Treatment with risankizumab, an interleukin-23 (IL-23) inhibitor, is not effective in reducing the signs and symptoms of ankylosing spondylitis (AS), according to the results of a phase 2, randomized, placebo-controlled, double-blind, proof-of-concept study ( identifier: NCT02047110) published in the Annals of the Rheumatic Diseases.

The study was conducted at 47 centers in North America, Europe, and East Asia between March 2014 and December 2014. A total of 159 patients with biologic-naïve AS who had active disease (Bath Ankylosing Spondylitis Disease Activity score ≥4) were randomly assigned to receive risankizumab 18 mg single dose (n=40), risankizumab 90 mg (n=39), risankizumab 180 mg (n=40), or placebo (n=40). All medication was administered at baseline and then at 8, 16, and 24 weeks. Treatment occurred over a 24-week blinded period.

The primary study outcome was the percentage of participants attaining a 40% improvement in the Assessment in Spondyloarthritis International Society (ASAS40) response at 12 weeks. The key secondary end point was the change from baseline in the AS Disease Activity Score-C reactive protein (ASDAS-CRP) at 12 weeks.

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The primary study outcome was not met. The ASAS40 response at 12 weeks was achieved by 25.5%, 20.5%, and 15.0% of patients in the risankizumab 18 mg-, 90 mg-, and 180 mg-groups, respectively, compared with 17.5% in the placebo group. The estimated difference in the percentage of ASAS40 responders between the risankizumab 180 mg-group and the placebo group was −2.5% (95% CI, −21.8 to 17.0; P =.42). In addition, the difference between the risankizumab 90 mg-group and the placebo group was 3.0% (95% CI, –15.9 to 20.8; P =.41) and the difference between the risankizumab 18 mg-group and the placebo group was 7.5% (95% CI, –12.1 to 26.6; P =.27).

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Prolongation of risankizumab therapy for up to 40 weeks in participants receiving escape treatment (risankizumab 180 mg) did not significantly improve ASAS40 achievement rates. Rates of adverse events were similar across all treatment groups.

The investigators concluded that the lack of efficacy of risankizumab implies that, despite a genetic association with the IL-23 pathway, the agent may not be a relevant driver of disease pathogenesis and symptoms in patients with AS.

Disclosures: DB reports grants from AbbVie, Pfizer, UCB, MSD, Novartis, and Eli Lilly and part-time employment at UCB. MØ reports grants, personal fees, and nonfinancial support from AbbVie, BMS, Merck, UCB, and Novartis; grants and personal fees from Celgene; personal fees and nonfinancial support from Janssen, Pfizer, and Roche; and personal fees from Boehringer Ingelheim, Eli Lilly, Sanofi, Regeneron, Orion, and Hospira. JS reports personal fees from Boehringer Ingelheim, AbbVie, Janssen, Lilly, Merck, Novartis, Pfizer, and UCB. PJ reports grants from AbbVie, Daiichi Sankyo, Boehringer Ingelheim, Lilly, Novartis, Roche, and UCB and grants and personal fees from BMS and Pfizer. YD, CP, SV, DBH, SA, PS and SJP report being employees of Boehringer Ingelheim.

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Baeten D, Østergaard M, Wei JC, et al. Risankizumab, an IL-23 inhibitor, for ankylosing spondylitis: results of a randomised, double-blind, placebo-controlled, proof-of-concept, dose-finding phase 2 study [published online June 26, 2018].  Ann Rheum Dis. doi:10.1136/annrheumdis-2018-213328