TNF inhibitor

From Wikipedia, the free encyclopedia

Tumor necrosis factor (TNF) promotes the inflammatory response, which in turn causes many of the clinical problems associated with autoimmune disorders such as rheumatoid arthritis, ankylosing spondylitis, Crohn's disease, psoriasis and refractory asthma. These disorders are sometimes treated by using a TNF inhibitor. This inhibition can be achieved with a monoclonal antibody such as infliximab (Remicade) or adalimumab (Humira), or with a circulating receptor fusion protein such as etanercept (Enbrel).

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[edit] Thereapeutic applications

[edit] Skin disease

Clinical trials regarding the effectiveness of these drugs on hidradenitis suppurativa are currently ongoing. A fourth anti-TNF biologic, certolizumab pegol, is expected to receive approval for human use in the near future.

[edit] Tuberculosis

In patients with latent Mycobacterium tuberculosis infection, active tuberculosis (TB) may develop soon after the initiation of treatment with infliximab.[1] Before prescribing the drug, physicians should screen patients for latent TB infection or disease. The anti-TNF monoclonal antibody biologics, Infliximab and adalimumab, and the fusion protein etanercept which are all currently Food and Drug Administration (FDA) approved for human use, have label warnings which state that patients should be evaluated for latent TB infection and treatment should be initiated prior to starting therapy with these medications.

[edit] Rheumatoid arthritis

This potential applicability of anti-TNF therapies in the treatment of RA is based on the recognition of the role of TNF-alpha is the "master regulator" (as coined by Marc Feldmann and Ravinder N. Maini, recipients of the 2003 Lasker Award for their anti-TNF research in rheumatoid arthritis) of the inflammatory response in many organ systems. [2] In the Jan 15, 2008 issue of the Journal of Immunology, a team from Rochester University observed[3] that "anti-TNF compounds help eliminate abnormal B cell activity in patients, raising the possibility that the drugs improve the health of patients in a way no one has realized before."[4]

[edit] Anti-TNF agents in nature

TNF or the effects of TNF are also inhibited by a number of natural compounds, including curcumin [5] [6] [7] [8] (a compound present in turmeric) and catechins (in green tea).

[edit] References

  1. ^ "Tuberculosis associated with infliximab, a tumor necrosis factor alpha-neutralizing agent" (2001). N Engl J Med 345 (15): 1098–104. doi:10.1056/NEJMoa011110. PMID 11596589. 
  2. ^ TNF defined as a therapeutic target for rheumatoid arthritis and other autoimmune diseases - Nature Medicine. Retrieved on 2008-01-10.
  3. ^ "Anti-Tumor Necrosis Factor Therapy in Rheumatoid Arthritis Inhibits Memory B Lymphocytes via Effects on Lymphoid Germinal Centers and Follicular Dendritic Cell Networks" (2008). J Immunol 180 (2): 688–692. 
  4. ^ A new view of drugs used to treat rheumatoid arthritis
  5. ^ "The anti-inflammatory effect of curcumin in an experimental model of sepsis is mediated by up-regulation of peroxisome proliferator-activated receptor-gamma" (2006). Crit Care Med 34 (7): 1874–82. doi:10.1097/01.CCM.0000221921.71300.BF. PMID 16715036. 
  6. ^ "Curcumin protects against radiation-induced acute and chronic cutaneous toxicity in mice and decreases mRNA expression of inflammatory and fibrogenic cytokines" (2006). Int J Radiat Oncol Biol Phys 65 (3): 890–8. PMID 16751071. 
  7. ^ "Effects of curcumin on tumour necrosis factor-alpha and interleukin-6 in the late phase of experimental acute pancreatitis" (2006). J Vet Med A Physiol Pathol Clin Med 53 (1): 49–54. PMID 16411910. 
  8. ^ "The effect of turmeric extracts on inflammatory mediator production" (2005). Phytomedicine 12 (6-7): 445–52. doi:10.1016/j.phymed.2003.12.011. PMID 16008121. 
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Immunomodulators - Immunosuppressants - Immunosuppressive drugs (L04)
Monoclonal antibodies
TNF inhibitors (Infliximab, Adalimumab, Certolizumab pegol), Afelimomab, Aselizumab, Atlizumab, Atorolimumab, Basiliximab, Belimumab, Bertilimumab, Cedelizumab, Clenoliximab, Daclizumab, Dorlimomab aritox, Dorlixizumab, Eculizumab, Efalizumab, Elsilimomab, Erlizumab, Faralimomab, Fontolizumab, Galiximab, Gantenerumab, Gavilimomab, Golimumab, Gomiliximab, Ibalizumab, Inolimomab, Ipilimumab, Keliximab, Lebrilizumab, Lerdelimumab, Lumiliximab, Maslimomab, Mepolizumab, Metelimumab, Morolimumab, Muromonab-CD3, Natalizumab, Nerelimomab, Ocrelizumab, Odulimomab, Omalizumab, Otelixizumab, Pascolizumab, Pexelizumab, Reslizumab, Rovelizumab, Ruplizumab, Siplizumab, Talizumab, Telimomab aritox, Teneliximab, Teplizumab, Tocilizumab, Toralizumab, Vapaliximab, Vepalimomab, Visilizumab, Zanolimumab, Ziralimumab, Zolimomab aritox
-imus
-cept (Fusion protein)
Other