Dual inhibition of IL-17A & IL-17F with bimekizumab may be a promising treatment option for AS, suggests BE MOBILE 2 trial

EULAR 2022: IL-17A & IL-17F with bimekizumab

Bimekizumab in patients with active ankylosing spondylitis: 24-week efficacy and safety from BE MOBILE 2, a Phase III, multicenter, randomized, placebo-controlled study (Abstract # OP0019)

Bimekizumab is a monoclonal IgG1 antibody that selectively inhibits interleukin (IL)-17F in addition to IL-17A. The BE MOBILE 2 trial, displayed a positive safety and efficacy results in patients who were affected by ankylosing spondylitis and poor response or intolerance to two nonsteroidal anti-inflammatory drugs and prior exposure to no more than one TNF inhibitor.


In Week-16, the bimekizumab group showed 44.8% ASAS40 response rates, in contrast to 22.5% response rates in the placebo group. In Week-24, the follow-up for ASAS40 response rates were 53.8% for patients who received bimekizumab throughout the study and 56.8% response rates for those who switched to placebo at Week-16. 54.3% of the patients experienced treatment-emergent adverse events (TEAEs), who were treated with bimekizumab at weeks 0-16. Patients with active As who were treated with bimekizumab showed rapid and clinically positive reductions in key signs and symptoms of the disease, with ASDAS <2.1 by week 24. In terms of secondary endpoints, objective signs of inflammation, as described by CRP levels and MRI inflammation of the sacroiliac joints and spine, were notably reduced in bimekiumab-treated patients. Commonly, around 7.7% of the individuals treated with bimekizumab were affected by Nasopharyngitis.


Conclusion


The BE MOBILE 2 Phase III study met all its primary and secondary endpoints. Between the TNFi-navie and TNFi-experienced patients, consistent ASA40 response rates were observed.

In patients with active AS, dual inhibition of IL-17A and IL-17F with bimekizumab resulted in rapid, clinically relevant improvements in efficacy outcomes versus placebo. These results will open up the scope for further exploration of humanized monoclonal IgG1 for AS.


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