Characterization of responder groups to secukinumab treatment in moderate to severe plaque psoriasis

Abstract

Background: Secukinumab is a fully human monoclonal antibody that neutralizes interleukin-17A (IL-17A), a key cytokine involved in the development of psoriasis. Here, we characterized secukinumab treatment-responder profiles and identified baseline factors affecting response.

Methods: Pooled phase 3 data from moderate to severe plaque psoriasis patients treated with secukinumab for 16 weeks (FIXTURE [NCT01358578], ERASURE [NCT01365455], and CLEAR [NCT02074982]) were analyzed to characterize responder groups, identifying factors associated with treatment response, and to evaluate early response kinetics as a biomarker for treatment response. Etanercept and ustekinumab were evaluated as comparators.

Results: Patients treated with secukinumab 300 mg (n = 867), ustekinumab 45/90 mg (n = 318), and etanercept 50 mg (n = 298) were evaluated. For secukinumab 300 mg, more patients were in higher responder groups than etanercept and ustekinumab. In higher response groups, fewer patients had previous systemic or biologic treatment, metabolic syndrome, hypertension, diabetes, and fewer were current smokers. Mean body weight, waist circumference, and BMI decreased as response level increased. Early onset of response (PASI50 at Week 4 or 8) correlated with sustained efficacy at Week 16.

Conclusions: Baseline factors, including weight and cardiometabolic status, were associated with response to secukinumab. Early onset of response may indicate treatment efficacy later on.

Keywords:

• Secukinumab
• psoriasis
• IL-17A
• responder groups
• baseline factors

Acknowledgments

The authors thank Evelyn Altemeyer and Jackie L. Johnson, PhD of Novartis Ireland Ltd. for providing medical writing support/editorial support, which was funded by Novartis Pharma GmbH, Germany in accordance with Good Publication Practice (GPP3) guidelines (http://www.ismpp.org/gpp3).

Disclosure statement

AP is a speaker for AbbVie, Allmirall-Hermal, Amgen, Biogen Idec, Celgene, Eli-Lilly, Galderma, Janssen, LEO-Pharma, Medac, Novartis, Pfizer and UCB Pharma, an advisor for AbbVie, Allmirall-Hermal, Amgen, Celgene, Eli-Lilly, Janssen, LEO-Pharma, and Novartis and has participated in clinical trials funded by AbbVie, Allmirall-Hermal, Amgen, Biogen Idec, Boehringer-Ingelheim, Celgene, GSK, Eli-Lilly, Galderma, Hexal, Janssen, LEO-Pharma, Medac, Merck Serono, Mitsubishi, MSD, Novartis, Pfizer, Tigercat Pharma, Regeneron, Roche, Sandoz Biopharmaceuticals, Schering-Plough and UCB Pharma. SG has been an advisor and/or received speakers’ honoraria and/or received grants and/or participated in clinical trials of the following companies: Abbott/AbbVie, Affibody AB, Akari Therapeutics Plc, Almirall-Hermal, Amgen, Anaptys Bio, Baxalta, Bayer Health Care, Biogen Idec, Bioskin, Boehringer-Ingelheim, Celgene, Centocor, Dermira, Eli Lilly, Foamix, Forward Pharma, Galderma, Hexal AG, Isotechnika, Janssen-Cilag, Leo Pharma, Medac, Merck Serono, Mitsubishi Tanabe, MSD, Novartis, Pfizer, Polichem SA, Regeneron Pharmaceutical, Sandoz Biopharmaceuticals, Sanofi-Aventis, Schering-Plough, Sienna Biopharmaceuticals, Takeda, Teva, UCB Pharma, VBL therapeutics, and Wyeth Pharma. CP is an employee of Novartis Pharma AG. MR is an employee of Novartis Pharma GmbH.

Data availability

Novartis is committed to sharing with qualified external researchers, access to patient-level data and supporting clinical documents from eligible studies. These requests are reviewed and approved by an independent review panel on the basis of scientific merit. All data provided is anonymized to respect the privacy of patients who have participated in the trial in line with applicable laws and regulations.

Additional information

Funding

This analysis was funded by Novartis Pharma GmbH, Nürnberg, Germany. All authors participated in data collection and/or analysis design/conduct.