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SAN DIEGO -- An investigational biologic drug that inhibits interleukin-23 without also targeting IL-12 easily met its primary and secondary endpoints in a phase II trial among psoriatic arthritis patients, a researcher reported here.

Risankizumab, a monoclonal antibody against the p19 subunit of IL-23, produced ACR20 responses (20% reduction in symptoms by American College of Rheumatology criteria, the study's primary endpoint) at week 16 in 60% of patients receiving either three or five doses at 150 mg, compared with 36% of a placebo group, said Philip Mease, MD, of Swedish Medical Center and the University of Washington in Seattle in a late-breaker session at the .

ACR50 and ACR70 responses followed a similar pattern, with progressively lower proportions of patients achieving these greater reductions in symptoms, as is typically the case in rheumatoid and psoriatic arthritis trials.

For a host of other secondary endpoints evaluating joint and skin symptoms at treatment week 16, the drug generally outperformed placebo. The only outcome for which at least one risankizumab dosing group did not improve significantly more than the placebo group was change in dactylitis count. That was out of 10 secondary endpoints reported.

Phase III studies are planned, but dosing will be decided when data through week 24 from this phase II study are fully analyzed, Mease said.

Another IL-23 inhibitor is already approved for psoriatic arthritis and psoriasis: ustekinumab (Stelara). However, that drug also inhibits IL-12 because its specific target is the p40 subunit that both cytokines share. By binding to the p19 subunit instead, risankizumab (a humanized IgG1 antibody) is hypothesized to induce a more focused change in immune activity, Mease explained.

The current trial randomized 185 patients to five treatment arms: placebo; a single subcutaneous 75-mg injection of risankizumab at week 0; 150 mg at weeks 0 and 12; 150 mg at weeks 0, 4, and 16; and 150 mg at weeks 0, 4, 8, 12, and 16. These last two groups were pooled as well as reported individually in Mease's statistical presentation.

There was not a clear dose response in the results he presented. The five doses of 150 mg did not consistently produce the greatest efficacy, nor were the best results always seen in the two highest-dose groups when pooled. Those groups did not show the highest rates of adverse events, either -- and the placebo group didn't have the lowest.

About 20% of patients in each group, including placebo, had adverse events considered drug-related. A total of 10 patients had severe events, including four in the placebo group and three of the other six in the highest-dose risankizumab arm. Rates of infection were similar across all groups at 30%-40% and only two cases were considered serious.

Perhaps the most dramatic efficacy results were in measures of skin symptoms. So-called PASI75 responses -- 75% reduction in Psoriasis Activity Severity Index -- were achieved by 67%-75% of patients in the active drug arms, compared to just 10% of the placebo group. From 35% to 56% of drug-treated patients achieved PASI100 responses, versus 7% of those on placebo.

Other secondary measures showing advantages for risankizumab include DAS28 disease activity scores, the proportion of patients having minimal disease activity, SPARCC and Leeds scores for enthesitis, and pain scores.

Efficacy built over time, Mease noted, with proportions of patients achieving benchmarks such as ACR20 and PASI75 building steadily through the 16 weeks of treatment and follow-up.

Another 8 weeks of follow-up is part of the study and those results will be analyzed and reported later.

Risankizumab is also being developed for Crohn's disease (a phase II study was reported in 2016), psoriasis (now in phase III), and asthma (phase II), by AbbVie in collaboration with Boehringer Ingelheim.