Responses More Likely With Bimekizumab Over Ustekinumab, Risankizumab in Treating PsA
A retrospective analysis compared data from the BE OPTIMAL and BE COMPLETE trials with data from pivotal trials of the IL-23–targeting therapies.
Philip J Mease, MD
Credit: tregmd.com
Bimekizumab seems to be more efficacious than both ustekinumab and risankizumab in treating psoriatic arthritis (PsA), according to new findings published in 2 separate papers in Rheumatology and Therapy.1,2
“PsA is a heterogeneous, systemic inflammation that occurs in up to 30% of patients with psoriasis and can impart a large burden on the patient’s quality of life as a result of irreversible joint damage if not adequately treated,” first author Philip J Mease, MD, Clinical Professor, University of Washington School of Medicine and Director, Rheumatology Research, Swedish Medical Center, and coauthors wrote.1
Mease and coauthors compared patient data from the BE OPTIMAL (NCT03895203; N = 431) and BE COMPLETE (NCT03896581; N = 267) trials that evaluated bimekizumab with data from the PSUMMIT 1 (NCT01009086; 45 mg, N = 205; 90 mg; N = 204) and PSUMMIT 2 trials (NCT01077362; 45 mg, N = 60; 90 mg, N = 58) of ustekinumab and with data from the KEEPsAKE-1 (NCT03675308; N = 483) and KEEPsAKE-2 (NCT03671148; N = 106) trials of risankizumab. Patients from the bimekizumab trials were reweighted to match the baseline characteristics of patients in the comparator trials and missing data were imputed. The investigators compared outcomes on American College of Rheumatology (ACR) 20/50/70 response criteria and minimal disease activity (MDA) index at week 52.1,2
Looking at bimekizumab compared with ustekinumab, investigators found that in patients who were biologic disease-modifying anti-rheumatic drug naïve (bDMARD naïve), bimekizumab had a greater likelihood of achieving ACR20 (45 mg: OR, 2.14 [95% CI, 1.35-3.40]; 90 mg: OR, 1.98 [95% CI, 1.24-3.16]), ACR50 (45 mg: OR, 2.74 [95% CI, 1.75-4.29]; 90 mg: OR, 2.29 [95% CI, 1.48-3.55]), and ACR70 (45 mg: OR, 3.33 [95% CI, 2.04-5.46]; 90 mg: OR, 3.05 [95% CI, 1.89-4.91]) at week 52.In patients with a previous inadequate response or an intolerance to tumor necrosis factor inhibitors (TNFi-IR disease), bimekizumab had a greater likelihood of achieving ACR20 (45 mg: OR, 4.17 [95% CI, 2.13-8.16]; 90 mg: OR, 4.19 [95% CI, 2.07-8.49]), ACR50 (45 mg: OR, 5.00 [95% CI, 2.26-11.05]; 90 mg: OR, 3.86 [95% CI, 1.70-8.79]), and ACR70 (45 mg: OR, 9.85 [95% CI, 2.79-34.79]; 90 mg: OR, 6.29 [95% CI, 1.98-20.04]) at week 52.1
Looking at bimekizumab compared with risankizumab, investigators found that in patients who were bDMARD naïve, risankizumab had a greater likelihood of achieving ACR50 (OR, 1.52 [95% CI, 1.11-2.09]) and ACR70 (OR, 1.80 [95% CO, 1.29-2.51) at week 52. In patients with TNFi-IR disease, bimekizumab had a greater likelihood of achieving ACR20 (OR, 1.78 [95% CI, 1.08-2.96]), ACR50 (OR, 2.05 [95% CI, 1.74-5.32]), ACR70 (OR, 3.69 [95% CI, 1.82--7.46]), and MDA (OR, 2.43 [95% CI, 1.37-4.32]).2
“Although both the IL-17 and IL-23 pathways are interconnected in the pathogenesis of PsA, it has been suggested that targeting IL-17 can provide greater potential for disease specificity and a rapid onset of action. The results of this study suggest that most patients achieve higher treatment targets in PsA with the dual inhibition of IL-17A/F compared to IL-12/23 inhibition,” Mease and coauthors concluded.1
