How it works:

Each of the diseases ENBREL is approved to treat affects the immune system - the body’s protection against invasion of infections and toxins. In these diseases, the immune system attacks the body’s own healthy cells, mistaking them for cells that don’t belong. This causes inflammation of the skin or in the lining or connective tissue of the joints.

Tumor necrosis factor (TNF) is one of the chemical messengers that helps regulate the inflammatory process. When the body produces too much TNF, it overwhelms the immune system’s ability to control inflammation of the joints or of psoriasis-affected skin areas. ENBREL is similar to a protein that the body produces naturally, and like this protein, it binds and deactivates some TNF molecules before they can trigger inflammation. 

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ENBREL is a fully human anti-TNF receptor approved for use to reduce the signs and symptoms and inhibit the progression of structural damage in patients with moderately to severely active Rheumatoid Arthritis (RA).  It is also approved to reduce the signs and symptoms of active arthritis in patients with psoriatic arthritis, moderately to severely active polyarticular juvenile idiopathic arthritis in patients ages 2 and older, ankylosing spondylitis, and chronic moderate to severe plaque psoriasis. ENBREL acts by binding TNF, one of the dominant inflammatory cytokines or regulatory proteins that play an important role in both normal immune function and the cascade of reactions that causes the inflammatory process.
 

WARNING RISK OF INFECTIONS Infections, including serious infections leading to hospitalization or death, have been observed in patients treated with ENBREL (see WARNINGS and ADVERSE REACTIONS). Infections have included bacterial sepsis and tuberculosis. Patients should be educated about the symptoms of infection and closely monitored for signs and symptoms of infection during and after treatment with ENBREL. Patients who develop an infection should be evaluated for appropriate antimicrobial treatment and, in patients who develop a serious infection, ENBREL should be discontinued. Tuberculosis (frequently disseminated or extrapulmonary at clinical presentation) has been observed in patients receiving TNF-blocking agents, including ENBREL. Tuberculosis may be due to reactivation of latent tuberculosis infection or to new infection. Data from clinical trials and preclinical studies suggest that the risk of reactivation of latent tuberculosis infection is lower with ENBREL than with TNF-blocking monoclonal antibodies. Nonetheless, postmarketing cases of tuberculosis reactivation have been reported for TNF blockers, including ENBREL. Patients should be evaluated for tuberculosis risk factors and be tested for latent tuberculosis infection prior to initiating ENBREL and during treatment. Treatment of latent tuberculosis infection should be initiated prior to therapy with ENBREL. Treatment of latent tuberculosis in patients with a reactive tuberculin test reduces the risk of tuberculosis reactivation in patients receiving TNF blockers. Some patients who tested negative for latent tuberculosis prior to receiving ENBREL have developed active tuberculosis. Physicians should monitor patients receiving ENBREL for signs and symptoms of active tuberculosis, including patients who tested negative for latent tuberculosis infection.