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The proinflammatory cytokine tumor necrosis factor-alpha (TNF-α) has been implicated as the primary mediator of articular inflammation in diseases such as RA, PsA, and AS. Targeting TNF-a has been a successful strategy in the intervention of a range of immunoinflammatory disorders. Biologics have risen to the forefront of TNF-α blockade with infliximab, a chimeric monoclonal antibody (mAb), and etanercept, a fusion protein comprised of the ligand-binding segment of the soluble TNF receptor, reaching the market in the late 1990s for the initial indication of RA. Since then, their use has expanded to other diseases of inflammatory etiology, and two additional TNF-α inhibitors have joined the competition. Golimumab, a human anti-TNF-α mAb that binds to both soluble and transmembrane forms of TNF-a, is the first once-monthly subcutaneous agent to enter the market and is currently approved for the treatment of RA in combination with methotrexate (MTX), PsA alone or in combination with MTX, and AS. .

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Treatment of allergic asthma.

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The most common adverse reactions, occurring with an incidence >5%, were upper respiratory tract infection and nasopharyngitis. Regarding drug interactions, live vaccines should not be administered while being treated with golimumab. As an increased risk of serious infection has been associated with concomitant use of abatacept and anakinra, combination of these drugs is not recommended. Also, golimumab treatment should not be initiated in patients with an active infection. Furthermore, patients should be warned about the higher incidence of malignancies observed with anti-TNF-a therapy and increased risks of worsening or new onset of heart failure, of exacerbation or new onset of demyelinating disease, and of hepatitis B reactivation.

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