Karla Machlab, MD1; Jensen Yeung, MD, FRCPC2,3; Melinda Gooderham, MSc, MD, FRCPC4-6

1Department of Medicine, University of Toronto, ON, Canada
2Division of Dermatology, Department of Medicine, University of Toronto, ON, Canada
3Department of Dermatology, Women’s College Hospital, Toronto, ON, Canada
4Probity Medical Research, Peterborough, ON, Canada
5SKiN Center for Dermatology, Peterborough, ON, Canada
6Queen’s University, Kingston, ON, Canada

Conflict of interest: Karla Machlab has no conflicts of interest. Jensen Yeung has served as an investigator, speaker, and/or advisory board member for, and/or received grants/honoraria from: AbbVie, Amgen, Anacor, Astellas, Arcutis, Bausch Health, Baxalta, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Centocor, Coherus, Dermira, Eli Lilly, Forward, Galderma, Incyte, Janssen, Leo Pharma, MedImmune, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi Genzyme, Sun Pharma, Takeda, UCB, and Xenon. Melinda Gooderham serves as the Vice President of the Dermatology Association of Ontario and has served as an investigator, speaker, advisor and/or consultant for, and/or received grants/honoraria from: AbbVie, Akros, Amgen, Arcutis, Aslan, Aristea, AnaptysBio, Bausch Health, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Coherus, Dermira, Dermavant, Eli Lilly, Galderma, GlaxoSmithKline, Incyte, Janssen, Kyowa Kirin, Leo Pharma, MedImmune, Meiji, Merck, Moonlake, Nimbus, Novartis, Pfizer, Regeneron, Reistone, Sanofi Genzyme, Sun Pharma, and UCB. Funding sources: None.

Abstract: Psoriatic arthritis (PsA) is a chronic inflammatory musculoskeletal disease associated with psoriasis. Its major clinical domains include peripheral and axial arthritis, enthesitis, dactylitis and skin and nail involvement. Approximately 30% of patients with psoriasis develop psoriatic arthritis. The pathophysiology of PsA is complex and involves a dysregulated immune response. In particular, interleukin (IL)-23 is a major regulatory cytokine that has been implicated in PsA, including bone remodeling, enthesitis, synovitis and psoriatic lesions. Risankizumab is a humanized immunoglobulin G1 monoclonal antibody that targets the p19 subunit of IL-23. It has been approved for the treatment of moderate-to-severe plaque psoriasis and, more recently, PsA. The efficacy and safety of risankizumab for the treatment of PsA has been demonstrated in phase 2 and phase 3 clinical trials. Risankizumab showed efficacy in decreasing the number of swollen and tender joints, clearing psoriatic plaque and improving quality of life. Treatment with risankizumab was well-tolerated, with the most common adverse event being upper respiratory tract infection. Overall, the current literature demonstrates that risankizumab is both a safe and effective therapeutic option for the treatment of PsA. Herein, week 24 and 52 results are reviewed.

Keywords: risankizumab, Skyrizi®, IL-23, psoriatic arthritis


Psoriatic arthritis (PsA) is an inflammatory musculoskeletal disease characterized by a range of clinical features including arthritic inflammation, dactylitis, enthesitis, and skin and nail changes. PsA may also be associated with multiple comorbidities including type 2 diabetes, hypertension, metabolic syndrome and cardiovascular disease.1,2 Accordingly, PsA can greatly impair one’s quality of life (QoL) and therefore prompt intervention is crucial.3,4

PsA affects males and females equally with an estimated prevalence of 1-2 in 1000.5 Approximately 30% of patients with psoriasis will develop PsA.6-8sup> Given the high prevalence of PsA, it is important to continue to find effective and safe therapeutic options. This review focuses on the current literature regarding the efficacy and safety of risankizumab for the treatment of PsA up to 52 weeks of treatment.


The pathophysiology of PsA is complex and multifactorial. Although the exact mechanism is not completely understood, genetic and environmental factors interact to trigger immune pathways. PsA is associated with class II major histocompatibility complex (MHC) alleles, including HA-B*27, B*0801, B*3801 and B*3901.9 Risk factors include severe psoriasis, scalp, inverse or nail psoriasis, obesity and trauma (Koebner phenomenon).10 T-cells are major effectors in PsA and the role of CD8+ T-cells is supported by a strong association with HLA-1 alleles.11 Type 17 T-cells, which include CD4+ type 17 helper T (Th17) cells, and type 3 innate lymphocytes, which produce interleukin (IL)-17 and IL-22, are increased in synovial fluid in patients with PsA.12

IL-23/IL-17 and tumor necrosis factor (TNF) pathways also play a central role and contribute to most domains of PsA, including synovitis, enthesitis, axial inflammation and psoriatic plaques. Dendritic cells produce IL-23, which triggers the differentiation and proliferation of Th17 cells, and activates other cytokine pathways including IL-17, IL-22 and TNF-α.13 These subsequently activate downstream effector cells, including keratinocytes, fibroblasts, osteoclast precursors, B-cells and macrophages. An inflammatory immune response is initiated resulting in keratinocyte proliferation, bone erosion and pathologic bone formation. Murine models have shown that administration of IL-23 leads to entheseal inflammation, inflammatory arthritis, bone erosion, periosteal bone formation, and increased production of IL-17.14,15

Overview of Therapy

Treatment of PsA is initially guided by severity of disease and, importantly, the degree of activity in each of the domains. Mild PsA can be managed with non-steroidal anti-inflammatory drugs (NSAIDs) or intra-articular steroids. However, in moderateto- severe PsA, conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) such as methotrexate, leflunomide or sulfasalazine are typically used first line. Newer novel agents, such as phosphodiesterase-4 (PDE4) inhibitors, Janus kinase (JAK) inhibitors, and biologic DMARDs (bDMARDs) are also approved efficacious agents. Biologics include TNF, IL-17, and IL-12/23 or IL-23 inhibitors.

TNF inhibitors were previously considered gold standard and are effective at improving clinical signs and symptoms of PsA and reducing radiographic progression of disease.16 Currently, five TNF inhibitors (etanercept, adalimumab, golimumab, certolizumab and infliximab) are approved for the treatment of PsA. The efficacy and safety of these agents are comparable;17,18 ultimately, the choice of agent depends on factors such as patient preference for route and frequency of administration, physician experience, availability, and cost. Patients must be screened for latent tuberculosis and hepatitis B virus (HBV) infections and treated prophylactically if there is evidence of current or prior infection.19 Moreover, TNF inhibitors are contraindicated in patients with significant heart failure, recent malignancy or a family history of multiple sclerosis.20,21 Newer classes of biologics have also been approved for the treatment of PsA and these include cytokine inhibitors anti-IL-17 (secukinumab and ixekizumab), anti-IL-12/23 (ustekinumab), and anti-IL-23 (guselkumab and risankizumab). These cytokine inhibitors have proven to be effective in treating PsA and are especially useful in patients who have contraindications to TNF inhibitors, but caution should be exercised with IL-17 inhibitors in patients with a history of inflammatory bowel disease.

Risankizumab for the Treatment of Psoriasis

Risankizumab is a humanized immunoglobulin G1 (IgG1) monoclonal antibody that targets the p19 subunit of IL-23. In 2019, it was approved for the treatment of moderate-to-severe plaque psoriasis. Administration follows a dosing schedule of 150 mg at week 0, week 4, and then every 12 weeks thereafter. Several clinical trials have established its ability to treat psoriasis with high efficacy and safety compared to biologics from each of the other classes. Two randomized, double-blinded phase 3 trials, UltIMMA-1 (n = 506) and UltIMMa-2 (n = 491), showed that risankizumab has significantly greater efficacy than ustekinumab and placebo.22 Skin clearance was seen as early as 4 weeks of treatment. Treatmentrelated adverse events (TEAEs) were comparable across all groups. Risankizumab was also proven superior to adalimumab in the phase 3 trial IMMvent (n = 605) where subjects were randomly assigned to a standard dosing regimen of risankizumab or adalimumab.23 Efficacy was measured by the Psoriasis Area and Severity Index (PASI) and after 16 weeks of treatment 70% of patients on risankizumab achieved a 90% decrease in their PASI score from baseline (PASI90), compared to 44% those on adalimumab. In the phase 3b trial IMMerge, risankizumab was found to be superior to secukinumab at week 52 with PASI90 rates of 86.6% for risankizumab versus 57.1% for secukinumab.24 These head-to-head studies have demonstrated risankizumab’s superior efficacy for plaque psoriasis when compared to adalimumab, ustekinumab and secukinumab.

Risankizumab for the Treatment of PsA

Given the critical role that IL-23 plays in the pathogenesis, risankizumab is an important therapeutic option for PsA. In a phase 2 trial, 185 subjects with active PsA were randomized into five groups: risankizumab 150 mg at week 0, 4, 8, 12 and 16 (arm 1); risankizumab 150 mg at week 0, 4 and 16 (arm 2); risankizumab at week 0 and 12 (arm 3); risankizumab 75 mg at week 0 (arm 4), or placebo.25 The primary endpoint at week 16 was American College of Rheumatology 20 (ACR20) response. ACR20 is a composite measure defined as a 20% improvement from baseline in the number of tender and swollen joints, and a 20% improvement in three or more of five variables: patient-assessed global activity, evaluator-assessed global activity, patient pain activity, functional disability, and acute phase response (ESR or CRP). Secondary endpoints included ACR50/70, dactylitis count, Spondyloarthritis Research Consortium of Canada (SPARCC) enthesitis index, and health assessment questionnaire and disability index (HAQDI), a questionnaire designed to evaluate functional status and QoL in patients with arthritis. After 16 weeks of treatment, ACR20 was significantly higher across all treatment arms (57.1- 65.0%) compared to placebo (35.7%). ACR50 was higher across all treatment arms, and significant in arm 3 (39%) compared to placebo (12%). ACR70 was also higher across all treatment arms, and significant in arms 1, 1+2, 3 and 4 (14.3-25.6%) compared to placebo (0.0%). PASI75/90/100 responses were also significantly greater in all treatment groups (PASI75: 67-75%, PASI90: 52- 67%; PASI100: 33-56%) compared to placebo (10%; 10%; 7%, respectively). Dactylitis counts were similar across all groups, and improvements in enthesitis and HAQ-DI were greater in treatment groups compared to placebo but not statistically significant. Of the 185 subjects enrolled in the study, 145 continued in a 52-week single arm open-label extension (OLE). Subjects received 150 mg of risankizumab every 12 weeks for 36 weeks and continued to respond positively over all efficacy measures during this period. TEAEs were comparable in all arms and were similar in the 24- week study and OLE. Approximately 60% of subjects experienced a TEAE, with the most common being viral upper respiratory tract infection (11%). There was one serious adverse event (SAE) reported, but no malignancies, deaths or active cases of tuberculosis. Overall, risankizumab was well-tolerated and only 3.4% of patients discontinued due to side effects.

Notably, risankizumab was not found to be effective in the treatment of ankylosing spondylitis (AS)26 in a double-blinded phase 2 study. In this trial, 159 subjects were randomized to four treatment groups (risankizumab 18 mg one dose at week 0; risankizumab 90 or 180 mg at week 0, 8, 16 and 24; and placebo) over a 24-week period. The primary endpoint was Ankylosing Spondylitis Disease Activity Score (ASDAS) 40, a composite measure defined as a 40% improvement from baseline in three or more out of four variables: back pain, peripheral pain and swelling, duration of morning stiffness and patient global assessment. After 12 weeks of treatment, risankizumab failed to meet the primary endpoint as ASDAS40 responses were comparable and non-significant in treatment groups (15.0-25.0%) and placebo (17.5%). Similarly, in three multicentered, randomized, placebo-controlled studies, patients with AS were treated with ustekinumab.22 However, ustekinumab also did not demonstrate clinical efficacy in treating AS, as it failed to meet both primary and secondary endpoints including Assessment in Ankylosing Spondylitis (ASAS)20/40. These studies support the hypothesis that axial disease is driven by different mechanisms that are less reliant on IL-23.27,28

Development Program for PsA

Pivotal phase 3 studies of risankizumab in PsA are currently ongoing. Two randomized, double-blinded studies compare risankizumab to placebo in subjects with active PsA who have failed to respond to at least one csDMARD (KEEPsAKE-1, NCT03675308) or bDMARD (KEEPsAKE-2, NCT03671148).29,30 Subjects were randomized 1:1 to the treatment group (risankizumab at week 0, 4, 16 or 24) or placebo for a 24-week period. The study design for these trials is shown in Figure 1.

Risankizumab in Adults with Psoriatic Arthritis - image
Figure 1. KEEPsAKE-1 and KEEPsAKE-2 study design. Patients were randomized into a treatment group (risankizumab [RZB] 150 mg at week 0, 4, 16 or 24) or placebo for a 24-week period. At week 16, patients were classified as non-responders if they did not achieve a 20% or more improvement in their tender joint count and/or swollen joint count at weeks 12 and 16. Non-responders were given the option to change or add concomitant therapy, and were discontinued from the study drug at 36 weeks. Patients were given the choice to enroll in an open label extension for a total of a 208-week period. csDMARD-IR, conventional systemic disease-modifying antirheumatic drug inadequate responder.
The primary endpoint of ACR20 was assessed after 24 weeks, and key secondary endpoints included ACR50/70, HAQ-DI, PASI90, and minimal disease activity (MDA) index as well as resolution of enthesitis and dactylitis (Table 1a). In KEEPsAKE-1, ACR20/50/70 response rates were significantly higher in subjects on risankizumab (57/33/15%) compared to those in the placebo group (34/11/5%) (Figure 2). Subjects receiving risankizumab achieved greater resolution of enthesitis at week 24 (risankizumab: 51%, placebo: 37%) and dactylitis (risankizumab: 67%, placebo: 54%) as well as a greater change from baseline in HAQ-DI compared to placebo (risankizumab: -0.31, placebo: -0.11). Significantly higher response rates were also observed with PASI90 and MDA for subjects on risankizumab (PASI90: 52%; MDA: 25%) compared to placebo (10%; 10%).

Risankizumab in Adults with Psoriatic Arthritis - image
Figure 2. Proportion of patients (%) on risankizumab or placebo achieving ACR20/50/70 response at week 24 (Period 1) and week 52 (Period 1 and 2); *p<0.001.

Similarly in KEEPsAKE-2, ACR20/50/70 response rates at week 24 were significantly higher with risankizumab (risankizumab: 51/26/12%; placebo:27/9/6%) (Figure 3). Subjects in the treatment group achieved greater resolution of enthesitis at week 24 (risankizumab: 43%, placebo: 30%) and dactylitis (risankizumab: 73%, placebo: 42%) and a greater change from baseline in HAQ-DI (risankizumab: -0.22; placebo: -0.05). In addition, PASI90 and MDA response rates were significantly higher with treatment (PASI90: 55%; MDA: 26%) compared to placebo (10%; 11%). Overall, in both trials, risankizumab produced more favorable outcomes in reducing disease activity, the number of affected joints, as well as improving psoriasis clearance and QoL.

Risankizumab in Adults with Psoriatic Arthritis - image
Figure 3. Proportion of patients (%) on risankizumab or placebo achieving ACR20/50/70 response at week 24 (Period 1) and week 52 (Period 1 and 2); *p<0.001, †p<0.05.

After week 24, patients continued in an open label extension (OLE, Period 2) and received risankizumab 150 mg every 12 weeks until week 208. ACR 20/50/70 rates continued to improve to week 52 in KEEPsAKE-1 (risankizumab: 70/43/26% and placebo to risankizumab: 63/37/20%) and KEEPsAKE-2 (risankizumab: 59/32/17% and placebo to risankizumab: 56/32/21%) (Table 1b). Pooled data from both studies showed resolution of enthesitis in 55% of patients receiving risankizumab from baseline and in 57% of patients who transitioned from placebo to risankizumab in Period 2. Similarly, pooled data for resolution of dactylitis was reported in 76% of risankizumab patients and 73% of placebo to risankizumab patients in Period 2. The mean change in HAQ-DI at week 52 was -0.41 and -0.32 in risankizumab and placebo to risankizumab, respectively, in KEEPSaKE-1 and -0.26 and -0.34 in risankizumab and placebo to risankizumab, respectively, in KEEPSaKE-2. PASI90 responses were stable (risankizumab: 68% and placebo to risankizumab: 60%) in KEEPSaKE-1 and (risankizumab: 64% and placebo to risankizumab: 60%) in KEEPSaKE-2. The proportion of patients achieving MDA improved through week 52 (risankizumab: 38% and placebo to risankizumab: 27%) in KEEPSaKE-1 and (risankizumab: 27% and placebo to risankizumab: 34%) in KEEPSaKE-2 (Table 1b).

Adverse events were similar across all groups as of the data cut-off for week 52 analysis. By week 24, serious infection was reported in 2.7-2.9 events per 100 patient years (E/100PYs) of patients on risankizumab and did not increase in the long-term 52-week analysis (2.8 and 2.0E/100PY in KEEPsAKE-1 and -2, respectively). Serious TEAEs also did not increase from week 24 with 7.4E/100PY in KEEPsAKE-1 and 9.4E/100PY in KEEPSaKE-2 in the long-term. There were no reports of active tuberculosis or anaphylaxis in either study, but there was one case of oropharyngeal candidiasis in each study. There were no deaths in KEEPsAKE-2 but there were two deaths in KEEPsAKE-1; an 81-year-old male with dementia who was hospitalized with pneumonia and died of urosepsis and a 41-year-old male experienced sudden death on day 502. There were no reports of major cardiovascular events in KEEPsAKE-1 and three events in KEEPsAKE-2 which were reported as a non-fatal stroke in a patient with a history of hypertension and two non-fatal myocardial infarctions in patients with risk factors. Once again, risankizumab proved to be well-tolerated and discontinuation due to adverse events was low and occurred in 2.3E/100PY in KEEPSaKE-1 and 1.6E/100PY in KEEPSaKE-2.

Future Outlook

PsA is a multi-faceted, complex disease affecting multiple domains including skin, entheses, peripheral and axial joints. Although there are currently many options for treatment, there remains an unmet need for more efficacious and safer options. The addition of IL-23 inhibitors to the therapeutic landscape is welcomed given their tolerability, safety, and convenience of use. Conventional treatments for PsA including methotrexate, sulfasalazine, and leflunomide are burdened with tolerability issues, adverse effects, and end-organ toxicity. Newer oral agents also present challenges. Apremilast provides modest benefit but has issues with gastrointestinal intolerance and headaches. The JAK inhibitors are efficacious but have a boxed warning for serious infection and venous thromboembolism; more recent warnings for tofacitinib of cardiovascular events and malignancy, based on results from the ORAL Surveillance study,31 may make their use unsuitable in high-risk patients. The strength of IL-23 inhibition is the proven safety of this class in the psoriatic population. There is no signal for tuberculosis or other serious infections and can safely be used in patients with other comorbidities such as cardiac, renal, or hepatic disease. The convenient dosing schedule of injections as frequent as every 8 weeks to as infrequent as every 12 weeks will contribute favorably to QoL for patients by reducing the treatment burden and improving adherence. The current agents approved for use in PsA to target IL-23 are guselkumab, risankizumab and ustekinumab.

Risankizumab provides efficacy similar to that of other biologic agents for PsA, however the effect may take longer as we have not observed the early responses seen with other agents such as JAK inhibitors or IL-17 blocking agents. Guselkumab has shown in a network meta-analysis to have efficacy similar to IL-17 and TNF-α inhibiting biologic therapies supporting the important role of blocking IL-23 in the management of PsA.32 For patients with a prominent skin domain, targeting IL-23 may be preferred as it is very effective at clearing the skin in the majority of patients. Limiting its use will be the lack of efficacy in AS and further research will be required to understand the impact of risankizumab on axial PsA.


When choosing a treatment for PsA, ACR scores only tell part of the story, and we need to consider other disease measures such as enthesitis, dactylitis and QoL scores such as HAQ-DI, which were all shown to be significantly improved with risankizumab compared to baseline. Risankizumab has the potential to offer a treatment with a combination of efficacy, safety, convenience and overall improvement in QoL. However, more data is required and the complete long-term 208-week results from clinical studies for the management of PsA are eagerly anticipated.


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