117.
122. Mascarenhas J., Hoffman R. A comprehensive review and analysis of the effect of ruxolitinib therapy on the survival of patients with myelofibrosis // Blood. 2013. Vol. 121. №. 24. P. 4832-4837.
123. Kalota A, Jeschke GR, Carroll M, Hexner EO. Intrinsic resistance to JAK2 inhibition in myelofi- brosis. // Clin Cancer Res. 2013. Vol. 19. №. 7. P. 1729-1739.
124. Sonbol M. B. et al. Comprehensive review of JAK inhibitors in myeloproliferative neoplasms // Therapeutic advances in hematology. 2013. Vol. 4. №. 1. P. 15-35.
125. Alinari L., Quinion C., Blum K. A. Bruton's tyrosine kinase inhibitors in B- cell non- Hodgkin's lymphomas // Clinical Pharmacology & Therapeutics. 2015. Vol. 97. №. 5. P. 469-477.
126. Kawakami Y. et al. Terreic acid, a quinone epoxide inhibitor of Bruton’s tyrosine kinase // Proceedings of the National Academy of Sciences. 1999. Vol. 96. №. 5. P. 2227-2232.
127. Mahajan S. et al. Rational design and synthesis of a novel anti-leukemic agent targeting Bruton' s tyrosine kinase (BTK), LFM-A13 [a- cyano-P-hydroxy-0-methyl-N-(2, 5-dibromophenyl) propenamide] // Journal of Biological Chemistry. 1999. Vol. 274. №. 14. P. 9587-9599.
128. Pan Z. et al. Discovery of selective irreversible inhibitors for Bruton’s tyrosine kinase // ChemMedChem. 2007. Vol. 2. №. 1. P. 58-61.
129. Honigberg L. A. et al. The Bruton tyrosine kinase inhibitor PCI- 32765 blocks B-cell activation and is efficacious in models of autoimmune disease and B-cell malignancy // Proceedings of the National Academy of Sciences. 2010. Vol. 107. №. 29. P. 13075-13080.
130. Lee B. Y. et al. FAK signaling in human cancer as a target for therapeutics // Pharmacology & therapeutics. 2015. Vol. 146. P. 132-149.
131. Yoon H. et al. Understanding the roles of FAK in cancer: inhibitors, genetic models, and new insights // Journal of Histochemistry & Cytochemistry. 2015. Vol. 63. №. 2. P. 114-128.
132. Sulzmaier F. J., Jean C., Schlaepfer D. D. FAK in cancer: mechanistic findings and clinical applications // Nature reviews Cancer. 2014. Vol. 14. №. 9. P. 598-610.
133. Iwatani M. et al. Discovery and characterization of novel allosteric FAK inhibitors // European journal of medicinal chemistry. 2013. Vol. 61. P. 49-60.

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