P115 Real-world experience of bimekizumab for plaque psoriasis in adult patients with prior exposure to interleukin-23 inhibitors: a 52-week multicentre retrospective review

Abstract For adult patients with plaque psoriasis, limited information exists on switching between classes from an IL-23 inhibitor (IL-23i) to bimekizumab. We conducted a real-world, multicentre, retrospective study of bimekizumab following IL-23i exposure. Twenty-three subjects with prior exposure to an IL-23i were identified. Effectiveness outcomes included Investigator Global Assessment (IGA), psoriasis area and severity index (PASI), body surface area (BSA), and IGA × BSA scores. Safety was assessed via treatment-related adverse events (AEs). For 23 patients included, the mean age was 43 (range: 20–73) years, with 56.5% (13/23) being male. Prior IL-23i exposures included guselkumab only (52.2%, 12/23), risankizumab only (21.7%, 5/23), and both guselkumab and risankizumab (26.1%, 6/23). Reasons for discontinuation included lack of efficacy (95.7%, 22/23) and persistent psoriatic arthritis (4.3%, 1/23). Primary non-response to prior IL-23i was defined as lack of IGA 0/1 and/or 75% improvement in PASI (PASI75) at Week 16, whereas secondary non-response to prior IL-17i was defined as loss of IGA 0/1 and/or PASI75 response at any point afterwards. At Weeks 52 ± 6: IGA 0/1 was achieved by 66.7% (12/18); mean PASI, BSA, and IGA × BSA improvements from baseline were 69.6% (8.5–0.8), 71.8% (8.2–0.7%), and 74.6% (22.6–1.4), respectively; 65.2% (15/23), 56.5% (13/23), and 47.8% (11/23) achieved PASI75, 90% improvement in PASI (PASI90), and 100% improvement in PASI (PASI100), respectively; 78.3% (18/23), 69.6% (16/23), and 65.2% (14/23) achieved absolute PASI scores <3, <2, and <1; and 73.9% (17/23) achieved BSA <1%. In prior IL-23i primary non-responders (n = 6), 83.3% (5/6) achieved IGA 0/1 and/or PASI90 and 50% (3/6) achieved PASI100 with bimekizumab at Week 52 ± 6. In prior IL-23i secondary non-responders (n = 12), 66.7% (8/12) achieved IGA 0/1 and/or PASI90 and 50% (6/12) achieved PASI100 with bimekizumab at Week 52 ± 6. Four treatment-related AEs occurred (17.4%, 4/23), including oral candidiasis (8.7%, 2/23) and bacterial folliculitis (4.3%, 1/23). There were 3 (13%) treatment-related discontinuations [lack of efficacy (n = 2); AE: anxiety (n = 1)]. While our real-world results of patients with prior IL-23i exposure demonstrated lower achievement of effectiveness endpoints (IGA 0/1: 66.7%; PASI90: 56.5%; PASI100: 47.8%) at Week 52 ± 6 as compared with clinical trials, the discrepancy between clinical trials and this study may be explained by a more difficult-to-treat population with multiple biologic failures (56.5% utilized >3 biologics and 26.1% used several IL-23i). Our real-world study also included patients with >1 biologic failure, while Phase III clinical trials excluded this population. Our results highlight the long-term utility of bimekizumab in the setting of prior IL-23i exposure. Study limitations include its small sample and retrospective nature.

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