Anti-TNF-Α Biotherapies
Anti-TNF-Α Biotherapies
This article discusses the rationale behind recommending immunopharmacological guidance of long-term therapies with genetically engineered anti-TNF-α immunoglobulin constructs. Arguments why therapeutic decision-making should not rely on clinical outcome alone are presented. Central to this is that the use of theranostics (i.e., monitoring circulating levels of functional anti-TNF-α drugs and antidrug antibodies) would markedly improve treatment because therapies can be tailored to individual patients and provide more effective and economical long-term therapies with minimal risk of side effects. Large-scale immunopharmacological knowledge of how patients 'handle' TNF-α biopharmaceuticals would also help industry develop more effective and safer TNF-α inhibitors.
The last decade has seen a revolution in the treatment of patients with chronic immunoinflammatory diseases. These include arthritic diseases (e.g., rheumatoid arthritis [RA], juvenile idiopathic arthritis and ankylosing spondylitis), inflammatory bowel diseases (e.g., Crohn's disease [CD] and ulcerative colitis), inflammatory skin diseases (e.g., psoriasis with or without joint involvement), eye diseases (e.g., uveitis, Behçets disease) and vasculitic diseases, possibly including atherosclerosis, and various autoinflammatory syndromes. It started with an appreciation of the possible role of TNF-α in the pathogenesis of autoimmune and autoinflammatory diseases, and this understanding provided the basis for development and use of genetically engineered biopharmaceuticals specifically targeting TNF-α in patients with a number of chronic inflammatory disorders.
Abstract and Introduction
Abstract
This article discusses the rationale behind recommending immunopharmacological guidance of long-term therapies with genetically engineered anti-TNF-α immunoglobulin constructs. Arguments why therapeutic decision-making should not rely on clinical outcome alone are presented. Central to this is that the use of theranostics (i.e., monitoring circulating levels of functional anti-TNF-α drugs and antidrug antibodies) would markedly improve treatment because therapies can be tailored to individual patients and provide more effective and economical long-term therapies with minimal risk of side effects. Large-scale immunopharmacological knowledge of how patients 'handle' TNF-α biopharmaceuticals would also help industry develop more effective and safer TNF-α inhibitors.
Introduction
The last decade has seen a revolution in the treatment of patients with chronic immunoinflammatory diseases. These include arthritic diseases (e.g., rheumatoid arthritis [RA], juvenile idiopathic arthritis and ankylosing spondylitis), inflammatory bowel diseases (e.g., Crohn's disease [CD] and ulcerative colitis), inflammatory skin diseases (e.g., psoriasis with or without joint involvement), eye diseases (e.g., uveitis, Behçets disease) and vasculitic diseases, possibly including atherosclerosis, and various autoinflammatory syndromes. It started with an appreciation of the possible role of TNF-α in the pathogenesis of autoimmune and autoinflammatory diseases, and this understanding provided the basis for development and use of genetically engineered biopharmaceuticals specifically targeting TNF-α in patients with a number of chronic inflammatory disorders.
Source...