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Bimekizumab initiation resulted in greater or comparable efficacy regarding minimal disease activity and achievement of ACR50/70 compared with guselkumab.
Compared with guselkumab, treatment with bimekizumab demonstrated a more favorable likelihood of achieving treatment outcomes in patients with psoriatic arthritis (PsA)who were biologic disease-modifying antirheumatic drug (bDMARD)-naïve or had an intolerance or inadequate response to tumor necrosis factor inhibitors (TNF-IR) at week 48/52, according to a study published in Rheumatology and Therapy.1
Bimekizumab initiation resulted in greater or comparable efficacy in terms of minimal disease activity and achievement of 50%/70% improvement in American College of Rheumatology score (ACR50/70).
bDMARD-naïve patients receiving bimekizumab, an interleukin (IL)-17F/IL-17A inhibitor, were evaluated in the BE OPTIMAL trial while BE COMPLETE enrolled TNF-IR patients. Guselkumab, a selective IL-23 inhibitor, was assessed in the DISCOVER-2 and COSMOS randomized controlled trials (RCTs). Although the efficacy of bimekizumab compared with other DMARDs has been established in previous research, there is a lack of long-term comparative network meta-analyses due to a lack of a placebo common comparator after the 24-week mark.2
“Head-to-head studies of available treatments for PsA are sparse, and no head-to-head trials have been conducted between bimekizumab and guselkumab,” wrote Richard B Warren, PhD, professor of Dermatology and Therapeutics and Honorary Consultant Dermatologist at the University of Manchester, UK. “With an increasing number of targeted therapies becoming available in PsA, clinicians face treatment decisions concerning the variety of modes of action available to them.”
The relative efficacy of guselkumab 100 mg every 4 weeks (Q4W) or 8 weeks (Q8W) was compared with bimekizumab 160 mg Q4W using matching-adjusted indirect comparisons (MAIC) at weeks 48 and 52 in bDMARD-naïve and TNF-IR patients with PsA. The systematic literature review used individual patient data from bDMARD-naïve patients in the BE OPTIMAL (n = 431) and compared results with summary data from DISCOVER-2 (Q4W, n = 245; Q8W, n = 248). In the TNF-IR group, investigators used patient data from BE COMPLETE (n = 267) and summary data from COSMOS (Q8W, n = 189). Unanchored comparisons evaluated ACR20/50/70 and MDA.
For those who were bDMARD-naïve, initiation of bimekizumab was linked to a greater likelihood of ACR50 (odds ratio [OR] [95% confidence interval (CI)] 1.62 [1.07, 2.44]; P = .021), ACR70 (2.20 [1.43, 3.38]; P < .001), and MDA (1.82 [1.20, 2.76]; P = .005) when compared with guselkumab Q4W at week 52. Similarly, patients receiving bimekizumab were more likely to achieve ACR70 response (2.08 [1.34, 3.22]; P = .001) and MDA (2.07 [1.35, 3.17]; P < .001) compared with guselkumab Q8W at week 52.
In the TNF-IR cohort, bimekizumab treatment more frequently resulted in achievement of all evaluated outcomes compared with guselkumab Q8W at week 48/52 (ACR20, 1.77 [1.15, 2.72]; P = .010; ACR50, 1.56 [1.03, 2.36]; P = .037; ACR70, 1.66 [1.05, 2.61]; P = .028; and MDA, 1.95 [1.27, 3.02]; P = .003).
Investigators mentioned limitations including introducing the data from BE VITAL OLE trial, a long-term extension of BE COMPLETE, making it difficult to control for unobserved or unreported variables. Additionally, the duration of the placebo-controlled portion varied among RCTs. However, as none were placebo-controlled at week 48/52, all patients were aware they were receiving active treatment. Further, other outcomes, including enthesitis resolution, dactylitis resolution, inhibition of radiographic progression, and safety could not be assessed using the available data.
“The results of this analysis should be viewed in the context of the limitations for an indirect comparison, yet the use of individual patient data and established MAIC methodology provides comparative evidence in the absence of a confirmatory head-to-head RCT,” investigators concluded.
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