IL-23 Inhibitor Fails in Ankylosing Spondylitis Save

A study of the IL-23 risankizumab in active ankylosing spondylitis (AS) patients failed to show efficacy and did not meet primary efficacy endpoints in a 6-month trial.

Risankizumab (RIZ) is a new, humanised anti-IL-23 monoclonal antibody that targets the p19 subunit of interleukin-23 (IL-23). It was studied in a 24-week trial involving 159 biologic-naïve, active AS patients. The primary outcome was a 40% improvement in Assessment in Spondylo Arthritis International Society (ASAS40) at week 12. 

In this placebo-controlled trial, the ASAS40 response rates were nearly the same for all groups 25.5%, 20.5%, 15.0%, and 17.5% (RIZ 18 mg, 90 mg, 180 mg and placebo groups). Adverse event rates were similar in all treatment groups.

While IL-23 inhibition (with this agent and another-guselkumab) has shown significant efficacy and benefits in cutaneous psoriasis and psoratic arthritis, the same has not been shown for patients with AS or axial spondyloarthritis. This in contrast to the efficacy of biologic inhibition of IL-17 (eg, secukinumab) and IL-12/23 (ustekinumab) that have shown efficay in SpA.

These data suggest that IL-23 alone may not be a primary driver of inflammation in AS.