Drugs for treating rheumatoid arthritis (RA) and related conditions that mimic the effects of proteins that are naturally manufactured by the body’s immune system. These genetically-engineered drugs inhibit cells and chemicals that normally cause or worsen inflammation, reducing inflammation and protecting joints.
Biologics, as they are sometimes called, do this in different ways. Adalimumab (brand name Humira), etanercept (Enbrel), infliximab (Remicade), and golimumab (Simponi) are drugs called TNF-inhibitors and all block a cytokine (chemical messenger) called tumor necrosis factor (TNF)-alpha, which plays an important role in inflammation and the immune response. Tocilizumab (Actemra) inhibits a different cytokine called interleukin-6 (IL-6). Anakinra (Kineret) blocks a cytokine called interleukin-1 (IL-1). Tofacitinib (Xeljanz), approved for marketing in November 2012, blocks inflammation-promoting chemicals called janus kinases. Abatacept (Orencia) blocks T-cells, a kind of white blood cell involved in inflammation. Rituximab (Rituxan) prevents the activation of another kind of white blood cell called B cells, which manufacture antibodies and promote inflammation in people with RA.
The US Food and Drug Administration (FDA) has approved biologic response modifiers for treating moderate-to-severe RA that hasn’t responded adequately to traditional disease-modifying antirheumatic drugs (DMARDs) such as methotrexate. However, emerging research suggests that using such drugs early in treatment could dramatically slow the progression of RA.
Etanercept, golimumab, adalimumab, and anakinra, are given by subcutaneous (under-the-skin) injection. Infliximab, rituximab, and tocilizumab are given by intravenous infusion. Tofacitinib is taken orally. All of these medicines may increase the risk of infections.