Secukinumab, a human anti-IL-17A monoclonal antibody, for moderate to severe Crohn's disease: unexpected results of a randomised, double-blind placebo-controlled trial (original) (raw)
Original articles
Inflammatory bowel disease
Secukinumab, a human anti-IL-17A monoclonal antibody, for moderate to severe Crohn's disease: unexpected results of a randomised, double-blind placebo-controlled trial
- Wolfgang Hueber1,
- Bruce E Sands2,
- Steve Lewitzky3,
- Marc Vandemeulebroecke4,
- Walter Reinisch5,
- Peter D R Higgins6,
- Jan Wehkamp7,
- Brian G Feagan8,
- Michael D Yao9,
- Marek Karczewski10,
- Jacek Karczewski10,
- Nicole Pezous4,
- Stephan Bek1,
- Gerard Bruin1,
- Bjoern Mellgard1,
- Claudia Berger1,
- Marco Londei11,
- Arthur P Bertolino1,
- Gervais Tougas4,
- Simon P L Travis12,
- for the Secukinumab in Crohn's Disease Study Group
- 1Novartis Institutes for BioMedical Research, Basel, Switzerland
- 2Mount Sinai Medical Centre, New York, USA
- 3Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, USA
- 4Novartis Pharma, Basel, Switzerland
- 5Medical University Vienna, Vienna, Austria
- 6University of Michigan, Ann Arbor, Michigan, USA
- 7IKB Robert-Bosch-Krankenhaus, Stuttgart, Germany
- 8Robarts Research Institute University of Western Ontario, London, Ontario, Canada
- 9National Institutes of Health, Bethesda, Maryland, USA
- 10Solumed Research Unit, Poznan, Poland
- 11Novartis Genomics Institute of the Novartis Research Foundation, San Diego, USA
- 12Translational Gastroenterology Unit, Nuffield Department of Experimental Medicine, University of Oxford, Oxford, UK
- Correspondence to Dr Wolfgang Hueber, Novartis Institutes for BioMedical Research, Basel, Switzerland; wolfgang.hueber{at}novartis.com
Abstract
Objective The authors tested whether the anti-interleukin (IL)-17A monoclonal antibody secukinumab was safe and effective for the treatment of active Crohn's disease.
Design In a double-blind, randomised, placebo-controlled proof-of-concept study, 59 patients with moderate to severe Crohn's disease (Crohn's Disease Activity Index (CDAI) ≥220 to ≤450) were assigned in a 2:1 ratio to 2×10 mg/kg intravenous secukinumab or placebo. The primary end point, addressed by Bayesian statistics augmented with historical placebo information, was the probability that secukinumab reduces the CDAI by ≥50 points more than placebo at week 6. Ancillary analyses explored associations of 35 candidate genetic polymorphisms and faecal calprotectin response.
Results 59 patients (39 secukinumab, 20 placebo, mean baseline CDAI 307 and 301, respectively) were recruited. 18/59 (31%) patients discontinued prematurely (12/39 (31%) secukinumab, 6/20 (30%) placebo), 10/59 (17%) due to insufficient therapeutic effect (8/39 (21%) secukinumab, 2/20 (10%) placebo). Fourteen serious adverse events occurred in 10 patients (seven secukinumab, three placebo); 20 infections, including four local fungal infections, were seen on secukinumab versus none on placebo. Primary end point analysis estimated <0.1% probability (∆CDAI (SD) =33.9 (19.7), 95% credible interval −4.9 to 72.9) that secukinumab reduces CDAI by ≥50 points more than placebo. Secondary area under the curve analysis (weeks 4–10) showed a significant difference (mean ΔCDAI=49; 95% CI (2 to 96), p=0.043) in favour of placebo. Post hoc subgroup analysis showed that unfavourable responses on secukinumab were driven by patients with elevated inflammatory markers (CRP≥10 mg/l and/or faecal calprotectin≥200 ng/ml; mean ΔCDAI=62; 95% CI (−1 to 125), p=0.054 in favour of placebo). Absence of the minor allele of tumour necrosis factor-like ligand 1A was strongly associated with lack of response measured by baseline-adjusted changes in calprotectin at week 6 (p=0.00035 Bonferroni-corrected).
Conclusions Blockade of IL-17A was ineffective and higher rates of adverse events were noted compared with placebo.
Clinical trial registration This trial was registered at ClinicalTrial.gov with the number NCT01009281.
- Crohn's disease
- clinical trials
- inflammatory bowel disease
- ulcerative colitis
- genetic polymorphisms
- genetics
- genotype
- pharmacogenetics
- statistics
- chronic IBD
- antibody targeted therapy
- immune response
- antibacterial mucosal immunity
- mucosal defense
- antibacterial peptide
- IBD basic research
- gut immunology
- gut inflammation
- cytokines
- immunoregulation
- immunology
- inflammation
- inflammatory mediators
- pharmacokinetics
- pharmacology
- infliximab
- 5-aminosalicylic acid
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Gut 2013; 62 1392-1393 Published Online First: 11 Jan 2013. doi: 10.1136/gutjnl-2012-303920