Emerging monoclonal antibody therapies for multiple sclerosis

被引:36
作者
Cree, Bruce [1 ]
机构
[1] Univ Calif San Francisco, Multiple Sclerosis Ctr, San Francisco, CA 94117 USA
关键词
multiple sclerosis; relapsing remitting multiple sclerosis; secondary progressive multiple sclerosis; primary progressive multiple sclerosis; neuromyelitis optica; Devic's disease; monoclonal antibody; alemtuzumab; rituximab; daclizumab; natalizumab;
D O I
10.1097/01.nrl.0000204859.15501.6b
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Monoclonal antibodies constitute a relatively new class of therapeutic agent designed to interact with specific target antigens. Monoclonal antibodies can be created to deplete cell lineages or antagonize receptors for which small molecule drugs are not available. Because of their accessibility, proteins expressed on the surface of immune system cell lineages are appealing targets for monoclonal antibody therapies. Review Summary: To review monoclonal antibodies currently under investigation for treatment of multiple sclerosis (MS). This was a review of the literature and ongoing clinical trials. Alemtuzumab, daclizumab, rituximab, and natalizumab are monoclonal antibodies at different stages of clinical development that show promise as MS disease modifying therapies. Conclusions: Several monoclonal antibodies directed against antigens present on the cell surface of immune system cell lines are promising candidates for immune suppression therapies in MS. Because these drugs are still in development, their clinical benefits and safety profiles are not fully established. Nevertheless, it seems possible that their specificity will offer advantages over broad-spectrum immune suppressing therapies.
引用
收藏
页码:171 / 178
页数:8
相关论文
共 51 条
  • [1] [Anonymous], COCHRANE DATABASE SY, DOI DOI 10.1002/14651858.CD003897.PUB2
  • [2] Humanized anti-CD25 (daclizumab) inhibits disease activity in multiple sclerosis patients failing to respond to interferon β
    Bielekova, B
    Richert, N
    Howard, T
    Blevins, G
    Markovic-Plese, S
    McCartin, J
    Würfel, J
    Ohayon, J
    Waidmann, TA
    McFarland, HF
    Martin, R
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (23) : 8705 - 8708
  • [3] Campath-1H treatment of multiple sclerosis: lessons from the bedside for the bench
    Coles, A
    Deans, J
    Compston, A
    [J]. CLINICAL NEUROLOGY AND NEUROSURGERY, 2004, 106 (03) : 270 - 274
  • [4] Coles AJ, 1999, ANN NEUROL, V46, P296, DOI 10.1002/1531-8249(199909)46:3<296::AID-ANA4>3.0.CO
  • [5] 2-#
  • [6] Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis
    Coles, AJ
    Wing, N
    Smith, S
    Coraddu, F
    Greer, S
    Taylor, C
    Weetman, A
    Hale, G
    Chatterjee, VK
    Waldmann, H
    Compston, A
    [J]. LANCET, 1999, 354 (9191) : 1691 - 1695
  • [7] The natural history of multiple sclerosis: a geographically based study - 5. The clinical features and natural history of primary progressive multiple sclerosis
    Cottrell, DA
    Kremenchutzky, M
    Rice, GPA
    Koopman, WJ
    Hader, W
    Baskerville, J
    Ebers, GC
    [J]. BRAIN, 1999, 122 : 625 - 639
  • [8] An open label study of the effects of rituximab in neuromyelitis optica
    Cree, BAC
    Lamb, S
    Morgan, K
    Chen, A
    Waubant, E
    Genain, C
    [J]. NEUROLOGY, 2005, 64 (07) : 1270 - 1272
  • [9] Effect of natalizumab on conversion of gadolinium enhancing lesions to T1 hypointense lesions in relapsing multiple sclerosis
    Dalton, CM
    Miszkiel, KA
    Barker, GJ
    MacManus, DG
    Pepple, TI
    Panzara, M
    Yang, M
    Hulme, A
    O'Connor, P
    Miller, DH
    [J]. JOURNAL OF NEUROLOGY, 2004, 251 (04) : 407 - 413
  • [10] DARDEN CE, 2002, REV CLIN EXP HEMATOL, V6, P435