Bimekizumab Effective in Active Psoriatic Arthritis Save

Interleukin 17 IIL-17) is important in the pathogenesis of psoriatic disease, with most current approaches targeting IL-17A. Now there is a novel approach showing that dual neutralisation of IL-17A and IL-17F in psoriatic arthritis arthritis patients results in clinically significant improvement. 

Bimekizumab (BMK) is a monoclonal antibody that selectively neutralises IL17A and IL17 and has been studied in the BE ACTIVE trial; a phase 2b randomised, double-blind, placebo-controlled, worldwide study done in patients with active psoriatic arthritis.

Adults (n=206) with active psoriatic arthritis randomized to receive placebo, or 4 different doses of bimekizumab (16 mg, 160 mg, 160 mg after a 320 mg loading dose), or 320 mg bimekizumab, given subcutaneously every 4 weeks for 12 weeks. The primary endpoint was the ACR50 response rate at week 12, although patients were followed till week 48. 

At 12 weeks, the odds of achieving an ACR50 response (compared with placebo) was: 

• BMK 16 mg - odds ratio [OR] 4·2 [95% CI 1·1–15·2]; p=0·032)
• BMK 160 mg - OR 8·1 [2·3–28·7]; p=0·0012
• BMK 160 mg + 320 mg Loading - OR 9·7 [2·7–34·3]; p=0·0004

ACR50 response rates were:

• Placebo 7%
• 16 mg 27%
• 160 mg 41%
• 160 + 320mg Loading 47%
• 320 mg 24% (not significant p=0.51)

By week 24, 37–60% of patients who remained on the same dose of bimekizumab from baseline had minimal disease activity, and these were maintained out to week 48.

Skin responses in patients with psoriasis affecting at least 3% of their BSA, showed bimekizumab groups were significantly more likely to achieve PASI75 (p≤0·0048) and that those in the 160 mg, 160 mg (loading dose), and 320 mg bimekizumab groups were significantly more likely to achieve PASI90 (p≤0·0020).

Adverse events were similar between groups (57% placebo vs. 41% BMK) with mild or moderate.  However eight of nince serious adverse events were with bimekizumab, but there were no deaths or cases of inflammatory bowel disease reported.