BIMEKIZUMAB MAINTAINED EFFICACY RESPONSES THROUGH 52 WEEKS IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS: RESULTS FROM TWO PHASE 3 STUDIES

Background: Bimekizumab (BKZ), a monoclonal IgG1 antibody that selectively inhibits interleukin (IL)-17F in addition to IL-17A, achieved significantly greater improvements in efficacy outcomes at Week (Wk) 16 vs placebo (PBO) and sustained efficacy to Wk 52 in two phase 3 studies in patients (pts) with psoriatic arthritis (PsA). Due to the chronic, long-term nature of PsA, sustaining high levels of disease control with treatment is important, and assessing long-term maintenance of response in pts achieving early treatment targets is of interest. Objectives: To report the proportion of Wk 16 responders maintaining their response at Wk 52, or demonstrating no loss of response at all visits to Wk 52, for joint and skin efficacy outcomes in pts with PsA from two phase 3 studies. Methods: Two phase 3 trials assessed BKZ 160 mg every 4 weeks (Q4W) in pts with PsA: BE OPTIMAL (biologic disease-modifying antirheumatic drug [bDMARD-naïve]; NCT03895203) and BE COMPLETE (tumour necrosis factor inhibitor intolerance/inadequate response [TNFi-IR]; NCT03896581). Both were PBO-controlled to Wk 16. BE OPTIMAL Wk 52 and BE COMPLETE Wk 16 completers could enrol in BE VITAL (open-label extension; NCT04009499). BE COMPLETE plus BE VITAL is referred to as ‘BE COMPLETE’ hereafter. Data are reported for pts randomised to BKZ at baseline (BL). Efficacy outcomes include ≥20/50/70% improvement from BL in American College of Rheumatology (ACR20/50/70) and ≥90/100% improvement from BL in Psoriasis Area and Severity Index (PASI90/100). Maintenance of response is defined as pts who achieved a response at Wk 16 and maintained that response at Wk 52. No loss of response is defined as pts who achieved a response at Wk 16 and all subsequent visits to Wk 52. Number of visits after Wk 16 varied by study and outcome (7 for ACR and 4 for PASI in BE OPTIMAL; 3 for ACR and PASI in BE COMPLETE); no loss of response data may appear higher for outcomes with fewer visits. Data are reported using non-responder imputation (NRI). Results: Of the pts randomised to BKZ, 388/431 (90.0%) bDMARD-naïve and 236/267 (88.4%) TNFi-IR pts completed Wk 52. High proportions of patients achieving ACR50 and PASI90 at Wk 16 maintained responses at Wk 52. At Wk 16, ACR50 was achieved by 189 (43.9%) bDMARD-naïve and 116 (43.4%) TNFi-IR pts; of those, 164 (86.8%) bDMARD-naïve and 93 (80.2%) TNFi-IR pts maintained response at Wk 52. Similarly, for pts with BL psoriasis affecting ≥3% body surface area, 133/217 (61.3%) bDMARD-naïve and 121/176 (68.8%) TNFi-IR pts achieved PASI90 at Wk 16; of those, 110 (82.7%) bDMARD-naïve and 107 (88.4%) TNFi-IR pts maintained response at Wk 52. The majority of pts also did not lose response at any visit to Wk 52: 110/189 (58.2%) bDMARD-naïve and 74/116 (63.8%) TNFi-IR pts did not lose ACR50 response, and 97/133 (72.9%) bDMARD-naïve and 96/121 (79.3%) TNFi-IR pts did not lose PASI90 response at any visit to Wk 52 ( Figure 1 ). Many Wk 16 ACR70 and PASI100 responders never lost response, with the majority achieving good efficacy response (ACR50/70 or PASI90/100) at every timepoint to Wk 52 ( Figure 2 ). At Wk 16, 105 (24.4%) bDMARD-naïve and 71 (26.6%) TNFi-IR pts achieved ACR70; of those, 87 (82.9%) bDMARD-naïve and 59 (83.1%) TNFi-IR pts maintained ACR70 response at Wk 52, and 51 (48.6%) bDMARD-naïve and 41 (57.7%) TNFi-IR pts never lost response to Wk 52. PASI100 was achieved at Wk 16 by 103/217 (47.5%) bDMARD-naïve and 103/176 (58.5%) TNFi-IR pts; of those, 82 (79.6%) bDMARD-naïve and 87 (84.5%) TNFi-IR pts maintained the response at Wk 52, and 63 (61.2%) bDMARD-naïve and 76 (73.8%) TNFi-IR pts never lost response to Wk 52. Similar trends were seen for Wk 16 ACR50 responders never losing ACR50 or ACR20 response to Wk 52 ( Figure 2 ). Conclusion: With BKZ treatment, high proportions of Wk 16 responders maintained robust efficacy responses at Wk 52 or did not lose response at any time point to Wk 52 across joint and skin outcomes, demonstrating durable improvement irrespective of prior bDMARD use. REFERENCES: [1] Ritchlin CT. Ann Rheum Dis 2023;82:1404–14. [2] Coates LC. Ann Rheum Dis 2023;82:346–7. Acknowledgements: Funded by UCB Pharma. Medical writing support provided by Costello Medical and funded by UCB Pharma. Disclosure of Interests: William Tillett Research grants, consulting fees, speaking fees and/or honoraria from AbbVie, Amgen Inc., BMS, Celgene, Eli Lilly, GSK, Janssen, MSD, Novartis, Ono Pharma, Pfizer and UCB Pharma, Yoshiya Tanaka Speaking fees and/or honoraria from AbbVie, AstraZeneca, BMS, Boehringer Ingelheim, Chugai, Eisai, Eli Lilly, Gilead, GSK, Pfizer, Taiho and Taisho, Received grants from Chugai, Eisai, Mitsubishi-Tanabe and Taisho, Diamant Thaçi Investigator and/or consultant/advisor for AbbVie, Almirall, Amgen, BMS, Boehringer Ingelheim, Celltrion, Eli Lilly and Company, Galderma, Janssen-Cilag, Kyowa Kirin, LEO Pharma, L’Oreal, New Bridge, Novartis, Pfizer, Regeneron, Sanofi, Target-RWE and UCB Pharma, Received grants from AbbVie, LEO Pharma and Novartis, Barbara Ink Shareholder of AbbVie, GSK and UCB Pharma, Employee of UCB Pharma, Vanessa Taieb Shareholder of UCB Pharma, Employee of UCB Pharma, Heather Edens Shareholder of UCB Pharma, Employee of UCB Pharma, Rajan Bajracharya Shareholder of UCB Pharma, Employee of UCB Pharma, Jessica A. Walsh Consultant for/grant support from AbbVie, Amgen, Eli Lilly, Janssen, Merck, Novartis, Pfizer and UCB Pharma DOI: 10.1136/annrheumdis-2024-eular.1239 Keywords: Skin, Outcome measures, Biological DMARD, Randomized controlled trial Citation: , volume 83, supplement 1, year 2024, page 691Session: Psoriatic arthritis (Poster View)

Skin, Outcome measures, Biological DMARD, Randomized controlled trial