Abstract
Introduction
Bimekizumab and brodalumab are characterized by a different mechanism of action if compared to the other anti-interleukin (IL)-17s which target IL-17A. Indeed, brodalumab acts on IL-17RA whereas bimekizumab acts on IL-17A, IL-17F, and IL-17AF cytokines. Currently, despite real-life data on the efficacy and safety of bimekizumab and brodalumab have been reported, data comparing these two drugs are absent. However, these data are mandatory to evaluate whether a different target of the same IL can be correlated with a different profile in terms of effectiveness and safety. Moreover, it should be underlined that bimekizumab and brodalumab stood out as the psoriasis treatments with the fastest onset of action, delivering quicker therapeutic responses compared to other drugs acting on IL-17.
Methods
A monocentric retrospective study was carried out enrolling patients affected by moderate to severe psoriasis undergoing treatment with brodalumab or bimekizumab. At baseline, clinical demographic details were collected. Clinical improvement [Psoriasis Area Severity Index (PASI), body surface area (BSA)] was collected at weeks 4, 16, and 36. Safety data were analyzed at the same timepoints.
Results
A total of 125 patients were enrolled in the study [bimekizumab: 53 (42.40%); brodalumab: 72 (57.6%)]. Psoriasis severity at baseline was similar between the two cohorts. Both PASI and BSA significantly reduced at each follow-up for both treatment cohorts. The bimekizumab group reached a higher percentage of PASI90/PASI100 response at each timepoint as compared to the brodalumab cohort. In particular, the percentage of PASI100 response was significantly higher in the bimekizumab group as compared to the brodalumab cohort at week 4 (41.5% vs 23.6%, p < 0.05) and at week 16 (67.9% vs 48.6%). Discontinuation for ineffectiveness was higher in the brodalumab cohort (8.3%) as compared to the bimekizumab group (3.8%), without statistical significance. As regards safety, two cases of eczematous reactions (bimekizumab: 2, brodalumab: 0), and five cases of candidiasis (bimekizumab: 4, brodalumab: 1) were collected. Overall, 3 (5.7%) and 1 (1.4%) patients discontinued bimekizumab and brodalumab because of adverse events, respectively.
Conclusion
Our study confirmed the efficacy and safety of both bimekizumab and brodalumab, up to 36 weeks of treatment. Although both drugs showed a significant improvement of the investigated scores from week 4, some differences in terms of PASI90 and PASI100 responses (higher for bimekizumab at each follow-up, with only PASI100 response significantly higher at week 4 and 16) were registered. No statistical significance was found for safety data and treatment failure.
Keywords: Bimekizumab, Brodalumab, Comparison, Real-world evidence, Real-life setting, Psoriasis, Anti-IL-17, Biologics
Key Summary Points
| Why carry out this study? |
| Bimekizumab and brodalumab are characterized by a different mechanism of action if compared to the other anti-interleukin (IL)-17s which target IL-17A. Currently, although real-life data on the efficacy and safety of bimekizumab and brodalumab have been reported, data comparing these two drugs are absent. However, these data are mandatory to evaluate whether a different target of the same IL can be correlated with a different profile in terms of effectiveness and safety. |
| This study aimed to indirectly compare the efficacy and safety of bimekizumab and brodalumab in patients with psoriasis, in a real-life setting. |
| What was learned from the study? |
| Our study confirmed the efficacy and safety of both bimekizumab and brodalumab, up to 36 weeks of treatment. Although both drugs showed a significant improvement of the investigated scores from week 4, some differences in terms of PASI90 and PASI100 responses (higher for bimekizumab at each follow-up, with only PASI100 response significantly higher at week 4 and 16) were registered. No statistical significance was found for safety data and treatment failure. |
Introduction
Psoriasis is a long-lasting inflammatory cutaneous disease, affecting up to 3% of the global population [1]. Although several clinical phenotypes can be distinguished, plaque psoriasis is the commonest, accounting for 90% of cases and presenting as sharply demarcated, erythematous plaques covered by silvery scales, most often on the scalp, elbows, or knees, but other parts of the body can be affected as well [2, 3]. Other clinical presentations include guttate psoriasis, pustular psoriasis, erythrodermic psoriasis, and inverse psoriasis [2, 3].
Psoriasis should not be considered only a skin disease. Indeed, several comorbidities can be associated with psoriasis, such as psoriatic arthritis (PsA), cardiovascular diseases, mental health problems, and inflammatory bowel diseases leading to the need for considering psoriasis as a “systemic disease”, better defined as “psoriatic disease” [4]. In consequence, the management of psoriasis should consider all the aspects of this disease, including its impact on quality of life of patients and caregivers [5].
Currently, several drugs have been approved, ranging from topical formulations (mainly based on the combination of calcipotriol and betamethasone) used for mild forms of the disease to systemic drugs for moderate to severe forms [6–8]. Systemic drugs are divided into conventional systemic drugs (cyclosporine, methotrexate, dimethyl fumarate, acitretin), oral small molecules (apremilast and deucravacitinib), and biological drugs [6–8]. The last group are represented by four different mechanisms of action, based on the target of interleukins (ILs) directly involved in psoriasis pathogenesis: anti-tumor necrosis factor alpha (TNFα), anti-IL-12/23, and the two most recently approved classes anti-IL-17 and anti-IL-23 [6–8]. Indeed, although psoriasis pathogenesis is not completely understood, the key role of the IL-23/IL-17 axis has been suggested by several studies [9]. In consequence, the introduction of biologics targeting these ILs represented a breakthrough in the psoriasis treatment scenario [9].
Of interest, the development of anti-IL-17 and anti-IL-23 resulted in the switching of treatment goals from Psoriasis Area Severity Index (PASI)75 to PASI90 or PASI100 as a result of their high efficacy profile, also characterized by promising safety data [10]. Among existing anti-IL-17 drugs, ixekizumab and secukinumab are characterized by their therapeutic action selectively binding to IL-17A, thus preventing its binding to the IL-17 receptor (IL-17R) [11]. In contrast, brodalumab binds with high affinity to human IL-17RA and blocks the biological activities of the pro-inflammatory cytokines IL-17A, IL-17F, IL-17A/F heterodimer, and IL-25 [12]. Finally, bimekizumab is the latest drug introduced that targets IL-17A, IL-17F, and IL-17AF cytokines [13].
It should be noted that although these four biologics belong to the same class (anti-IL-17), they are characterized by a unique mechanism of action. In consequence, they may have different effectiveness and safety profiles in real life. These data are necessary in clinical practice, to allow clinicians to select the right drug for the right patient at the right moment. Currently, real-life data comparing the efficacy and safety profiles of bimekizumab and brodalumab to highlight eventual differences are still lacking. Thus, the aim of our study was to indirectly compare the efficacy and safety of bimekizumab and brodalumab in patients with psoriasis, in a real-life setting.
Bimekizumab and Brodalumab
Bimekizumab is a humanized IgG1 monoclonal antibody that selectively targets interleukin-17A, IL-17F, and IL-17AF cytokines, effectively blocking their interaction with the IL-17RA/IL-17RC receptor complex. Currently, bimekizumab has been approved for the management of adult patients with moderate to severe plaque psoriasis, PsA, axial spondyloarthritis, and hidradenitis suppurativa [13]. The recommended dosage in psoriatic disease is 320 mg (given as two subcutaneous injections of 160 mg or one subcutaneous injection of 320 mg) at weeks 0, 4, 8, 12, and 16, and every 8 weeks thereafter [13]. Data on its efficacy and safety in psoriasis treatment have been reported in clinical trials (BE READY, BE SURE, BE RADIANT, BE VIVID, BE BRIGHT), which also showed its superiority over adalimumab (BE SURE), ustekinumab (BE VIVID), and secukinumab (BE RADIANT) [14–17]. Moreover, a number of real-life experiences confirming these data are emerging [18–24].
Brodalumab is a recombinant fully human monoclonal immunoglobulin IgG2 antibody that binds with high affinity to human IL-17RA and blocks the biological activities of the pro-inflammatory cytokines IL-17A, IL-17F, IL-17A/F heterodimer, and IL-25 [12]. Brodalumab has been approved for the management of moderate to severe plaque psoriasis in adult patients, at the dosage of 210 mg administered by subcutaneous injection at weeks 0, 1, and 2 followed by 210 mg every 2 weeks [12]. Its efficacy and safety have been reported in AMAGINE-1, AMAGINE-2, and AMAGINE-3, also showing its superiority over ustekinumab (AMAGINE-2 and AMAGINE-3) [25–27]. Moreover, several real-life experiences confirmed these data [28–30].
Methods
A monocentric retrospective study was carried out enrolling patients affected by moderate to severe psoriasis undergoing treatment with brodalumab and/or bimekizumab, attending the Psoriasis Care Centre of Dermatology at the University of Naples “Federico II”, with the aim of indirectly comparing the effectiveness and safety of these two biologic drugs. Inclusion criteria were presence of moderate to severe plaque psoriasis confirmed by a dermatologist; treatment with bimekizumab and brodalumab for at least 16 weeks. Exclusion criteria were patients < 18 years old; concomitant systemic treatment for psoriasis; other clinical phenotypes of psoriasis (erythrodermic, guttate, inverse, palmoplantar, or generalized pustular psoriasis). Bimekizumab and brodalumab were administered at the labelled dosage.
The following data were collected for each patient at baseline: demographic details (age, sex) and psoriasis clinical features and clinical history [psoriasis duration, comorbidities, previous and current psoriasis treatments, presence of PsA, psoriasis severity by using PASI and body surface area (BSA)]. Clinical improvement (PASI, BSA) was collected at weeks 4, 16, and 36. At these timepoints, the mean percentage change from baseline and percentage of patients with a PASI reduction ≥ 90% (PASI90) and 100% (PASI100) were assessed as well. Lack of PASI75 response after 12 weeks was considered primary inefficacy whereas loss of PASI75 response after 12 weeks as a secondary lack of efficacy. Safety data were analyzed at the same timepoints. The present study was conducted respecting the Declaration of Helsinki, and all patients signed an informed consent before starting the study. The patients in this manuscript have given written informed consent to publication of their case details.
Statistical Analysis
Demographic and clinical data were analyzed by using descriptive statistics. Mean ± standard deviation was used to present continuous variables whereas number and proportion of patients were used to present categorical ones. Student’s t test and chi-square test were used to assess the statistical significance of differences in the quantitative and qualitative features of the cohort of patients treated with bimekizumab and brodalumab at the different timepoints. p values < 0.05 were considered to be statistically significant. GraphPad Prism 8.0 (GraphPad Software Inc., La Jolla, CA, USA) was used to perform the statistical investigation.
Results
A total of 125 patients were enrolled in the study. Of these, 53 (42.40%) were treated with bimekizumab (32 male, 60.4%; mean age 50.2 ± 15.5 years), and 72 (57.6%) undergoing treatment with brodalumab (41 male, 56.9%; mean age 49.2 ± 15.6 years). Bimekizumab and brodalumab groups were comparable in terms of sex, age, presence of PsA [8 (15.1%) vs 7 (9.7%)], comorbidities, and previous conventional systemic treatments. However, the mean duration of psoriasis was significantly higher in the brodalumab cohort [13.4 ± 9.2 vs 19.3 ± 7.9, p < 0.001].
As regards previous biologic treatments, the two groups were comparable except in terms of the use of etanercept [bimekizumab: 3 (5.7%), brodalumab: 13 (18.1%), p < 0.05], ustekinumab [bimekizumab: 4 (7.5%), brodalumab: 15 (20.8%), p < 0.05], and guselkumab [bimekizumab: 7 (13.2%), brodalumab: 2 (2.8%), p < 0.05]. Of interest, 21 (39.6%) and 17 (23.6%) subjects receiving bimekizumab and brodalumab were bio-naïve, respectively. Demographic data and previous conventional and biological treatments for the two groups are summarized in Table 1.
Table 1.
Demographic data and clinical outcomes of patients treated with bimekizumab and brodalumab
| Treatment groups | Bimekizumab | Brodalumab | p |
|---|---|---|---|
| Number of patients | 53 | 72 | NS |
| Sex | |||
| Male | 32 (60.4%) | 41 (56.9%) | NS |
| Female | 21 (39.6%) | 31 (43.1%) | NS |
| Mean age (years) | 50.2 ± 15.5 | 49.2 ± 15.6 | NS |
| Mean duration of psoriasis (years) | 13.4 ± 9.2 | 19.3 ± 7.9 | p < 0.001 |
| Psoriatic arthritis | 8 (15.1%) | 7 (9.7%) | NS |
| Comorbidities | |||
| Hypertension | 13 (24.5%) | 22 (30.6%) | NS |
| Dyslipidemia | 10 (18.9%) | 16 (22.2%) | NS |
| Obesity | 12 (22.6%) | 25 (34.7%) | NS |
| Diabetes | 6 (11.3%) | 11 (15.3%) | NS |
| Cardiopathy | 3 (5.7%) | 5 (6.9%) | NS |
| Thyropathy | 2 (3.8%) | 4 (5.6%) | NS |
| Depression | 1 (1.9%) | 2 (2.8%) | NS |
| Previous conventional systemic treatments | |||
| Cyclosporine | 14 (26.4%) | 21 (29.2%) | NS |
| Acitretin | 9 (17.0%) | 18 (25.0%) | NS |
| Methotrexate | 31 (58.5%) | 37 (51.4%) | NS |
| Nb-UVB phototherapy | 7 (13.2%) | 8 (11.1%) | NS |
| Naïve | 7 (13.2%) | 12 (16.7%) | NS |
| Apremilast | 2 (3.8%) | 3 (4.2%) | NS |
| Previous biologic treatments | |||
| Bio-naïve | 21 (39.6%) | 17 (23.6%) | NS |
| Anti-TNFα | |||
| Adalimumab | 12 (22.6%) | 23 (31.9%) | NS |
| Etanercept | 3 (5.7%) | 13 (18.1%) | < 0.05 |
| Infliximab | 4 (7.5%) | 2 (2.8%) | NS |
| Certolizumab | 2 (3.8%) | 5 (6.9%) | NS |
| Anti-IL-12/23 | 4 (7.5%) | 15 (20.8%) | < 0.05 |
| Anti-IL-17 | |||
| Secukinumab | 13 (24.5%) | 11 (15.3%) | NS |
| Ixekizumab | 9 (17.0%) | 9 (12.5%) | NS |
| Brodalumab | 5 (9.4%) | NA | NS |
| Bimekizumab | NA | 0 (0%) | NS |
| Anti-IL-23 | |||
| Risankizumab | 7 (13.2%) | 3 (4.2%) | NS |
| Guselkumab | 7 (13.2%) | 2 (2.8%) | < 0.05 |
| Tildrakizumab | 2 (3.8%) | 1 (1.4%) | NS |
| Baseline | |||
| Mean PASI | 18.1 ± 8.2 | 16.8 ± 5.6 | NS |
| Mean BSA | 27.2 ± 12.4 | 25.4 ± 9.8 | NS |
| Week 4 | |||
| Mean PASI | 4.8 ± 3.7 | 5.4 ± 3.1 | NS |
| Mean BSA | 5.3 ± 4.8 | 7.3 ± 5.8 | NS |
| PASI90 | 27 (50.9%) | 27 (37.5%) | NS |
| PASI100 | 22 (41.5%) | 17 (23.6%) | p < 0.05 |
| Week 16 | |||
| Mean PASI | 1.0 ± 1.2 | 2.7 ± 1.9 | NS |
| Mean BSA | 1.3 ± 2.0 | 3.8 ± 2.6 | NS |
| PASI90 | 40 (75.5%) | 47 (65.3%) | NS |
| PASI100 | 37 (67.9%) | 35 (48.6%) | p < 0.05 |
| Week 36 | |||
| Mean PASI | 0.6 ± 1.0 | 1.0 ± 1.4 | NS |
| Mean BSA | 1.0 ± 1.2 | 1.2 ± 1.6 | NS |
| PASI90 | 44 (83.0%) | 55 (76.4%) | NS |
| PASI100 | 39 (73.6%) | 48 (66.7%) | NS |
| Adverse events | |||
| Eczematous reactions | 2 (3.8%) | 0 (0%) | NS |
| Candidiasis | 4 (7.5%) | 1 (1.4%) | NS |
| Treatment discontinuation | |||
| Adverse events | 3 (5.7%) | 1 (1.4%) | NS |
| Treatment failure | 2 (3.8%) | 6 (8.3%) | NS |
BSA body surface area, NS not significant, PASI Psoriasis Area Severity Index, NA not applicable
Psoriasis severity at baseline was similar between the two cohorts (bimekizumab: PASI 18.1 ± 8.2, BSA 27.2 ± 12.4; brodalumab: PASI 16.8 ± 5.6, BSA 25.4 ± 9.8). Both scores significantly reduced at each follow-up for both treatment cohort (Fig. 1). In particular, in the bimekizumab group, mean PASI score reduced to 4.8 ± 3.7 (p < 0.0001) at week 4, to 1.0 ± 1.2 (p < 0.0001) at week 16, and to 0.6 ± 1.0 (p < 0.0001) at week 36. As regards the brodalumab group, mean PASI decreased to 5.4 ± 3.1 (p < 0.0001) at week 4, to 2.7 ± 1.9 (p < 0.0001) at week 16, and to 1.0 ± 1.4 (p < 0.0001) at week 36. BSA showed a similar trend for both groups (Table 1). No significant differences in mean PASI and BSA were observed between the treatments at all follow-ups.
Fig. 1.
Psoriasis Area Severity Index (a) and body surface area (b) improvement in bimekizumab and brodalumab groups
Overall, the bimekizumab group reached a higher percentage of PASI90/PASI100 response at each timepoint as compared to the brodalumab cohort (week 4: PASI90 50.9% vs 37.5%, PASI100 41.5% vs 23.6%; week 16: PASI90 75.5% vs 65.3%, PASI100 67.9% vs 48.6%; week 36: PASI90 83.0% vs 76.4%, PASI100 73.6% vs 66.7%) (Fig. 2).
Fig. 2.
PASI90 (a) and PASI100 (b) responses in bimekizumab and brodalumab groups
In particular, the percentage of PASI100 response was significantly higher in the bimekizumab group as compared to the brodalumab cohort at week 4 (41.5% vs 23.6%, p < 0.05) and at week 16 (67.9% vs 48.6%, p < 0.05).
Discontinuation for ineffectiveness was higher in the brodalumab cohort (8.3%) as compared to the bimekizumab group (3.8%), without statistical significance.
As regards the safety, two cases of eczematous reactions (bimekizumab: 2, brodalumab: 0), and five cases of candidiasis were collected (bimekizumab: 4, brodalumab: 1). Overall, 3 (5.7%) patients discontinued bimekizumab because of adverse events (AEs), whereas 1 (1.4%) subject interrupted treatment with brodalumab because of AEs. Treatment outcomes, including mean PASI and BSA, PASI90 and PASI100 responses, reported AEs, and data on treatment discontinuation are summarized in Table 1.
Discussion
Recent knowledge on psoriasis pathogenesis has suggested the IL-23/Th17 axis as the key immune pathway [31]. As regards the IL-17, there are six subunits (A–F) [32, 33]. Among these, IL-17A and IL-17F represent the most studied. IL-17A exists as a homodimer or as a heterodimer with IL-17F, binding to an IL-17 receptor comprising IL-17RA and IL-17RC, resulting in the activation of multiple and complex pathways [32, 33]. Four drugs targeting IL-17 are currently approved for psoriasis management: secukinumab, ixekizumab, bimekizumab, and brodalumab.
Bimekizumab and brodalumab are characterized by a different mechanism of action than the other anti-IL-17s which target IL-17A. Indeed, brodalumab acts on IL-17RA and blocks the biological activities of the pro-inflammatory cytokines IL-17A, IL-17F, and IL-17A/F whereas bimekizumab acts on IL-17A, IL-17F, and IL-17AF cytokines, effectively blocking their interaction with the IL-17RA/IL-17RC receptor complex [12, 13].
Currently, although real-life data on the efficacy and safety of bimekizumab and brodalumab have been reported, real-life data comparing these two drugs are absent. However, these data are mandatory to evaluate whether a different target of the same IL can be correlated with a different profile in terms of effectiveness and safety. Moreover, it should be underlined that bimekizumab and brodalumab stood out as the psoriasis treatments with the fastest onset of action, delivering quicker therapeutic responses compared to other drugs acting on the IL-17 [34].
Our study was the first to indirectly compare the effectiveness and safety of these drugs, investigating their use in patients undergoing treatment for at least 16 weeks. Our experience confirmed the high efficacy of both bimekizumab and brodalumab treatments, showing significant reduction of PASI and BSA at each follow-up (p < 0.0001), reaching PASI100 in 73.6% and 66.7% of patients receiving bimekizumab and brodalumab at week 36, respectively.
At baseline, the two cohorts of our study were comparable in terms of demographic and clinical data, including psoriasis severity, except for mean duration of psoriasis (p < 0.001), previous use of etanercept (p < 0.05) and ustekinumab (p < 0.05), which were significantly higher in the brodalumab cohort, whereas guselkumab failure was more common in the bimekizumab group (p < 0.05).
Regarding clinical outcomes, both treatments resulted in highly effective treatment of psoriasis. However, the percentage of patients achieving PASI100 response at weeks 4 and 16 was significantly higher in the bimekizumab cohort (p < 0.05). A slightly higher percentage of PASI90 was noted for bimekizumab at each follow-up, however without approaching statistical significance. These data suggest that bimekizumab is the fastest anti-IL-17 in terms of PASI90/100 achievement time.
Moreover, the discontinuation rate for ineffectiveness was lower for bimekizumab than brodalumab (8.3% vs 3.8%), without being statistically significant.
Our results also confirmed the safety profiles of bimekizumab and brodalumab. In particular, although a higher percentage of candidiasis and eczematous reactions have been reported in the bimekizumab cohort (candidiasis: 7.5% vs 1.4%; eczematous reactions: 3.8% vs 0%), no significant differences were detected, with only 5.7% and 1.4% of patients discontinuing therapy because of AEs.
Strengths and Limitations
The main strengths of the study are data accuracy, the homogeneous evaluation, and the comparability of baseline features of the study cohorts.
Major limitations of the study are the retrospective design, the limited number of patients in the study population, the limited follow-up (36 weeks), and a different sample size between bimekizumab and brodalumab groups.
Conclusion
Our study confirmed the efficacy and safety of both bimekizumab and brodalumab, up to 36 weeks of treatment. Although both drugs showed a significant improvement of both investigated scores (PASI and BSA) from week 4, some differences in terms of PASI90 and PASI100 responses (higher for bimekizumab at each follow-up, with only PASI100 response significantly higher at weeks 4 and 16) were registered. These differences seem to support the hypothesis that bimekizumab is the better-performing anti-IL-17 in terms of treatment response time for PASI100 achievement. In terms of AEs, a higher rate of candidiasis and eczematous reactions in the bimekizumab cohort, without statistical significance, was observed while discontinuation for inefficacy was higher for brodalumab, without statistical significance.
To the best of our knowledge, this is the first study evaluating and comparing bimekizumab and brodalumab in real-life settings. Certainly, more data are needed to confirm our results, with a larger study population to better evaluate any differences among these drugs.
Acknowledgements
We thank the participants of the study.
Author Contributions
Luca Potestio: conceptualization; methodology; validation; formal analysis; investigation; resources; data curation; writing—original draft; writing—review and editing; visualization; supervision; project administration; funding acquisition. Fabrizio Martora: conceptualization; methodology; validation; investigation; writing—review and editing; visualization. Flavia Raia: conceptualization; methodology; validation; investigation; writing—review and editing; visualization. Gioacchino Lucagnano: conceptualization; methodology; validation; investigation; writing—review and editing; visualization. Claudio Brescia: conceptualization; methodology; validation; investigation; writing—review and editing; visualization. Ginevra Torta: conceptualization; methodology; validation; investigation; writing—review and editing; visualization. Matteo Megna: conceptualization; methodology; validation; formal analysis; investigation; resources; data curation; writing—original draft; writing—review and editing; visualization; supervision; project administration; funding acquisition. Maria Esposito. All authors read and approved the final version of the manuscript.
Funding
No funding was received for this study or the publication of this article.
Data Availability
Data that support the findings of this study are available from the corresponding author, upon reasonable request.
Declarations
Conflict of Interest
Luca Potestio, Fabrizio Martora, Flavia Raia, Gioacchino Lucagnano, Claudio Brescia, Ginevra Torta, and Matteo Megna confirm that they have no conflicts of interest to declare.
Ethical Approval
The present study was conducted respecting the Declaration of Helsinki, and all patients signed an informed consent before starting the study. The patients in this manuscript have given written informed consent to publication of their case details.
References
- 1.Boehncke WH, Schön MP. Psoriasis. Lancet. 2015;386(9997):983–94. 10.1016/S0140-6736(14)61909-7. [DOI] [PubMed] [Google Scholar]
- 2.Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet. 2007;370(9583):263–71. 10.1016/S0140-6736(07)61128-3. [DOI] [PubMed] [Google Scholar]
- 3.Langley RG, Krueger GG, Griffiths CE. Psoriasis: epidemiology, clinical features, and quality of life. Ann Rheum Dis. 2005;64(Suppl 2):ii18–25. 10.1136/ard.2004.033217. [DOI] [PMC free article] [PubMed]
- 4.Armstrong AW, Read C. Pathophysiology, clinical presentation, and treatment of psoriasis: a review. JAMA. 2020;323(19):1945–60. 10.1001/jama.2020.4006. [DOI] [PubMed] [Google Scholar]
- 5.Camela E, Potestio L, Fabbrocini G, Ruggiero A, Megna M. New frontiers in personalized medicine in psoriasis. Expert Opin Biol Ther. 2022;22(12):1431–3. 10.1080/14712598.2022.2113872. [DOI] [PubMed] [Google Scholar]
- 6.Armstrong AW, Puig L, Joshi A, et al. Comparison of biologics and oral treatments for plaque psoriasis: a meta-analysis. JAMA Dermatol. 2020;156(3):258–69. 10.1001/jamadermatol.2019.4029. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Nast A, Smith C, Spuls PI, et al. EuroGuiDerm guideline on the systemic treatment of psoriasis vulgaris—Part 1: treatment and monitoring recommendations. J Eur Acad Dermatol Venereol. 2020;34(11):2461–98. 10.1111/jdv.16915. [DOI] [PubMed] [Google Scholar]
- 8.Nast A, Smith C, Spuls PI, et al. EuroGuiDerm guideline on the systemic treatment of psoriasis vulgaris—Part 2: specific clinical and comorbid situations. J Eur Acad Dermatol Venereol. 2021;35(2):281–317. 10.1111/jdv.16926. [DOI] [PubMed] [Google Scholar]
- 9.Carrascosa JM, Del-Alcazar E. New therapies versus first-generation biologic drugs in psoriasis: a review of adverse events and their management. Expert Rev Clin Immunol. 2018;14(4):259–73. 10.1080/1744666X.2018.1454835. [DOI] [PubMed] [Google Scholar]
- 10.Ten Bergen LL, Petrovic A, Krogh Aarebrot A, Appel S. The TNF/IL-23/IL-17 axis-head-to-head trials comparing different biologics in psoriasis treatment. Scand J Immunol. 2020;92(4):e12946. 10.1111/sji.12946. [DOI] [PubMed] [Google Scholar]
- 11.Ly K, Smith MP, Thibodeaux Q, Reddy V, Liao W, Bhutani T. Anti IL-17 in psoriasis. Expert Rev Clin Immunol. 2019;15(11):1185–94. 10.1080/1744666X.2020.1679625. [DOI] [PubMed] [Google Scholar]
- 12.Farahnik B, Beroukhim K, Abrouk M, et al. Brodalumab for the treatment of psoriasis: a review of phase III trials. Dermatol Ther (Heidelb). 2016;6(2):111–24. 10.1007/s13555-016-0121-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Ruggiero A, Potestio L, Martora F, Villani A, Comune R, Megna M. Bimekizumab treatment in patients with moderate to severe plaque psoriasis: a drug safety evaluation. Expert Opin Drug Saf. 2023;22(5):355–62. 10.1080/14740338.2023.2218086. [DOI] [PubMed] [Google Scholar]
- 14.Gordon KB, Foley P, Krueger JG, et al. Bimekizumab efficacy and safety in moderate to severe plaque psoriasis (BE READY): a multicentre, double-blind, placebo-controlled, randomised withdrawal phase 3 trial [published correction appears in Lancet. 2021 Mar 27;397(10280):1182. 10.1016/S0140-6736(21)00669-3]. Lancet. 2021;397(10273):475–86. 10.1016/S0140-6736(21)00126-4. [DOI] [PubMed]
- 15.Thaçi D, Vender R, de Rie MA, et al. Safety and efficacy of bimekizumab through 2 years in patients with moderate-to-severe plaque psoriasis: longer-term results from the BE SURE randomized controlled trial and the open-label extension from the BE BRIGHT trial. Br J Dermatol. 2023;188(1):22–31. 10.1093/bjd/ljac021. [DOI] [PubMed] [Google Scholar]
- 16.Strober B, Paul C, Blauvelt A, et al. Bimekizumab efficacy and safety in patients with moderate to severe plaque psoriasis: two-year interim results from the open-label extension of the randomized BE RADIANT phase 3b trial. J Am Acad Dermatol. 2023;89(3):486–95. 10.1016/j.jaad.2023.04.063. [DOI] [PubMed] [Google Scholar]
- 17.Reich K, Papp KA, Blauvelt A, et al. Bimekizumab versus ustekinumab for the treatment of moderate to severe plaque psoriasis (BE VIVID): efficacy and safety from a 52-week, multicentre, double-blind, active comparator and placebo controlled phase 3 trial [published correction appears in Lancet. 2021 Feb 20;397(10275):670. 10.1016/S0140-6736(21)00387-1]. Lancet. 2021;397(10273):487–98. 10.1016/S0140-6736(21)00125-2. [DOI] [PubMed]
- 18.Potestio L, Ruggiero A, Martora F, Megna M. Long-term efficacy and safety of bimekizumab in real-world setting: a 52-week prospective study. Arch Dermatol Res. 2024;317(1):102. 10.1007/s00403-024-03594-w. [DOI] [PubMed] [Google Scholar]
- 19.Megna M, Orsini D, Assorgi C, et al. The risk of candidiasis during treatment with bimekizumab for the management of plaque psoriasis: a 16-week multicenter real-world experience—IL PSO (Italian Landscape Psoriasis). Clin Exp Dermatol. 2024. 10.1093/ced/llae400. [DOI] [PubMed] [Google Scholar]
- 20.Orsini D, Megna M, Assorgi C, et al. Efficacy and Safety of bimekizumab in elderly patients: real-world multicenter retrospective study—IL PSO (Italian Landscape Psoriasis). J Dermatol Treat. 2024;35(1):2393376. 10.1080/09546634.2024.2393376. [DOI] [PubMed] [Google Scholar]
- 21.Gargiulo L, Narcisi A, Ibba L, et al. Effectiveness and safety of bimekizumab for the treatment of plaque psoriasis: a real-life multicenter study-IL PSO (Italian landscape psoriasis). Front Med (Lausanne). 2023;10:1243843. 10.3389/fmed.2023.1243843. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Megna M, Battista T, Potestio L, et al. A case of erythrodermic psoriasis rapidly and successfully treated with bimekizumab. J Cosmet Dermatol. 2023;22(3):1146–8. 10.1111/jocd.15543. [DOI] [PubMed] [Google Scholar]
- 23.Orsini D, Malagoli P, Balato A, et al. Bimekizumab for the treatment of plaque psoriasis with involvement of genitalia: a 16-week multicenter real-world experience—IL PSO (Italian Landscape Psoriasis). Dermatol Pract Concept. 2024;14(2):e2024052. 10.5826/dpc.1402a52. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 24.Campione E, Artosi F, Shumak RG, et al. Fast clinical response of bimekizumab in nail psoriasis: a retrospective multicenter 36-week real-life study. Pharmaceuticals (Basel). 2024;17(10):1378. 10.3390/ph17101378. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.Papp K, Menter A, Leonardi C, et al. Long-term efficacy and safety of brodalumab in psoriasis through 120 weeks and after withdrawal and retreatment: subgroup analysis of a randomized phase III trial (AMAGINE-1). Br J Dermatol. 2020;183(6):1037–48. 10.1111/bjd.19132. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Puig L, Lebwohl M, Bachelez H, Sobell J, Jacobson AA. Long-term efficacy and safety of brodalumab in the treatment of psoriasis: 120-week results from the randomized, double-blind, placebo- and active comparator-controlled phase 3 AMAGINE-2 trial. J Am Acad Dermatol. 2020;82(2):352–9. 10.1016/j.jaad.2019.05.095. [DOI] [PubMed] [Google Scholar]
- 27.Reich K, Iversen L, Puig L, et al. Long-term efficacy and safety of brodalumab in moderate-to-severe plaque psoriasis: a post hoc pooled analysis of AMAGINE-2 and -3. J Eur Acad Dermatol Venereol. 2022;36(8):1275–83. 10.1111/jdv.18068. [DOI] [PubMed] [Google Scholar]
- 28.Cacciapuoti S, Potestio L, Guerrasio G, et al. Effectiveness of brodalumab in patients with moderate-to-severe plaque psoriasis located in difficult-to-treat areas. Clin Cosmet Investig Dermatol. 2023;16:2637–44. 10.2147/CCID.S423234. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 29.Kojanova M, Turkova B, Gkalpakiotis S, et al. Real-world data on brodalumab treatment in patients with moderate-to-severe plaque psoriasis: an observational study from the Czech Republic BIOREP Registry. Adv Ther. 2024;41(10):3951–71. 10.1007/s12325-024-02952-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 30.Caldarola G, Galluzzo M, Bernardini N, et al. Long-term effectiveness of brodalumab for the treatment of moderate-to-severe psoriasis: a real-life multicenter study of up to 3 years in a real-life Italian cohort. Dermatol Pract Concept. 2024;14(2):e2024152. 10.5826/dpc.1402a152. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 31.Potestio L, Martora F, Lauletta G, Vallone Y, Battista T, Megna M. The role of interleukin 23/17 axis in psoriasis management: a comprehensive review of clinical trials. Clin Cosmet Investig Dermatol. 2024;17:829–42. 10.2147/CCID.S462797. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 32.Blauvelt A, Chiricozzi A. The immunologic role of IL-17 in psoriasis and psoriatic arthritis pathogenesis. Clin Rev Allergy Immunol. 2018;55(3):379–90. 10.1007/s12016-018-8702-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 33.Brembilla NC, Senra L, Boehncke WH. The IL-17 family of cytokines in psoriasis: IL-17A and beyond. Front Immunol. 2018;9:1682. 10.3389/fimmu.2018.01682. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 34.Abdin R, Gharib R, Bunick CG, Issa NT. Rapid remission of plaque psoriasis with bimekizumab treatment. J Drugs Dermatol. 2024;23(8):694–6. 10.36849/JDD.8381. [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
Data that support the findings of this study are available from the corresponding author, upon reasonable request.