From the Masterclasses in Dermatology 2024 Meeting: Updates in Psoriasis Treatments

J Clin Aesthet Dermatol. 2025;18(2):16–22.

by Beth Childs, MS*; Sarah Romanelli, BS*; Joseph F. Merola, MD, MMSc**;
and Alice B. Gottlieb, MD, PhD**
Ms. Childs and Dr. Merola are with the Department of Dermatology and Department of Medicine, Division of Rheumatology at UT Southwestern Medical Center in Dallas, Texas. Ms. Romanelli and Dr. Gottlieb are with the Department of Dermatology and Department of Medicine, Division of Rheumatology at Icahn School of Medicine at Mount Sinai in New York, New York.

*Ms. Childs and Ms. Romanelli share co-primary authorship of this article.

**Drs. Merola and Gottlieb share co-primary senior authorship of this article.

FUNDING: No funding was provided for this article. 

DISCLOSURES: Dr. Merola is a consultant and/or investigator for Amgen, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, AbbVie, Dermavant, Eli Lilly, Incyte, Moonlake, Novartis, Janssen, UCB, Sanofi-Regeneron, Sun Pharma, Biogen, Pfizer and Leo Pharma. Dr. Gottlieb has received honoraria as an advisory board member and consultant for Amgen, AnaptysBio, Avotres Therapeutics, Boehringer Ingelheim, Bristol-Myers Squibb, Dice Therapeutics, Eli Lilly, Highlights Therapeutics, Janssen, Novartis, Sanofi, Teva, UCB, and XBiotech (stock options for a rheumatoid arthritis project); and research/educational grants from Highlights Therapeutics, Bristol-Myers Squibb, Janssen, and UCB Pharma, all paid to Mount Sinai School of Medicine; and has received honoraria as an advisory. Ms. Childs and Romanelli report no conflicts of interest relevant to the content of this article. 

ABSTRACT: Psoriasis (PsO) is an immune-mediated, chronic inflammatory skin disease that significantly impairs quality of life. Its treatment landscape is rapidly evolving, providing better disease control. Here, we highlight updates in biologics, obtaining coverage for biologics under Medicare, the PsO-to-psoriatic arthritis (PsA) transition, and orally administered drugs, as presented at the 2024 Masterclass in Dermatology in Puerto Rico. We provide a concise overview of the evolving therapeutic landscape and its impact on personalized care for patients with PsO. The toolkit of biologics is expanding, with agents that target interleukin (IL)-17 and IL-23 pathways addressing symptoms across multiple disease domains. Interchangeable biosimilars reduce financial barriers to access, particularly for tumor necrosis factor (TNF) inhibitors. An IL-36 receptor antibody, spesolimab, demonstrates efficacy in generalized pustular psoriasis. Further, Medicare has expanded coverage of certain biologics, addressing challenges to treating patients of this population. PsA is an important comorbidity that can significantly reduce quality of life. Recent studies suggest that biologic therapies—including TNF inhibitors, as well as anti-IL-17, anti-IL-23, and anti-IL-12/23 agents—protect against arthritis onset in PsO patients. In addition to traditional modes of delivery, novel formulations address widespread preference for orally administered therapies. Deucravacitinib, a tyrosine kinase (TYK) 2 inhibitor, is highly selective, effective, and safe. Additionally, JNJ-77242113, an investigational IL-23 receptor antagonist, constitutes an orally administered, targeted biologic therapy. Together, these developments are shaping the future for patients with PsO. It is our goal to simplify the complexities of emerging treatment options, offering clinicians a concise and useful guide for patient management.

KEYWORDS: Psoriasis, psoriatic arthritis, biologics, biosimilars, immune-mediated inflammatory disease, IL-17 inhibitors, IL-23 inhibitors

Introduction

Psoriasis (PsO), a chronic inflammatory skin condition, significantly affects patients’ quality of life and often coexists with other systemic conditions such as psoriatic arthritis (PsA), metabolic syndrome, cardiovascular disease and depression. With advancements in the characterization of immune pathways involved in disease pathogenesis, treatment options have expanded beyond conventional therapies to include a variety of targeted biologics and orals. Novel biologic and oral agents, which work by modulating immune responses, have demonstrated efficacy in treating not only the cutaneous symptoms of PsO but also associated systemic manifestations, including PsA. This paper provides an overview of recent developments in biologic therapies, focusing on agents that target interleukin (IL)-17 and IL-23 pathways, as well as updates on biosimilars and interchangeability for tumor necrosis factor (TNF) inhibitors. Furthermore, we discuss novel treatments modalities, such as the oral IL-23 receptor antagonist JNJ-77242113 and the oral TYK2 inhibitor deucravacitinib. By presenting the latest advancements in this field, as presented at the 2024 Masterclasses in Dermatology in Puerto Rico, we aim to offer a practical overview of the evolving therapeutic landscape and its impact on personalized care for psoriasis patients.

Updates in biologic therapies for psoriatic disease

Recent advances in biologic therapies have expanded treatment options for psoriatic disease, with tailored drugs targeting specific cytokines involved in disease pathogenesis. New data highlights the efficacy of IL-17 inhibitors in achieving rapid skin clearance while addressing symptoms of PsA, while IL-23 inhibitors provide promising alternatives for long-term PsO control. Additionally, TNF biosimilars offer cost-effective options. For generalized pustular psoriasis (GPP), IL-36 receptor monoclonal antibodies are emerging as targeted therapies, addressing unmet needs in this subtype.

IL-17 Inhibition. IL-17 inhibitors have demonstrated efficacy across multiple domains of PsO and PsA through numerous double-blind, randomized, placebo-controlled, Phase 3 clinical trials. Secukinumab, ixekizumab (IXE), and bimekizumab effectively treat peripheral arthritis, axial disease, enthesitis, and dactylitis with outstanding clearance of PsO in skin and nails. They also inhibit radiographic progression of PsA (Table 1).^1–18

Efficacy of bimekizumab in psoriasis. Bimekizumab, an IL-17A and IL-17F inhibitor, has been approved by the U.S. Food and Drug Administration (FDA) for the treatment of PsO, PSA, and ankylosing spondylitis.^1,2 In clinical trials, bimekizumab at 320mg every four weeks significantly outperformed secukinumab at 300mg in achieving complete skin clearance (PASI-100). Based on pooled data from 52-week (BE VIVID) and 56-week (BE READY and BE SURE) phase III trials, at 16 weeks, 61.7 percent of patients on bimekizumab achieved PASI-100 compared to 48.9 percent on secukinumab. By Week 48, 67.0 percent of patients maintained PASI-100 on a bimekizumab regimen of dosing every four weeks followed by every eight weeks, compared to 46.2 percent on secukinumab (p<0.001). Across PASI-100, PASI-90, PASI- 75, and IGA0/1 endpoints, bimekizumab consistently outperformed secukinumab with a similar safety profile.¹ Adverse events included upper respiratory infections (37.8% in bimekizumab vs. 41.6% in secukinumab) and a higher incidence of oral candidiasis in the bimekizumab group (19.3% vs. 3.0%).¹⁸ 

Administration and safety considerations for bimekizumab. The recommended dosage is 320mg (two 160mg injections) subcutaneously at Weeks 0, 4, 8, 12, and 16, followed by maintenance dosing every eight weeks. For patients weighing 120kg or greater, maintenance every four weeks after Week 16 may be considered. 

Overall, bimekizumab’s safety profile is comparable with other biologics. Bimekizumab has shown no significant increase in depression scores compared to other biologics, as evidenced by mean PHQ-9 scores in the BE VIVID/BE READY trials (against placebo), BE SURE (against adalimumab), BE RAIDANT (against secukinumab), and BE VIVID (against ustekinumab).^20–22 Additionally, laboratory abnormalities, such as liver enzyme elevations, were comparable between bimekizumab and other biologics, with a lower incidence compared to adalimumab and secukinumab but a higher incidence than ustekinumab. Further, based on pooled data from three phase III trials (BE VIVID, BE READY, and BE SURE) and their ongoing open-label study (BE BRIGHT), bimekizumab’s safety profile remains steady with long-term use.²² However, a notable adverse effect of bimekizumab includes a 19.3 percent incidence of oral candidiasis.¹⁸ 

Intravenous secukinumab. While IL-17 inhibitors are typically given through subcutaneous (SC) injection, a new intravenous (IV) form presents an alternative mode of delivery approved for Medicare patients with PsA or ankylosing spondylitis. In the INVIGORATE-2 trial (NCT04209205), IV secukinumab demonstrated efficacy and safety in patients with active PsA. This phase III, randomized, placebo-controlled study involved 381 patients who received either IV secukinumab (6mg/kg at baseline, then 3mg/kg every 4 weeks) or placebo, with placebo patients transitioning to IV secukinumab at Week 16. By Week 16, the ACR50 response was significantly higher in the secukinumab group compared to placebo (31.4% vs. 6.3%, adjusted p<0.0001). Rapid improvements were seen in those switched from placebo, and both groups achieved similar outcomes by Week 52. No unexpected safety concerns were noted, aligning with the safety profile of SC secukinumab.²³ These findings suggest that IV secukinumab offers a robust alternative for PsA management, complementing the results observed with other IL-17 inhibitors and illustrating the expanding therapeutic landscape for PsA.

Real-world observations. The prospective, international observational Psoriasis Study of Health Outcomes (PSoHO) elucidates the real-world effectiveness of anti-IL-17A biologics for treating moderate-to-severe PsO, confirming their substantial efficacy in achieving skin clearance and comparing efficacies between agents. At Week 12, 71.4 percent of patients receiving anti-IL-17A biologics achieved PASI-90 and/or sPGA 0/1, compared to 58.6 percent of those on other approved biologics, indicating a significant advantage for IL-17A inhibitors in delivering rapid results. Within the anti-IL-17A class, IXE demonstrated particularly favorable outcomes, with the highest response rates among all biologics studied. IXE-treated patients achieved PASI-90 at a rate approximately 7 to 9 percent higher than risankizumab, brodalumab, and secukinumab, and up to 20 percent higher than ustekinumab and adalimumab. While PASI-75 response rates were highest in the IXE group, comparative effectiveness relative to secukinumab and brodalumab were not statistically significant. These findings illustrate both the shared benefits of anti-IL-17A agents and relative intra-class efficacy for improving PsO severity.²⁴ Of note, at the time of this study, bimekizumab was not available.

IL-23 inhibition. IL-23 inhibitors have shown promising safety and efficacy across multiple domains of psoriatic disease, particularly in managing enthesitis, dactylitis, peripheral arthritis signs and symptoms as well as skin and nail manifestations (Table 1). Of note, IL-23 inhibition fails in inflammatory axial arthritis (eg ankylosing spondylitis). Moreover, combination therapy with agents like TNF inhibitors are emerging as a potential strategy for treatment-resistant cases, supported by recent findings in ulcerative colitis (UC).

VEGA study: golimumab and guselkumab combination therapy. The VEGA study explored the combination therapy of golimumab (GOL, anti-TNF) and guselkumab (GUS, anti-IL23) versus monotherapy in patients with UC, a chronic inflammatory disease that shares some pathophysiological mechanisms with PsO.²⁵ While the study was conducted in UC, its findings may hold relevance for psoriatic disease, as both medications are independently approved for PsO and PsA.^{26, 27} The study involved an initial 12-week combination phase followed by a 26-week monotherapy phase. At Week 12, patients in the combination group demonstrated significantly superior clinical remission rates compared to either monotherapy, without an increase in adverse events through Week 50, suggesting that combination therapy could provide enhanced efficacy in cases where monotherapy is insufficient.^25,28 

Although the VEGA trial was conducted in UC and focused on outcomes specific to that disease, like the Mayo score, its findings highlight the emerging potential of combination therapies to address the complexities of treating chronic inflammatory conditions like PsO. As dermatologists increasingly encounter refractory disease requiring novel strategies, lessons from studies like VEGA may inform future exploration of combination approaches in dermatology, though additional research specific to PsO is needed. The study underscores that targeting complementary pathways may yield synergistic benefits, potentially relevant to psoriatic disease.

TNF biosimilars

Biosimilarity versus interchangeability. Biosimilarity and interchangeability have distinct regulatory meanings under the FDA’s framework. A biosimilar product is one that is highly similar to an approved reference product, with no clinically meaningful differences in safety, purity, or potency, despite minor variations in inactive components. Interchangeability, however, is a separate designation that allows a biosimilar to be substituted for the reference product without the prescriber’s intervention. To achieve interchangeability, a biosimilar must demonstrate not only biosimilarity but also that it will produce the same clinical results as the reference product in any patient. Additionally, the safety and efficacy risks associated with switching between the biosimilar and reference product must be no greater than continuing the reference product alone.²⁹ 

VOLTAIRE-X study: adalimumab biosimilar interchangeability. The VOLTAIRE-X study investigated interchangeability between adalimumab (reference biologic) and BI 695501 (adalimumab-adbm, biosimilar). Patients with moderate-to-severe chronic plaque PsO were randomized to either continuous adalimumab or a switching group alternating between the biosimilar and adalimumab. At Weeks 30–32, pharmacokinetic equivalence was confirmed, with efficacy rates of 84.8 percent PASI-75 in the switching group and 79.0 percent in the continuous group (Table 2), demonstrating the interchangeability of BI 695501 with adalimumab. Multiple adalimumab biosimilars are now available in the US, with Cyltezo (Boehringer Ingelheim, Ingelheim am Rhein, Germany) being the first to receive FDA approval for interchangeability. Others, such as Hadlima (Organon & Co., Jersey City, New Jersey), Yuflyma (Celltrion, Jersey City, New Jersey), and adalimumab-atto, are undergoing clinical trials, while Abrilada (Pfizer, New York, New York) and AVT02 (Alvotech, Luxembourg) await approval.²⁹

Biologics for Medicare patients

Availability and dosing. Treating Medicare patients with PsO can be challenging due to difficulty obtaining coverage for some biologic agents. However, a range of biologics, including tildrakizumab, infliximab, golimumab (IV for PsA), certolizumab (lyophilized), and IV secukinumab, are available for this patient population with specific dosing regimens. Tildrakizumab is administered at a dose of 100mg subcutaneously at Weeks 0 and 4, followed by maintenance dosing every 12 weeks. Infliximab is given at 5mg/kg intravenously at Weeks 0, 2, and 6, then every eight weeks thereafter. For golimumab IV, a 2mg/kg dose is infused over 30 minutes at Weeks 0 and 4, followed by infusions every eight weeks. Certolizumab, in its lyophilized form, is administered as 400mg subcutaneously every other week at Weeks 0, 2, and 4, then maintained either with 400mg subcutaneously every four weeks or 200mg subcutaneously every two weeks. For psoriasis, 400mg subcutaneously every two weeks may be used as a maintenance dose. Finally, IV secukinumab requires a loading dose of 6mg/kg, followed by a maintenance dose of 1.75mg/kg every four weeks, with a maximum dose of 300mg (Table 3).

IL-36 receptor monoclonal antibody for generalized pustular psoriasis (GPP)

There remains an unmet need for biologics that effectively control GPP. Until recently, no GPP-specific treatments for acute flares were approved in the United States. Although the pathogenesis of GPP is not fully understood, it is believed to involve abnormal IL-36 signaling, often due to loss-of-function mutations in the IL36RN gene encoding the IL-36 receptor antagonist (IL-36Ra), a negative regulator of the IL-36 pathway. In GPP, dysregulated IL-36 activity drives excessive inflammation through NF-κB and MAP kinase signaling. Patients with deficiency of the IL-36 receptor antagonist (DITRA) typically show overactive NF-κB and MAP kinase responses, underscoring the therapeutic need for IL-36 pathway inhibition.³⁰

Spesolimab, an anti-IL-36 receptor monoclonal antibody, has been FDA-approved for treating GPP. In the Effisayil 1 trial, spesolimab demonstrated a favorable safety and efficacy profile for GPP flares. It was associated with rapid pustular and skin clearance within one week; primary efficacy endpoint was Generalized Pustular Psoriasis Physician Global Assessment (GPPGA) pustulation sub score of zero (occurred in 54.3% of patients on spesolimab vs. 5.6% on placebo, risk difference: 48.7%, 95% CI 21.5-67.22%, p<0.001) and key secondary endpoint GPPGA total score of 1 or fewer (42.9% in spesolimab vs 11.1% in placebo, risk difference 31.7%, 95% CI: 2.2-52.7%, p=0.012). Efficacy was independent of IL36RN mutation status and sustained through 12 weeks.³¹ 

Regarding safety, the trial reported a 6-percent rate of serious adverse events among patients receiving spesolimab at one week compared to 0 percent in the placebo group. Additionally, 17 percent of patients treated with spesolimab experienced infections at one week, versus 6 percent in the placebo group. Drug reaction with eosinophilia and systemic symptoms (DRESS) occurred in 4 percent of patients on spesolimab at 12 weeks (in the open-label extension), equating to an incidence rate of 15.9 per 100 patient-years. Overall, spesolimab has proven to be both effective and safe, providing swift relief for patients with GPP flares. It is administered as a single 900mg dose by IV infusion over 90 minutes, with an additional 900mg IV dose over 90 minutes recommended after one week if GPP flare symptoms persist.³¹

While Effisayil 1 evaluated spesolimab in the context of GPP flares, the phase IIb Effisayil 2 trial assessed the safety and efficacy of spesolimab as a maintenance treatment to prevent GPP flare recurrence.^{32, 33} In Effisayil 2, 157 patients with GPP were randomized into four groups: 1) high-dose spesolimab (600mg SC loading dose, then 300mg SC every 4 weeks), 2) medium-dose spesolimab (600mg SC loading dose, then 300mg SC every 12 weeks), 3) low-dose spesolimab (300 mg SC loading dose, then 150 mg SC every 12 weeks), and 4) placebo (SC loading dose, then SC every 4 weeks). During the randomized treatment period, patients who experienced a flare were given a single 900mg IV dose, with an optional additional dose after one week if symptoms persisted. Patients who responded to this acute treatment after 12 weeks were then placed on 300mg SC every 12 weeks.

The primary endpoint was time to GPP flare by Week 48, with a key secondary endpoint examining flare occurrence by Week 48. The study aimed to demonstrate a dose-response relationship and confirm the superiority of spesolimab over placebo. High-dose SC spesolimab reduced the risk of flare development by 84 percent compared to placebo (HR [95% CI] 0.16 [0.05, 0.54]; p=0.0004), with no flares reported after Week 4. Infection rates were similar across groups, and while localized injection site reactions were more common with spesolimab, they were generally mild and did not necessitate discontinuation of treatment.³³ Thus, spesolimab is emerging as a promising treatment that not only addresses acute GPP flares but may also help reduce their frequency and severity. 

Biologics and psoriatic arthritis progression

Biologics are increasingly recognized for their potential to not only manage PsO but also reduce the risk of developing PsA. In a retrospective cohort study of electronic medical records, Rosenthal et al³⁴ analyzed 1,326 PsO patients and found that those not receiving biologic treatments had significantly higher risk of PsA onset compared to those treated with biologics (adjusted HR=1.39, 95% CI: 1.03–1.87). These results suggest that biologic treatments may delay or reduce the onset of PsA, supporting their use for patients at risk for PsA development or progression.³⁴

Further, Singla et al³⁵ conducted a large-scale retrospective cohort study using TriNetX network to explore how specific biologics influence the risk of inflammatory arthritis in patients with PsO. Among newly prescribed biologics, compared with TNF inhibitors, both IL-17 and IL -23 inhibitors were associated with lower progression from PsO to PsA.³⁵ Thus, emerging targeted biologics, including IL-17 and IL-23 inhibitors, may protect against the development of PsA, along with the associated detriments to quality of life and potential for irreversible erosive damage that may accompany this progression.

Novel oral medications

Deucravacitinib versus apremilast. The advent of small molecule JAK inhibitors has significantly impacted PsO treatment, yet the selective allosteric inhibition of TYK2 offers an even more targeted therapeutic option. Deucravacitinib exhibits over 100-fold selectivity for TYK2 compared to JAK1/JAK3 and more than 2,000-fold selectivity compared to JAK2, making it substantially more selective than conventional JAK inhibitors.³⁶ This high selectivity allows TYK2 inhibitors to modulate pathways relevant to psoriasis—namely those associated with IL-12, IL-23, and type I interferons—while avoiding the broader toxicities associated with the inhibition of JAK1-3 catalytic domains, which affect multiple signaling pathways beyond PsO pathogenesis.³⁷ 

Deucravacitinib, a TYK2 inhibitor, is FDA-approved for moderate-to-severe PsO in patients eligible for phototherapy or systemic therapy, taken as a 6mg oral dose once daily. The phase III POETYK PSO-1 and PSO-2 trials demonstrated that deucravacitinib achieves superior PASI-75 response rates at Week 16 and sustained efficacy through Week 24 compared to placebo and apremilast. Notably, 82.5 percent (PSO-1) and 81.4 percent (PSO-2) of patients achieving PASI-75 at Week 24 maintained their response through Week 52. Additionally, deucravacitinib led to superior sPGA 0/1 outcomes at Week 16, with continued benefits over apremilast through Week 24.^36,38 Importantly, deucravacitinib also exhibited superior efficacy in treating scalp PsO, a notoriously difficult area to treat.³⁹

In terms of safety, deucravacitinib has a well-documented and tolerable profile. In the two-year, phase III POETYK trials, adverse events were infrequent, with an exposure-adjusted incidence rate (EAIR) of 6.1 per 100 person-years (PY) over two years. Commonly reported adverse events include diarrhea (which was more prevalent in the apremilast group), nasopharyngitis, upper respiratory tract infections, and COVID-19, most of which were mild or moderate in severity. Acne occurred in a small subset (EAIR 1.3 per 100 PY), but cases resolved spontaneously or with topical or oral antibiotics. Serious infections were rare, with no cases of herpes zoster or tuberculosis, and one serious adverse event involving venous thromboembolism occurred in a patient with an existing aortic dissection. Creatine phosphokinase (CPK) and triglyceride elevations were the most common grade ≥ 3 laboratory abnormalities observed, however most CPK elevations were transient and associated with recent physical exertion, and no changes in triglyceride levels were considered clinically meaningful. Importantly, no clinically significant changes were observed in other laboratory parameters, such as cholesterol or neutrophil counts, throughout the study.⁴⁰

Oral Anti-IL-23 receptor antagonist.In response to widespread preference for oral medications, traditionally SC biologic therapies may be reinvented as future oral formulations.⁴¹ JNJ-77242113, an oral peptide inhibitor targeting the IL-23 receptor, represents a novel treatment approach for PsO and is currently undergoing phase III trials. In a phase II trial with 255 participants, the 100mg twice-daily dose achieved higher rates of PASI-75, PASI-90, and PASI-100 responses compared to lower doses and placebo over a 16-week period. These findings underscore the potential efficacy of JNJ-77242113 as a targeted treatment with a more favorable mode of delivery for patients with moderate-to-severe plaque PsO.⁴² However, further validation through ongoing trials is necessary to confirm the safety and efficacy of this investigational drug.

Conclusion

The treatment landscape for PsO and PsA has evolved substantially, with biologics offering targeted approaches that provide better disease control and quality of life for patients. IL-17 inhibitors have shown promising results in managing both skin symptoms and PsA, providing both efficacy and tolerability. The ongoing development of IL-23 inhibitors, including a novel oral agent, further expands the toolkit of targeted agents that can help patients achieve disease remission with better quality of life. Deucravacitinib, a TYK2 inhibitor, provides a new choice for patients seeking more oral alternatives. Additionally, up-and-coming biosimilar therapies offer affordable and accessible alternatives, with recent studies validating their interchangeability with reference biologics. These advances not only broaden the spectrum of available treatments but also allow for more tailored therapeutic strategies, potentially improving long-term outcomes in PsO and PsA management (Figure 1).

Acknowledgements

The authors would like to extend their sincere thanks to IDEOM for their support in making the Masterclass in Dermatology series possible.

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