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Cited by 47Rheumatoid Arthritis Research and TherapiesAutoimmune and Inflammatory Disorders ResearchCytokine Signaling Pathways and Interactions

Are Janus kinase inhibitors superior over classic biologic agents in RA patients?

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Kotyla, Przemyslaw J.·2018·BioMed Research International
DOI 10.1155/2018/7492904PMC PMC5971265
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Abstract

The Janus Kinases (JAKs) are a family of intracellular tyrosine kinases that provide transmission signals from cytokine, interferons, and many hormones receptors to the nucleus resulting in synthesis of many biologically active compounds and changing cell metabolism and function. That was theoretical background to synthetize the JAK inhibitors (Jakinibs). In recent years a substantial battery of evidence has been collected indicating the potential role of Jakinibs to interact with the specific elements of the immune system, therefore changing the inflammatory response. JAK kinase blockade offers a unique opportunity to block most of the key cytokines enabling the deep interaction into immune system functioning. Following discovery first Jakinibs were intensively studied in various forms of autoimmune diseases, including rheumatoid arthritis, and finally two Jakinibs tofacitinib and Baricitinib have been approved for the treatment of rheumatoid arthritis. Some clinical data indicated that under special circumstances Jakinibs may be even superior to biologics in the treatment of RA; however this suggestion should be verified in large clinical and observational studies.

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  • Jakinibs are associated with immunosuppression, common early adverse effects include diarrhea, nasopharyngitis, headache, and urinary tract infection; prolonged treatment is associated with upper respiratory tract infections, nasopharyngitis, and bronchitis.

    “Jakinibs are associated with immunosuppression, and common early adverse effects include diarrhea, nasopharyngitis, headache, and urinary tract infection, whereas prolonged treatment has been associated with upper respiratory tract infections, nasopharyngitis, and bronchitis.”

    From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Kotyla, 2018

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  1. [1]Smolen J. S. Aletaha D. McInnes I. B. Rheumatoid arthritis 2016 388 10055 2023 2038 2-s2.0-84964773927 10.1016/S0140-6736(16)30173-8 27156434 · DOI
  2. [2]Firestein G. S. McInnes I. B. Immunopathogenesis of Rheumatoid Arthritis 2017 46 2 183 196 2-s2.0-85013957711 10.1016/j.immuni.2017.02.006 PMC5385708 28228278 · DOI · Paper page
  3. [3]Okada Y. Wu D. Trynka G. Genetics of rheumatoid arthritis contributes to biology and drug discovery 2014 506 7488 376 381 10.1038/nature12873 PMC3944098 24390342 · DOI · Paper page
  4. [4]McInnes I. B. Schett G. Pathogenetic insights from the treatment of rheumatoid arthritis 2017 389 10086 2328 2337 2-s2.0-85020875474 10.1016/S0140-6736(17)31472-1 28612747 · DOI
  5. [5]Alam J. Jantan I. Bukhari S. N. A. Rheumatoid arthritis: Recent advances on its etiology, role of cytokines and pharmacotherapy 2017 92 615 633 28582758
  6. [6]McInnes I. B. Schett G. The pathogenesis of rheumatoid arthritis 2011 365 23 2205 2219 10.1056/NEJMra1004965 2-s2.0-84855172814 22150039 · DOI · Paper page
  7. [7]Alam J. Jantan I. Bukhari S. N. A. Rheumatoid arthritis: Recent advances on its etiology, role of cytokines and pharmacotherapy 2017 92 615 633 2-s2.0-85020029836 10.1016/j.biopha.2017.05.055 28582758 · DOI
  8. [8]Feldmann M. Maini S. R. N. Role of cytokines in rheumatoid arthritis: An education in pathophysiology and therapeutics 2008 223 1 7 19 2-s2.0-47249153519 10.1111/j.1600-065X.2008.00626.x 18613827 · DOI
  9. [9]Luchetti M. M. Benfaremo D. Gabrielli A. Biologics in Inflammatory and Immunomediated Arthritis 2018 18 12 989 1007 10.2174/1389201019666171226151852 29278210 · DOI
  10. [10]Choy E. H. Bernasconi C. Aassi M. Molina J. F. Epis O. M. Treatment of Rheumatoid Arthritis With Anti–Tumor Necrosis Factor or Tocilizumab Therapy as First Biologic Agent in a Global Comparative Observational Study 2017 69 10 1484 1494 2-s2.0-85028929150 10.1002/acr.23303 PMC5656814 28622454 · DOI
  11. [11]Lampropoulos C. E. Orfanos P. Manoussakis M. N. Tzioufas A. G. Moutsopoulos H. M. Vlachoyiannopoulos P. G. Treat-to-target biologic therapy in patients with rheumatoid arthritis is more efficacious and safe compared to delayed initiation of biologics: A real-world study 2017 35 2 192 200 2-s2.0-85018191707 28094760
  12. [12]Narazaki M. Tanaka T. Kishimoto T. The role and therapeutic targeting of IL-6 in rheumatoid arthritis 2017 13 6 535 551 10.1080/1744666X.2017.1295850 2-s2.0-85019241339 28494214 · DOI
  13. [13]Smolen J. S. Landewé R. Breedveld F. C. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2013 update 2014 73 3 492 509 2-s2.0-84893772728 10.1136/annrheumdis-2013-204573 PMC3933074 24161836 · DOI
  14. [14]Ramiro S. Gaujoux-Viala C. Nam J. L. Safety of synthetic and biological DMARDs: a systematic literature review informing the 2013 update of the EULAR recommendations for management of rheumatoid arthritis 2014 73 3 529 535 10.1136/annrheumdis-2013-204575 2-s2.0-84893803131 24401994 · DOI
  15. [15]Nam J. L. Ramiro S. Gaujoux-Viala C. Efficacy of biological disease-modifying antirheumatic drugs: A systematic literature review informing the 2013 update of the EULAR recommendations for the management of rheumatoid arthritis 2014 73 3 516 528 2-s2.0-84893721202 10.1136/annrheumdis-2013-204577 24399231 · DOI
  16. [16]van Schouwenburg P. A. Rispens T. Wolbink G. J. Immunogenicity of anti-TNF biologic therapies for rheumatoid arthritis 2013 9 3 164 172 10.1038/nrrheum.2013.4 2-s2.0-84874656491 23399692 · DOI
  17. [17]Arstikyte I. Kapleryte G. Butrimiene I. Venalis A. Shi G. Influence of immunogenicity on the efficacy of long-term treatment with TNF α blockers in rheumatoid arthritis and spondyloarthritis patients 2015 2015 10 604872 10.1155/2015/604872 2-s2.0-84929358899 PMC4427010 26064930 · DOI
  18. [18]Smolen J. S. Landewé R. Bijlsma J. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2016 update 2017 76 6 960 977 2-s2.0-85019702082 10.1136/annrheumdis-2016-210715 28264816 · DOI
  19. [19]Wilks A. F. Two putative protein-tyrosine kinases identified by application of the polymerase chain reaction 1989 86 5 1603 1607 2-s2.0-0011280342 10.1073/pnas.86.5.1603 PMC286746 2466296 · DOI · Paper page
  20. [20]al-Obeidi F. A. Wu J. J. Lam K. S. Protein tyrosine kinases: structure, substrate specificity, and drug discovery 1998 47 3 197 223 10.1002/(sici)1097-0282(1998)47:3<197::aid-bip2>3.0.co;2-h 9817025 · DOI
  21. [21]Wilks A. F. Harpur A. G. Kurban R. R. Ralph S. J. Zurcher G. Ziemiecki A. Two novel protein-tyrosine kinases, each with a second phosphotransferase-related catalytic domain, define a new class of protein kinase 1991 11 4 2057 2065 2-s2.0-0026081302 10.1128/MCB.11.4.2057 PMC359893 1848670 · DOI · Paper page
  22. [22]Boussiotis V. A. Barber D. L. Nakarai T. Prevention of T cell anergy by signaling through the γc chain of the IL-2 receptor 1994 266 5187 1039 1042 2-s2.0-0028114542 10.1126/science.7973657 7973657 · DOI
  23. [23]Leonard W. J. O'Shea J. J. Jaks and STATs: biological implications 1998 16 293 322 10.1146/annurev.immunol.16.1.293 2-s2.0-0031919849 9597132 · DOI
  24. [24]Laurence A. Pesu M. Silvennoinen O. O'Shea J. JAK kinases in health and disease: an update 2012 6 2 232 244 10.2174/1874312901206010232 2-s2.0-84870982794 PMC3460320 23028408 · DOI
  25. [25]Ghoreschi K. Laurence A. O'Shea J. J. Janus kinases in immune cell signaling 2009 228 1 273 287 10.1111/j.1600-065x.2008.00754.x 2-s2.0-61849086101 PMC2782696 19290934 · DOI · Paper page
  26. [26]Kawamura M. Mcvicar D. W. Johnston J. A. Molecular cloning of L-JAK, a Janus family protein-tyrosine kinase expressed in natural killer cells and activated leukocytes 1994 91 14 6374 6378 2-s2.0-0028301958 10.1073/pnas.91.14.6374 PMC44204 8022790 · DOI
  27. [27]Goswami R. Kaplan M. STAT Transcription Factors in T Cell Control of Health and Disease 2017 331 123 180 10.1016/bs.ircmb.2016.09.012 28325211 · DOI
  28. [28]Liongue C. Sertori R. Ward A. C. Evolution of cytokine receptor signaling 2016 197 1 11 18 2-s2.0-84975318343 10.4049/jimmunol.1600372 27317733 · DOI
  29. [30]Bazan J. F. Structural design and molecular evolution of a cytokine receptor superfamily 1990 87 18 6934 6938 2-s2.0-0025162844 10.1073/pnas.87.18.6934 PMC54656 2169613 · DOI
  30. [31]Liongue C. Taznin T. Ward A. C. Signaling via the CytoR/JAK/STAT/SOCS pathway: Emergence during evolution 2016 71 166 175 2-s2.0-84958280151 10.1016/j.molimm.2016.02.002 26897340 · DOI
  31. [32]Waickman A. T. Park J. Y. Park J. H. The common γ-chain cytokine receptor: tricks-and-treats for T cells 2016 73 2 253 269 10.1007/s00018-015-2062-4 PMC6315299 26468051 · DOI
  32. [33]O'Shea J. J. Schwartz D. M. Villarino A. V. Gadina M. McInnes I. B. Laurence A. The JAK-STAT pathway: impact on human disease and therapeutic intervention 2015 66 311 328 10.1146/annurev-med-051113-024537 2-s2.0-84921325808 PMC5634336 25587654 · DOI
  33. [34]Roskoski Jr. R. Janus kinase (JAK) inhibitors in the treatment of inflammatory and neoplastic diseases 2016 111 784 803 10.1016/j.phrs.2016.07.038 2-s2.0-84979900297 27473820 · DOI
  34. [35]Broughton S. E. Hercus T. R. Lopez A. F. Parker M. W. Cytokine receptor activation at the cell surface 2012 22 3 350 359 2-s2.0-84862635898 10.1016/j.sbi.2012.03.015 22521507 · DOI
  35. [36]Kiu H. Nicholson S. E. Biology and significance of the JAK/STAT signalling pathways 2012 30 2 88 106 2-s2.0-84858961271 10.3109/08977194.2012.660936 PMC3762697 22339650 · DOI · Paper page
  36. [37]Ferrao R. Lupardus P. J. The Janus Kinase (JAK) FERM and SH2 domains: Bringing specificity to JAK-receptor interactions 2017 8, article no. 71 2-s2.0-85018305638 10.3389/fendo.2017.00071 PMC5394478 28458652 · DOI
  37. [38]Quintás-Cardama A. Kantarjian H. Cortes J. Verstovsek S. Janus kinase inhibitors for the treatment of myeloproliferative neoplasias and beyond 2011 10 2 127 140 2-s2.0-79551575494 10.1038/nrd3264 21283107 · DOI
  38. [39]Ghoreschi K. Laurence A. O'Shea J. J. Selectivity and therapeutic inhibition of kinases: to be or not to be? 2009 10 4 356 360 10.1038/ni.1701 2-s2.0-62849094732 PMC2758543 19295632 · DOI
  39. [40]Lupardus P. J. Ultsch M. Wallweber H. Kohli P. B. Johnson A. R. Eigenbrot C. Structure of the pseudokinase-kinase domains from protein kinase TYK2 reveals a mechanism for Janus kinase (JAK) autoinhibition 2014 111 22 8025 8030 2-s2.0-84901840527 10.1073/pnas.1401180111 PMC4050602 24843152 · DOI · Paper page
  40. [41]Haan C. Kreis S. Margue C. Behrmann I. Jaks and cytokine receptors-An intimate relationship 2006 72 11 1538 1546 2-s2.0-33750522675 10.1016/j.bcp.2006.04.013 16750817 · DOI
  41. [42]Wallweber H. J. Tam C. Franke Y. Starovasnik M. A. Lupardus P. J. Structural basis of recognition of interferon-α receptor by tyrosine kinase 2 2014 21 5 443 448 10.1038/nsmb.2807 PMC4161281 24704786 · DOI
  42. [43]O'Shea J. J. Murray P. J. Cytokine signaling modules in inflammatory responses 2008 28 4 477 487 10.1016/j.immuni.2008.03.002 2-s2.0-41549107522 PMC2782488 18400190 · DOI
  43. [44]Rawlings J. S. Rosler K. M. Harrison D. A. The JAK/STAT signaling pathway 2004 117 8 1281 1283 2-s2.0-2342445635 10.1242/jcs.00963 15020666 · DOI · Paper page
  44. [45]Zouein F. A. Duhé R. J. Booz G. W. JAKs go nuclear: Emerging role of nuclear JAK1 and JAK2 in gene expression and cell growth 2011 29 6 245 252 2-s2.0-80155146810 10.3109/08977194.2011.614949 PMC3595105 21892841 · DOI
  45. [46]Krebs D. L. Hilton D. J. SOCS proteins: negative regulators of cytokine signaling 2001 19 5 378 387 10.1634/stemcells.19-5-378 2-s2.0-0034801684 11553846 · DOI
  46. [47]Kershaw N. J. Murphy J. M. Lucet I. S. Nicola N. A. Babon J. J. Regulation of Janus kinases by SOCS proteins 2013 41 4 1042 1047 2-s2.0-84880560118 10.1042/BST20130077 PMC3773493 23863176 · DOI
  47. [48]McLornan D. P. Khan A. A. Harrison C. N. Immunological consequences of JAK inhibition: friend or foe? 2015 10 4 370 379 10.1007/s11899-015-0284-z 2-s2.0-84949534185 26292803 · DOI
  48. [50]Casanova J.-L. Holland S. M. Notarangelo L. D. Inborn errors of human JAKs and STATs 2012 36 4 515 528 10.1016/j.immuni.2012.03.016 2-s2.0-84859950150 PMC3334867 22520845 · DOI
  49. [51]Macchi P. Villa A. Giliani S. Mutations of jak-3 gene in patients with autosomal severe combined immune deficiency (SCID) 1995 377 6544 65 68 2-s2.0-0029164841 10.1038/377065a0 7659163 · DOI
  50. [52]Notarangelo L. D. Mella P. Jones A. Mutations in severe combined immune deficiency (SCID) due to JAK3 deficiency 2001 18 4 255 263 2-s2.0-0034804745 10.1002/humu.1188 11668610 · DOI
  51. [53]Lin J. Leonard W. J. The Common Cytokine Receptor γ Chain Family of Cytokines 2017 10.1101/cshperspect.a028449 PMC6120701 29038115 · DOI
  52. [54]Spolski R. Gromer D. Leonard W. J. The γc family of cytokines: fine-tuning signals from IL-2 and IL-21 in the regulation of the immune response 2017 6, article 1872 10.12688/f1000research.12202.1 PMC5657018 29123649 · DOI
  53. [55]Rosen F. S. Cooper M. D. Wedgwood R. J. The Primary Immunodeficiencies 1995 333 7 431 440 10.1056/NEJM199508173330707 7616993 · DOI
  54. [56]Noguchi M. Yi H. Rosenblatt H. M. Interleukin-2 receptor gamma chain mutation results in X-linked severe combined immunodeficiency in humans 1993 73 1 147 157 8462096
  55. [57]Kondo M. Takeshita T. Higuchi M. Functional participation of the IL-2 receptor γ chain in IL-7 receptor complexes 1994 263 5152 1453 1454 2-s2.0-0028327550 10.1126/science.8128231 8128231 · DOI
  56. [58]Kovanen P. E. Leonard W. J. Cytokines and immunodeficiency diseases: critical roles of the γc-dependent cytokines interleukins 2, 4, 7, 9, 15, and 21, and their signaling pathways 2004 202 67 83 10.1111/j.0105-2896.2004.00203.x 2-s2.0-9644295710 15546386 · DOI
  57. [59]Ozaki K. Spolski R. Feng C. G. A critical role for IL-21 in regulating immunoglobulin production 2002 298 5598 1630 1634 2-s2.0-0037159687 10.1126/science.1077002 12446913 · DOI · Paper page
  58. [60]Deng Y. Wang Z. Chang C. Lu L. Lau C. S. Lu Q. Th9 cells and IL-9 in autoimmune disorders: Pathogenesis and therapeutic potentials 2017 78 2 120 128 10.1016/j.humimm.2016.12.010 28040536 · DOI
  59. [61]Gernez Y. Freeman A. F. Holland S. M. Autosomal Dominant Hyper-IgE Syndrome in the USIDNET Registry 2017 2-s2.0-85029570324 10.1016/j.jaip.2017.06.041 PMC5858974 28939137 · DOI
  60. [62]Mogensen T. H. STAT3 and the Hyper- IgE syndrome: clinical presentation, genetic origin, pathogenesis, novel findings and remaining uncertainties 2013 2 2 10.4161/jkst.23435 e23435 PMC3710320 24058807 · DOI
  61. [63]Mogensen T. H. Primary Immunodeficiencies with Elevated IgE 2016 1 39 56 10.3109/08830185.2015.1027820 25970001 · DOI
  62. [64]Milner J. D. Brenchley J. M. Laurence A. Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome 2008 452 7188 773 776 10.1038/nature06764 PMC2864108 18337720 · DOI · Paper page
  63. [65]O'Sullivan J. M. Harrison C. N. JAK-STAT signaling in the therapeutic landscape of myeloproliferative neoplasms 2017 451 71 79 2-s2.0-85012885394 10.1016/j.mce.2017.01.050 28167129 · DOI
  64. [66]Patterson-Fortin J. Moliterno A. R. Molecular Pathogenesis of Myeloproliferative Neoplasms: Influence of Age and Gender 2017 12 5 424 431 2-s2.0-85029817871 10.1007/s11899-017-0411-0 28948454 · DOI
  65. [67]Huynh J. Etemadi N. Hollande F. Ernst M. Buchert M. The JAK/STAT3 axis: A comprehensive drug target for solid malignancies 2017 45 13 22 2-s2.0-85021086567 10.1016/j.semcancer.2017.06.001 28647610 · DOI
  66. [68]Salgado E. Maneiro J. R. Carmona L. Gomez-Reino J. J. Safety profile of protein kinase inhibitors in rheumatoid arthritis: Systematic review and meta-analysis 2014 73 5 871 882 2-s2.0-84898012375 10.1136/annrheumdis-2012-203116 23599436 · DOI
  67. [69]Meyer D. M. Jesson M. I. Li X. Anti-inflammatory activity and neutrophil reductions mediated by the JAK1/JAK3 inhibitor, CP-690,550, in rat adjuvant-induced arthritis 2010 7, article no. 41 2-s2.0-77955375143 10.1186/1476-9255-7-41 PMC2928212 20701804 · DOI
  68. [70]Fleischmann R. Kremer J. Tanaka Y. Efficacy and safety of tofacitinib in patients with active rheumatoid arthritis: review of key Phase 2 studies 2016 19 12 1216 1225 2-s2.0-84994452795 10.1111/1756-185X.12901 PMC5396326 27451980 · DOI
  69. [71]Kremer J. M. Cohen S. Wilkinson B. E. A phase IIb dose-ranging study of the oral JAK inhibitor tofacitinib (CP-690,550) versus placebo in combination with background methotrexate in patients with active rheumatoid arthritis and an inadequate response to methotrexate alone 2012 64 4 970 981 10.1002/art.33419 2-s2.0-84866156845 22006202 · DOI
  70. [72]Fleischmann R. Cutolo M. Genovese M. C. Phase IIb dose-ranging study of the oral JAK inhibitor tofacitinib (CP-690,550) or adalimumab monotherapy versus placebo in patients with active rheumatoid arthritis with an inadequate response to disease-modifying antirheumatic drugs 2012 64 3 617 629 2-s2.0-84857761516 10.1002/art.33383 21952978 · DOI
  71. [73]Tanaka Y. Takeuchi T. Yamanaka H. Nakamura H. Toyoizumi S. Zwillich S. Efficacy and safety of tofacitinib as monotherapy in japanese patients with active rheumatoid arthritis: A 12-week, randomized, phase 2 study 2015 25 4 514 521 10.3109/14397595.2014.995875 2-s2.0-84934900153 PMC4819568 25496464 · DOI
  72. [74]Kotyla P. Jankiewicz-Ziobro K. Owczarek A. Kucharz E. J. Etanercept increases tumor necrosis factor-alpha level but not sfas level in patients with rheumatoid arthritis 2015 17 1 14 18 2-s2.0-84921870721 25739170
  73. [75]Fleischmann R. Kremer J. Cush J. Placebo-controlled trial of tofacitinib monotherapy in rheumatoid arthritis 2012 367 6 495 507 2-s2.0-84864716411 10.1056/NEJMoa1109071 22873530 · DOI
  74. [76]Christina C.-S. Burmester G. Nash P. Efficacy and safety of tofacitinib following inadequate response to conventional synthetic or biological disease-modifying antirheumatic drugs 2016 75 7 1293 1301 2-s2.0-84940176223 10.1136/annrheumdis-2014-207178 PMC4941182 26275429 · DOI
  75. [77]Fleischmann R. Mysler E. Hall S. Efficacy and safety of tofacitinib monotherapy, tofacitinib with methotrexate, and adalimumab with methotrexate in patients with rheumatoid arthritis (ORAL Strategy): a phase 3b/4, double-blind, head-to-head, randomised controlled trial 2017 390 10093 457 468 10.1016/S0140-6736(17)31618-5 28629665 · DOI
  76. [78]Van Vollenhoven R. F. Fleischmann R. Cohen S. Tofacitinib or adalimumab versus placebo in rheumatoid arthritis 2012 367 6 508 519 2-s2.0-84864703156 10.1056/NEJMoa1112072 22873531 · DOI
  77. [79]Lee E. B. Fleischmann R. Hall S. Tofacitinib versus methotrexate in rheumatoid arthritis 2014 370 25 2377 2386 10.1056/nejmoa1310476 2-s2.0-84902593564 24941177 · DOI
  78. [80]Burmester G. R. Blanco R. Charles-Schoeman C. Tofacitinib (CP-690,550) in combination with methotrexate in patients with active rheumatoid arthritis with an inadequate response to tumour necrosis factor inhibitors: a randomised phase 3 trial 2013 381 9865 451 460 10.1016/S0140-6736(12)61424-X 2-s2.0-84873707288 23294500 · DOI
  79. [81]Rodig S. J. Meraz M. A. White J. M. Disruption of the Jak1 gene demonstrates obligatory and nonredundant roles of the Jaks in cytokine-induced biologic responses 1998 93 3 373 383 2-s2.0-0032076183 10.1016/S0092-8674(00)81166-6 9590172 · DOI
  80. [82]Neubauer H. Cumano A. Müller M. Wu H. Huffstadt U. Pfeffer K. Jak2 deficiency defines an essential developmental checkpoint in definitive hematopoiesis 1998 93 3 397 409 2-s2.0-18244432009 10.1016/S0092-8674(00)81168-X 9590174 · DOI
  81. [83]Fleischmann R. Schiff M. van der Heijde D. Baricitinib, Methotrexate, or Combination in Patients With Rheumatoid Arthritis and No or Limited Prior Disease-Modifying Antirheumatic Drug Treatment 2017 69 3 506 517 2-s2.0-85014083376 10.1002/art.39953 PMC5347954 27723271 · DOI
  82. [84]Keystone E. C. Taylor P. C. Drescher E. Safety and efficacy of baricitinib at 24 weeks in patients with rheumatoid arthritis who have had an inadequate response to methotrexate 2015 74 2 333 340 2-s2.0-84921475867 10.1136/annrheumdis-2014-206478 PMC4316868 25431052 · DOI
  83. [85]Tanaka Y. Emoto K. Cai Z. Efficacy and Safety of Baricitinib in Japanese Patients with Active Rheumatoid Arthritis Receiving Background Methotrexate Therapy: A 12-week, Double-blind, Randomized Placebo-controlled Study 2016 43 3 504 511 26834213
  84. [86]Dougados M. Van Der Heijde D. Chen Y.-C. Baricitinib in patients with inadequate response or intolerance to conventional synthetic DMARDs: Results from the RA-BUILD study 2017 76 1 88 95 2-s2.0-84991491965 10.1136/annrheumdis-2016-210094 PMC5264214 27689735 · DOI
  85. [87]Genovese M. C. Kremer J. Zamani O. Baricitinib in patients with refractory rheumatoid arthritis 2016 374 13 1243 1252 2-s2.0-84962375370 10.1056/NEJMoa1507247 27028914 · DOI
  86. [88]Taylor P. C. Keystone E. C. Van Der Heijde D. Baricitinib versus Placebo or Adalimumab in Rheumatoid Arthritis 2017 376 7 652 662 2-s2.0-85013393351 10.1056/NEJMoa1608345 28199814 · DOI
  87. [89]Gabay C. Emery P. van Vollenhoven R. Tocilizumab monotherapy versus adalimumab monotherapy for treatment of rheumatoid arthritis (ADACTA): a randomised, double-blind, controlled phase 4 trial 2013 381 9877 1541 1550 10.1016/s0140-6736(13)60250-0 2-s2.0-84877275257 23515142 · DOI · Paper page
  88. [90]Keystone E. C. Genovese M. C. Schlichting D. E. Safety and Efficacy of Baricitinib Through 128 Weeks in an Open-label, Longterm Extension Study in Patients with Rheumatoid Arthritis 2018 45 1 14 21 10.3899/jrheum.161161 28811354 · DOI
  89. [91]Fleischmann R. Alam J. Arora V. Safety and efficacy of baricitinib in elderly patients with rheumatoid arthritis 2017 3 2, article e000546 10.1136/rmdopen-2017-000546 PMC5640108 29071120 · DOI

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Authors
Kotyla, P. J.
Affiliations
Department of Internal Medicine and Rheumatology, Medical Faculty in Katowice, Medical University of Silesia, Katowice, Poland
ORCID
Kotyla, Przemyslaw J.
Venue
BioMed Research International
Publisher
Wiley
Published
2018
Volume
2018
Pages
1-9
ISSN
  • 1110-7243 (ISSN-L)
  • 2314-6133
  • 2314-6141
DOI
10.1155/2018/7492904
PMC
PMC5971265
OpenAlex
W2800650671
Cited by
47
References
2
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FWCI
1.03
Type
journal article
Language
en
Open access
Licence
Locations
  • BioMed Research International (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
University of Oxford
Topics
  • Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
  • Health Sciences › Medicine › Hematology › Autoimmune and Inflammatory Disorders Research
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
Keywords
JAK inhibitors, rheumatoid arthritis, tofacitinib, baricitinib, biologic agents, cytokine signaling, autoimmune disease, inflammation
MeSH terms
Animals, Azetidines, Humans, Piperidines, Purines, Pyrazoles, Pyrimidines, Pyrroles, Rheumatic Fever, Sulfonamides, Protein Kinase Inhibitors, Janus Kinases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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