Prospective new biological therapies for rheumatoid arthritis

Autoimmun Rev. 2009 Dec;9(2):102-7. doi: 10.1016/j.autrev.2009.03.010. Epub 2009 Mar 26.

Abstract

Advances in the current knowledge of pathogenetic mechanisms of rheumatoid arthritis have contributed to the development of biological therapy, and translated research findings into clinical practice. TNF-alpha (infliximab, etanercept, adalimumab), IL-1 (anakinra) and IL-6 (tocilizumab) inhibitors, a B-cell depleting agent (rituximab) and a drug blocking T-cell costimulation (abatacept) have been approved for rheumatoid arthritis. The progress in manufacturing biotechnology has contributed to the development of several other prospective agents that may form the basis for the therapy of rheumatoid arthritis in the near future. New or modified TNF-alpha inhibitors (golimumab, certolizumab pegol), new monoclonal antibodies against other cytokines (e.g. IL-1, IL-6, IL-12, IL-15, IL-17, IL-23), and other agents targeting B-cell depletion (e.g. ocrelizumab, ofatumumab) are in various stages of development. Many pharmaceutical companies have focused on developing small molecule inhibitors with possible peroral administration, which are considered promising drugs for rheumatoid arthritis. In most cases, these small molecules inhibit cellular kinases (e.g. p38, JAK or Syk) that mediate the signaling and transcription of proinflammatory genes. In this review, we describe the cytokine inhibitors and modulators of the immune response currently in ongoing clinical trials, the results of which may further expand the spectrum of efficient therapies for chronic autoimmune diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antibodies, Monoclonal
  • Antigens, Differentiation / immunology
  • Arthritis, Rheumatoid / genetics
  • Arthritis, Rheumatoid / immunology
  • Arthritis, Rheumatoid / therapy*
  • Biological Therapy* / trends
  • Cell Communication / drug effects
  • Cell Communication / immunology
  • Cytokines / immunology
  • Humans
  • Lymphocyte Depletion
  • Protein Kinase Inhibitors / therapeutic use*
  • RNA Interference
  • RNA, Small Interfering / genetics
  • Signal Transduction / drug effects
  • Signal Transduction / immunology

Substances

  • Antibodies, Monoclonal
  • Antigens, Differentiation
  • Cytokines
  • Protein Kinase Inhibitors
  • RNA, Small Interfering