How ENBREL Works
Although the exact cause of rheumatoid arthritis (RA) is unknown, elevated levels of TNF are found in the involved tissues and fluids of patients with RA. Elevated levels of TNF are also found in the tissues and fluids of patients with psoriatic arthritis and ankylosing spondylitis (AS).1
ENBREL is a moderate to severe rheumatoid arthritis treatment and fully human soluble tumor necrosis factor (TNF) receptor. ENBREL is a dimeric fusion protein consisting of the extracellular ligand-binding portion of the human 75 kilodalton (p75) tumor necrosis factor receptor (TNFR) linked to the Fc portion of human IgG1.1
ENBREL was designed to bind specifically to TNF and block its interaction with cell surface TNF receptors, thereby modulating the biological responses induced or regulated by TNF, including the inflammatory responses that play an important part in RA, psoriatic arthritis, AS, and juvenile idiopathic arthritis.1,2
ENBREL binds to TNF, limiting the amount of active TNF.1,3,4
Tumor necrosis factor (TNF; yellow) attaches to TNF "receptors" (purple) on immune cells, which trigger a cellular response.
This response can be modulated by soluble TNF receptors that are released from cells.
ENBREL (orange/purple) works like the body's soluble TNF receptors, capturing TNF before it attaches to these immune cells.
In medical studies, ENBREL was shown to be clinically effective in about 2 out of 3 adults with moderate to severe RA at 3 months. ENBREL has been shown to begin working in as few as 2 weeks, and most patients who benefit will do so within 3 months. In another medical study, 55% of patients who were evaluated 5 years after beginning ENBREL therapy had no further progression of joint damage.
In a medical study, ENBREL was shown to be effective in about 50% of psoriatic arthritis patients at 6 months. Clinical responses were apparent at the time of the first visit (4 weeks) and were maintained through 6 months of therapy.