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ENBREL combo therapy inhibits joint damage progression, offers significant RA symptom relief

er than that of methotrexate.

Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. If left untreated or improperly treated, RA can produce serious destruction of one or more joints, which frequently leads to permanent disability, significantly impacting quality of life.

ABOUT ENBREL
ENBREL is the only fully human, soluble TNF receptor approved to reduce the signs and symptoms and inhibit the structural damage in patients with moderately to severely active RA, and to reduce the signs and symptoms of active arthritis in patients with psoriatic arthritis. ENBREL is the only biologic therapy approved for first line treatment of RA patients, and can be used alone. It is also approved to reduce the signs and symptoms of moderately to severely active polyarticular-course juvenile rheumatoid arthritis (JRA) in patients who have had an inadequate response to disease-modifying medicines.

Physicians have become familiar with the benefits and proven long-term tolerability profile of ENBREL. It has been used to treat over 180,000 patients worldwide since becoming commercially available four years ago.

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 of psoriatic arthritis and RA. The binding of ENBREL to TNF renders the bound TNF biologically inactive, resulting in significant reduction in inflammatory activity.

Since the product was first introduced, the following have been reported in patients using ENBREL:

Serious Infections

  • Many occurred in people prone to infection, such as those with advanced or poorly controlled diabetes
  • Some serious infections were fatal
  • Rare cases of tuberculosis

What to do/Not do'"/>

Contact: Rebecca Hamm, Amgen
805-447-3872
Porter Novelli
20-Jun-2003


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