Risankizumab: A Review in Moderate to Severe Plaque Psoriasis

Blair, Hannah A.

doi:10.1007/s40265-020-01357-1

Cited by 24 publications

(19 citation statements)

References 36 publications

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“…Biologic therapies, such as secukinumab, an anti-interleukin (IL) 17A monoclonal antibody, have been highly effective in the management of resistant palmoplantar psoriasis, as shown in the 2PRECISE randomized controlled trial [ 3 ] and GESTURE trial [ 4 ]. Risankizumab, another biologic therapy, is a humanized immunoglobulin (Ig) G1 monoclonal antibody that targets the p19 subunit of IL-23 [ 5 ]. Risankizumab has been FDA approved since 2019 for the treatment of moderate to severe plaque psoriasis in adult patients, who are candidates for systemic therapy or phototherapy [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Palmoplantar Psoriasis Successfully Treated With Risankizumab

Alajlan¹,

Qadoumi²

2021

Cureus

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Palmoplantar psoriasis is a variant of psoriasis that affects the palms and soles. Despite the small body surface area affected, palmoplantar psoriasis can have significant implications on a patient’s mental health, justifying the urgency in treating this condition. Palmoplantar psoriasis is also known to be challenging to treat. In this case report, we present a male who presented with a 15-year history of psoriasis with significant palmoplantar involvement, managed with topical and systemic therapies, achieving a minimal response. After trying other therapies including acitretin and adalimumab, we eventually started the patient on risankizumab, an anti-IL-23 antibody. Following the fourth dose of risankizumab, the patient’s palmoplantar lesions completely resolved. We further discuss why risankizumab may be considered a treatment option in resistant palmoplantar psoriasis cases.

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Section: Introductionmentioning

confidence: 99%

Palmoplantar Psoriasis Successfully Treated With Risankizumab

Alajlan¹,

Qadoumi²

2021

Cureus

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“…Certolizumab is the anti‐TNFa biologic and about 50% of patients reach PASI-90 after a long-term treatment 38 . Risankizumab is a humanized monoclonal antibody that specifically targets interleukin (IL)-23 and around 50% patients treated with subcutaneous risankizumab show a clear skin 39 . Thus, although some patients have benefited, a significant portion of patients still cannot reach a completely clear skin even after extensive treatment with newest biologics.…”

Section: Discussionmentioning

confidence: 99%

The endoribonuclease N4BP1 prevents psoriasis by controlling both keratinocytes proliferation and neutrophil infiltration

Gou

et al. 2021

Cell Death Dis

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Psoriasis is a common chronic skin disease, characterized by abnormal interplay between hyperproliferative epidermal keratinocytes and self-reactive immune cells with not fully addressed molecular mechanism. N4BP1 (NEDD4-binding protein 1) is considered as an immune regulator for a long time but its physiological role is not determined yet. Here, we found that the expression of N4BP1 in skin was highest among all 54 tested tissues, and its expression was further upregulated in psoriatic skin. N4BP1-deficient mice exhibited normal grossly, but developed severe and prolonged IMQ-induced psoriasis-like disease comparing to controls. N4BP1 mainly expressed in keratinocytes and located on nucleus. Up- but not downregulated genes in N4BP1-deficient skin were specifically enriched in keratinocyte proliferation and differentiation. The proliferation of N4BP1-deficient primary keratinocytes was faster compared to that of controls. The upregulated genes upon ablation of N4BP1 were highly enriched in targets of AP-1 transcription factor. Knocking out N4BP1 resulted in upregulation of JunB and FosB, and conversely, overexpression of N4BP1 greatly reduced their expression. Furthermore, N4BP1 binds with JunB and FosB encoding mRNAs and greatly reduces their stability. In addition, with a high expression in neutrophils, N4BP1 limits survival of neutrophils in blood and infiltration of neutrophils in psoriatic skin by targeting CXCL1, CCL20, and S100A8. These findings demonstrate that N4BP1 controls the proper function of keratinocytes and neutrophils by negatively regulating JunB, FosB, and CXCL1, respectively, and that is critical for psoriasis prevention.

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“…In contrast, ustekinumab targets the p40 subunit shared by IL-12 and IL-23. Except for infliximab, which is administered via intravenous infusion, all the biologics currently used for psoriasis are administered subcutaneously [ 148 , 149 , 150 , 151 , 152 ]. Compared with the small-molecule drugs, these biologics demonstrate an improved efficacy.…”

Section: Mechanisms Of the Current Therapies For Psoriasismentioning

confidence: 99%

Therapeutic Development Based on the Immunopathogenic Mechanisms of Psoriasis

et al. 2021

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Psoriasis, a complex inflammatory autoimmune skin disorder that affects 2–3% of the global population, is thought to be genetically predetermined and induced by environmental and immunological factors. In the past decades, basic and clinical studies have significantly expanded knowledge on the molecular, cellular, and immunological mechanisms underlying the pathogenesis of psoriasis. Based on these pathogenic mechanisms, the current disease model emphasizes the role of aberrant Th1 and Th17 responses. Th1 and Th17 immune responses are regulated by a complex network of different cytokines, including TNF-α, IL-17, and IL-23; signal transduction pathways downstream to the cytokine receptors; and various activated transcription factors, including NF-κB, interferon regulatory factors (IRFs), and signal transducer and activator of transcriptions (STATs). The biologics developed to specifically target the cytokines have achieved a better efficacy and safety for the systemic management of psoriasis compared with traditional treatments. Nevertheless, the current therapeutics can only alleviate the symptoms; there is still no cure for psoriasis. Therefore, the development of more effective, safe, and affordable therapeutics for psoriasis is important. In this review, we discussed the current trend of therapeutic development for psoriasis based on the recent discoveries in the immune modulation of the inflammatory response in psoriasis.

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Risankizumab: A Review in Moderate to Severe Plaque Psoriasis

Cited by 24 publications

References 36 publications

Palmoplantar Psoriasis Successfully Treated With Risankizumab

Palmoplantar Psoriasis Successfully Treated With Risankizumab

The endoribonuclease N4BP1 prevents psoriasis by controlling both keratinocytes proliferation and neutrophil infiltration

Therapeutic Development Based on the Immunopathogenic Mechanisms of Psoriasis

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