PMID- 19689289
OWN - NLM
STAT- MEDLINE
DCOM- 20091106
LR  - 20240109
IS  - 1875-533X (Electronic)
IS  - 0929-8673 (Linking)
VI  - 16
IP  - 24
DP  - 2009
TI  - TNF-alpha as a therapeutic target in inflammatory diseases, ischemia-reperfusion 
      injury and trauma.
PG  - 3152-67
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a central regulator of inflammation, 
      and TNF-alpha antagonists may be effective in treating inflammatory disorders in 
      which TNF-alpha plays an important pathogenetic role. Recombinant or modified 
      proteins are an emerging class of therapeutic agents. To date, several 
      recombinant or modified proteins which acts as TNF antagonists have been 
      disclosed. In particular, antibodies that bind to and neutralise TNF have been 
      sought as a means to inhibit TNF activity. Inhibition of TNF has proven to be an 
      effective therapy for patients with rheumatoid arthritis and other forms of 
      inflammatory disease including psoriasis, psoriatic arthritis, and ankylosing 
      spondylitis, inflammatory bowel disease. Additionally, the efficacy of preventing 
      septic shock and AIDS has been questioned as a result of recent research. The 
      currently available therapies include a soluble p75 TNF receptor:Fc construct, 
      etanercept, a chimeric monoclonal antibody, infliximab, and a fully human 
      monoclonal antibody, adalimumab. Certolizumab pegol is a novel TNF inhibitor 
      which is an antigen-binding domain of a humanized TNF antibody coupled to 
      polyethylene glycol (PEG) to increase half-life, and thus is Fc-domain-free. In 
      this review, we discuss briefly the present understanding of TNF-alpha-mediated 
      biology and the current therapies in clinical use, and focus on some of the new 
      therapeutic approaches with small-molecule inhibitors. Moreover, we examine 
      recent reports providing important insights into the understanding of efficacy of 
      thalidomide and its analogs, as TNF-alpha activity inhibitories, especially in 
      therapies of several inflammatory diseases within the nervous system.
FAU - Esposito, E
AU  - Esposito E
AD  - IRCCS Centro Neurolesi Bonino-Pulejo, Messina, Italy.
FAU - Cuzzocrea, S
AU  - Cuzzocrea S
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Curr Med Chem
JT  - Current medicinal chemistry
JID - 9440157
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 4Z8R6ORS6L (Thalidomide)
SB  - IM
MH  - Anti-Inflammatory Agents/therapeutic use
MH  - Antibodies, Monoclonal/immunology/therapeutic use
MH  - Arthritis, Rheumatoid/drug therapy
MH  - Humans
MH  - Immunosuppressive Agents/pharmacology
MH  - Receptors, Tumor Necrosis Factor/metabolism
MH  - Reperfusion Injury/*drug therapy
MH  - Thalidomide/pharmacology
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors/metabolism
MH  - Wounds and Injuries/*drug therapy
RF  - 149
EDAT- 2009/08/20 09:00
MHDA- 2009/11/07 06:00
CRDT- 2009/08/20 09:00
PHST- 2009/08/20 09:00 [entrez]
PHST- 2009/08/20 09:00 [pubmed]
PHST- 2009/11/07 06:00 [medline]
AID - 10.2174/092986709788803024 [doi]
PST - ppublish
SO  - Curr Med Chem. 2009;16(24):3152-67. doi: 10.2174/092986709788803024.