0523: Bimekizumab Maintained Stringent Clinical Responses Through Week 52 in Patients with Axial Spondyloarthritis: Results from Two Phase 3 Studies

Fabian Proft¹, Désirée van der Heijde², Xenofon Baraliakos³, Joerg Ermann⁴, Carmen Fleurinck⁵, Ute Massow⁶, Natasha De Peyrecave⁷, Vanessa Taieb⁸, Astrid van Tubergen⁹ and Victoria Navarro-Compán¹⁰, ¹Department of Gastroenterology, Infectiology and Rheumatology (including Nutrition Medicine), Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany, ²Department of Rheumatology, Leiden University Medical Center, Leiden, Netherlands, ³Rheumazentrum Ruhrgebiet Herne, Ruhr-University Bochum, Herne, Germany, ⁴Division of Rheumatology, Inflammation and Immunity, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, ⁵UCB Pharma, Oosterzele, Belgium, ⁶UCB Pharma, Monheim am Rhein, Germany, ⁷UCB Pharma, Brussels, Belgium, ⁸UCB Pharma, Colombes, France, ⁹Department of Internal Medicine, Division of Rheumatology, Maastricht University Medical Centre, Maastricht, Netherlands, ¹⁰Department of Rheumatology, La Paz University Hospital, IdiPaz, Madrid, Spain

Background/Purpose: Axial spondyloarthritis (axSpA) is a chronic rheumatic disease which requires optimal management and disease control. Patients (pts) can experience loss of response in the long term and maintenance of response is an internationally recommended treatment target.¹

Bimekizumab (BKZ), a monoclonal IgG1 antibody that selectively inhibits IL‑17F in addition to IL‑17A, has demonstrated sustained clinical efficacy to Week (Wk) 52 in pts across the full disease spectrum of axSpA in the phase 3 studies BE MOBILE 1 and 2.²

Here, we report the maintenance of stringent clinical responses through 1 year of treatment with BKZ in pts with non‑radiographic axSpA (nr-axSpA) and radiographic-axSpA (r‑axSpA, i.e., AS).³

Methods: In BE MOBILE 1 (NCT03928704; nr-axSpA; pts met ASAS criteria for axSpA) and BE MOBILE 2 (NCT03928743; r‑axSpA; pts fulfilled ASAS and modified New York criteria for r-axSpA), pts were randomized to receive subcutaneous BKZ 160mg every 4 wks (Q4W) or placebo (PBO) to Wk 16. From Wks 16−52, all pts received BKZ 160mg Q4W.^4,5

Assessment of SpondyloArthritis international Society ≥40% improvement (ASAS40) and Ankylosing Spondylitis Disease Activity Score (ASDAS) < 2.1 (low disease activity [LDA]) or < 1.3 (inactive disease [ID]) responses to Wk 52 were assessed among BKZ‑randomized pts who responded at Wk 16. Non-responder imputation (NRI), and multiple imputation (MI) were used for missing ASAS40 and ASDAS data, respectively. Observed case (OC) data and Wk 16 and Wk 52 responder rates for all BKZ-randomized pts (NRI or MI) are also reported.

The number of treatment-emergent adverse events (TEAEs) to Wk 52 are reported for pts who received ≥1 dose of BKZ.

Results: A total of 128 and 221 pts were randomized to BKZ 160mg Q4W in BE MOBILE 1 and 2, respectively. At Wk 16, 47.7% and 44.8% of these pts achieved the primary endpoint, ASAS40, and this increased to 60.9% and 58.4% at Wk 52 (NRI, Figure). Of pts that achieved ASAS40 at Wk 16, 82.0% and 83.8% maintained this response at Wk 52 (NRI, Figure).

ASDAS LDA was achieved by 46.1% and 44.8% of BKZ-randomized pts at Wk 16 of BE MOBILE 1 and 2, respectively; this increased to 61.6% and 57.1% at Wk 52 (MI, Figure). Of pts that achieved ASDAS LDA at Wk 16, 88.9% and 88.4% maintained this response at Wk 52 (MI, Figure).

At Wk 16 of BE MOBILE 1 and 2, ASDAS ID was achieved by 18.8% and 16.4% of BKZ‑randomized pts, respectively; and this increased to 25.2% and 23.4% at Wk 52 (MI). Among Wk 16 ASDAS ID responders, ASDAS ID was maintained by 79.2% and 75.1% at Wk 24, 85.3% and 71.7% at Wk 36, and 88.0% and 58.7% at Wk 52 (MI).

To Wk 52 of BE MOBILE 1 and 2, 183/244 (75.0%) and 249/330 (75.5%) pts reported ≥1 TEAE whilst receiving BKZ, respectively; 9 (3.7%) and 20 (6.1%) reported serious TEAEs.

Conclusion: Dual inhibition of IL-17F and IL-17A with BKZ provided robust maintenance of stringent clinical responses from Wk 16 to Wk 52 across the full disease spectrum of axSpA.

References:1. Smolen J. Ann Rheum Dis 2018;77:3–17; 2. Baraliakos X. Arthritis Rheumatol 2022;74 (suppl 9); 3. Boel A. Ann Rheum Dis 2019;78:1545–9; 4. Deodhar A. Ann Rheum Dis 2022;81:772–3; 5. van der Heijde D. Ann Rheum Dis 2022;81:12–3.




F. Proft: AbbVie, 2, 6, Amgen, 2, 6, BMS, 2, 6, Celgene, 2, 6, Eli Lilly, 5, Hexal, 2, 6, Janssen, 2, 6, MSD, 2, 6, Novartis, 2, 5, 6, Pfizer, 2, 6, Roche, 2, 6, UCB Pharma, 2, 5, 6; D. van der Heijde: AbbVie, 2, Bayer, 2, BMS, 2, Eli Lilly, 2, Galapagos, 2, Gilead, 2, GSK, 2, Imaging Rheumatology BV, 12, Director, Janssen, 2, Novartis, 2, Pfizer, 2, Takeda, 2, UCB Pharma, 2; X. Baraliakos: AbbVie, 2, 6, BMS, 2, 6, Chugai, 2, 6, Eli Lilly, 2, 6, Galapagos, 2, 6, Gilead, 2, 6, MSD, 2, 6, Novartis, 2, 6, Pfizer Inc, 2, 6, UCB, 2, 6; J. Ermann: AbbVie, 2, 5, Boehringer Ingelheim, 5, Janssen, 2, Novartis, 2, 5, Pfizer, 2, 5, Takeda, 2, UCB Pharma, 2; C. Fleurinck: UCB Pharma, 3; U. Massow: UCB Pharma, 3; N. De Peyrecave: UCB Pharma, 3; V. Taieb: UCB Pharma, 3, 11; A. van Tubergen: MSD, 5, Novartis, 2, 5, Pfizer, 2, 5, 6, UCB Pharma, 2, 5; V. Navarro-Compán: AbbVie, 2, 5, 6, Eli Lilly, 2, 6, Galapagos, 2, Janssen, 6, MoonLake, 2, MSD, 2, 6, Novartis, 2, 5, 6, Pfizer, 2, 6, UCB, 2, 6.