Since TNF-α is a potent and pivotal mediator in the inflammatory process, considerable investment has been made in the research into – and development of – anti-TNF-α agents, for the purpose of reducing the severity of inflammatory responses in disease states (e.g., the medicine etanercept for treatment of rheumatoid arthritis). The inhibition of ADAM17 by a pharmacological agent may represent another means by which the effects of TNF-α can be modulated, although this is yet to be demonstrated clinically in humans.
Functional ADAM17 has been documented to be ubiquitously expressed in the human colon, with increased activity in the colonic mucosa of patients with ulcerative colitis, a main form of inflammatory bowel disease. These data will no doubt contribute to growing interest in the inhibition of ADAM17 as a potential therapeutic strategy.
Adapted from the Wikipedia article ADAM17, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki
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ADAM17 – ADAM17 as a target for future medicines?
Since TNF-α is a potent and pivotal mediator in the inflammatory process, considerable investment has been made in the research into – and development of – anti-TNF-α agents, for the purpose of reducing the severity of inflammatory responses in disease states (e.
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