LAUSR

Bimekizumab (BKZ) is a monoclonal IgG1 antibody that selectively inhibits IL-17F in addition to IL-17A and has demonstrated rapid and clinically meaningful improvements in disease activity (ASAS40, primary outcome measure) in patients across the full spectrum of axial spondyloarthritis (axSpA; active non-radiographic axSpA [nr-axSpA; BE MOBILE 1, NCT03928704] and ankylosing spondylitis [AS] / radiographic axSpA [r-axSpA; BE MOBILE 2, NCT03928743]). Here we report results related to HRQoL instruments (EQ-5D-3L, ASQoL and SF-36) from the two ongoing phase 3 studies at week (wk) 16. BE MOBILE 1 and 2 were conducted in parallel with similar study designs: 16-wk double-blind placebo-controlled period followed by a 36-wk maintenance period. Patients were randomised (1:1 in BE MOBILE 1 and 2:1 in BE MOBILE 2) to BKZ 160 mg Q4W or placebo (PBO). All patients received BKZ 160 mg Q4W from wk16. We report change from baseline (CfB) in the overall EQ-5D-3L utility index, ASQoL and SF-36 Physical component Summary (PCS) scores at wk16 compared to PBO. Missing data is imputed using multiple imputation. Overall, 240/254 (94.5%; nr-axSpA) and 313/332 (94.3%; r-axSpA) patients completed the studies up to wk24. Both studies met their primary and all ranked secondary endpoints at wk16. In both studies, BKZ treatment resulted in improved health status as measured with the EQ-5D-3L utility score versus PBO. This improvement at wk16 was consistent across both tumour necrosis factor inhibitor (TNFi)-naive and TNFi-inadequate responders (IR) patients. Significantly greater improvements were also observed with BKZ compared to PBO in ASQoL and SF-36 PCS in both studies (p < 0.001, all comparisons) at wk16 (Table). At wk16, a higher proportion of BKZ- versus PBO-treated patients achieved ≥5-point improvement in SF-36 PCS (nr-axSpA: 64.8% vs 41.3% and r-axSpA: 63.8% vs 49.5%) and ≥4-point improvement in ASQoL (nr-axSpA: 58.6% vs 33.3% and r-axSpA: 57.5% vs 45.0%), respectively. Dual inhibition of IL-17A and IL-17F with BKZ improved quality of life measured by EQ-5D-3L, ASQoL and SF-36 PCS scores compared with PBO in patients across the full spectrum of axSpA. Disclosure N. McKay: Member of speakers’ bureau; NM has received Speaker' bureau from Gilead. Other; NM has received travel fees from UCB Pharma and Gilead. A. Bennett: Honoraria; AB has received teaching honorarium from Abbvie Ltd, Pfizer, UCB Pharma, Novartis and Biogen. Grants/research support; AB has received research grants from Pfizer. Other; AB has received advisory board fees from Abbvie Ltd, Pfizer, UCB Pharma, MSD, Novartis and Eli Lilly. N. Goodson: Honoraria; NG has received honoraria from UCB Pharma and Novartis. C. Fleurinck: Other; CF is an employee of UCB Pharma. C. de la Loge: Consultancies; CdlL is a consultant to UCB Pharma, Brussels, Belgium. U. Massow: Other; UM is an employee of UCB Pharma. V. Taieb: Other; VT is employee of UCB Pharma. H. Marzo-Ortega: Grants/research support; HMO has received grants/research support from Janssen, Novartis and UCB Pharma. Other; HMO has received honoraria and/or consultancy and/or speaker fees from Abbvie, Biogen, Celgene, Janssen, Eli-Lilly, Moonlake, Novartis, Pfizer and UCB Pharma. K. Gaffney: Consultancies; KG has received honoraria or consultancy fees from Novartis, AbbVie, UCB Pharma, Eli Lilly and Pfizer. Shareholder/stock ownership; KG is a shareholder of Rheumatology Events. Member of speakers’ bureau; KG has paticipated in speaker's bureau for Novartis, UCB Pharma, AbbVie and Eli Lilly. Grants/research support; KG has received grants/research support from NASS, Versus Arthritis, AbbVie, Pfizer, UCB Pharma, Norvartis, Eli Lilly, Cellgene, Celltrion, Janssen, Gilead and Biogen. Other; KG has received meeting expenses from AbbVie, Eli Lilly, Roche, Novartis, Pfizer and UCB Pharma.