A Human Interleukin-12/23 Monoclonal Antibody for the Treatment of Psoriasis

Type 1 cytokines are overexpressed in psoriatic plaques. This trial evaluated a monoclonal antibody against interleukin-12 and interleukin-23 in patients with psoriasis. Response rates at 12 weeks were significantly higher in patients treated with interleukin-12/23 monoclonal antibody than in those...

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Veröffentlicht in:The New England journal of medicine 2007-02, Vol.356 (6), p.580-592
Hauptverfasser: Krueger, Gerald G, Langley, Richard G, Leonardi, Craig, Yeilding, Newman, Guzzo, Cynthia, Wang, Yuhua, Dooley, Lisa T, Lebwohl, Mark
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Sprache:eng
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Zusammenfassung:Type 1 cytokines are overexpressed in psoriatic plaques. This trial evaluated a monoclonal antibody against interleukin-12 and interleukin-23 in patients with psoriasis. Response rates at 12 weeks were significantly higher in patients treated with interleukin-12/23 monoclonal antibody than in those treated with placebo. Four percent of patients who received interleukin-12/23 monoclonal antibody and 1% of those who received placebo had serious adverse events. Larger studies of longer duration are needed to assess the effectiveness and safety of interleukin-12/23 monoclonal antibody for psoriasis. In patients with psoriasis, response rates at 12 weeks were significantly higher in those treated with interleukin-12/23 monoclonal antibody than in those treated with placebo. Psoriasis is a chronic inflammatory skin disorder affecting 2 to 3% of the world's population. 1 , 2 Psoriasis affects the physical and emotional well-being of patients, and its effect on quality of life is similar to that seen with other major medical diseases. 3 Significant unmet need remains for safe, highly effective, and convenient treatments. Aberrant type 1 immune responses have been linked to the pathogenesis of psoriasis, 4 – 7 and cytokines that elicit these immune responses (e.g., interleukin-12 and interleukin-23) may represent appropriate therapeutic targets. 8 Interleukin-12 p40 is overexpressed in psoriasis plaques, 9 and preclinical studies implicate this cytokine in the pathogenesis of . . .
ISSN:0028-4793
1533-4406
DOI:10.1056/NEJMoa062382