Psoriasis: Patient Impact and the Path to Innovation
Psoriasis is more than a skin condition, it is often a lifelong, systemic autoimmune disease that may increase the risk of other serious health complications such as heart disease and diabetes, and have a negative impact on patients’ mental health. According to the National Psoriasis Foundation, psoriatic disease affects approximately 125 million people globally, or 2 to 3 percent of the total population, and the condition’s prevalence is increasing. Recent U.S.-specific data indicate an 11.7% increase in new psoriasis cases and a 15.7% rise in the disease prevalence since 2010. It is estimated that 30% of people suffering from psoriasis also develop psoriatic arthritis, with both conditions sharing a common etiology. [1]
The global psoriasis market is projected to grow from USD 29.15 billion in 2025 to USD 57.68 billion by 2032. The rising prevalence of psoriasis across the globe is one of the major factors driving the demand for psoriasis treatment, which recently have been focusing on safer biologics that target specific checkpoints in the inflammatory pathways. Previously dominated by tumor necrosis factor (TNF) inhibitors, new therapeutics targeted at interleukins or kinases are getting a lot of traction, including IL-23, IL-17, and TYK2 (part of the JAK family). Despite several existing drugs for psoriasis on the market, dozens of new biologic candidates are being evaluated both preclinically and in advanced clinical trials for better and safer alternatives. [2][3]
Untangling the Pathways of Chronic Immune Disease
Psoriasis can be triggered by injury, trauma, infection, medications, or other factors, including genetic. The shift from managing symptoms to targeting the underlying mechanism of autoimmunity comes from a better understanding of molecular pathogenesis. Psoriasis and psoriatic arthritis share a common molecular mechanism with other chronic autoimmune disorders such as rheumatoid arthritis or inflammatory bowel disease. Although the immune system is a vast, intricate network of cells and molecules, a specific group of key players has been targeted since they have shown great therapeutic promise in preclinical and clinical studies.
Psoriasis pathogenesis. Inflammatory myeloid dendritic cells release IL-23 and IL-12 to activate T cells to produce psoriatic cytokines, with IL-17 being identified as one of the main effector cytokines in psoriasis. These cytokines cause additional chemokine flooding and inflammatory effects on keratinocytes, which further increase dendritic cell activity, closing the loop of self-amplifying chronicity [5]
The trickiest part of targeting an autoimmune disease is to target its molecular culprit without disrupting the immune system to the point where the body is at risk of being defenseless. For example, one of the known TNF-α inhibitor side effects is reactivation of the dormant tuberculosis pathogen residing in patients for years, requiring tuberculosis screening or prophylactic treatment before starting the therapy. Blocking key immune system components can leave a person with a compromised immune system, which requires them to be extra vigilant not to contract any infectious diseases.
Spotlight on Interleukins: Different Paths to Cure
Targeting TNF-α is a universal approach to autoimmune diseases, but other cytokines with a more favorable safety profile have been identified in psoriasis. IL-12 and IL-23 share a common subunit (p40) and have been double-targeted, however, IL-12 is considered one of the major switches of the immune system, thus better efficacy and a better safety profile have been observed with selective inhibitors of IL-23 (non-shared p19 subunit), such as guselkumab, risankizumab, and tildrakizumab, all currently approved medications. There are also several approved inhibitors against the effector cytokine IL-17A, but currently, more evidence suggests that targeting IL-23 is superior to IL-17A inhibition in achieving long-term clinical responses. Also, selective IL-23 inhibition has been shown to favorably shift the relative ratio of CD8+ TRM cells and Treg cells in lesional skin compared with IL-17A inhibition. Moreover, side effects such as Candida infections associated with direct IL-17A inhibition were not observed with IL-23 targeting. On the other hand, patients treated with ixekizumab (an IL-17A inhibitor) achieve skin clearance more rapidly than patients treated with guselkumab. IL-23 has been continuously pursued as the most promising target for psoriasis, displaying high levels of clinical response that are often sustained for up to five years of treatment, and it displays continued suppression of the disease even after treatment withdrawal. [4][5]
ChemPartner’s Integrated IL-23 Inhibitor Screening Platform
Proactively meeting the demand, we have developed a comprehensive suite of assays tailored for evaluating drug candidates targeting the IL-23 in psoriasis. Leveraging state-of-the-art in vitro techniques such as surface plasmon resonance (SPR), ELISA, HTRF, DM cell line/pSTAT3 signaling, and cytokine release assays, we provide seamless progression from biochemical to cellular evaluation.
Our in vitro toolbox allows for comprehensive screening to evaluate a therapeutic’s binding specificity, affinity, inhibition potency, and cytokine pathway activation before testing it in animals
Example data from our in vitro panel, testing different therapeutics: A) ELISA, mirikizumab (antibody targeting IL-23), B) Reporter cell line, ustekinumab (antibody targeting IL-23/IL-12) inhibition, C) Human PBMC pSTAT assay, ruxolitinib (small molecule targeting JAK1/JAK2)
Complementing these in vitro assays, we offer robust in vivo models, including IL-23-induced psoriasis in mice, and IMQ-induced psoriasis model, enabling preclinical validation of drug candidate efficacy and mechanism of action studies.
Our 4-day IL-23 induced psoriasis murine model allows for effective and fast screening for anti-IL-23 biologics
Our in vivo model uses C57BL/6 female mice during 4-day evaluation with daily IL-23 injections on day 0,1,2, and 3. Major readouts include body weight, ear thickness, H&E histopathology and ear tissue cytokine analysis.
H&E staining of ear tissue section shows remarkably thick dermis and histopathological changes characteristic to psoriasis. The model confirms inhibition of inflammatory mechanism induced by IL-23 injection.
Gross measurement of the injected ear also confirms model adequacy and responsiveness to treatment with biologics targeting IL-2.
Our cytokine release assay confirms pathway activation of the key effector interleukins – IL-17 and IL-22 – induced by the injection of IL-23, and displays inhibitory effect of anti-IL-23 antibody
Our IL-23 Platform: Proven Science. Adaptive Collaboration
Partner with us for discovery backed by decades of experience, and speed driven by experts. Psoriasis is a serious disease that affects millions, and it involves a highly competitive therapeutic industry, poised to grow at a significant rate in the next decade. Our integrated IL-23 platform allows for comprehensive screening of drug candidates from physicochemical properties to investigation of mechanism of action in animals. We are a preclinical CRO with expertise across all molecular modalities, leveraging our scale and flexible partnership model to work with visionary life science companies, helping them efficiently and rapidly bring scalable, life-changing drugs to market. Contact us today!
Bibliography
[1] National Psoriasis Foundation. World Psoriasis Day. Available from: https://www.psoriasis.org/world-psoriasis-day/
[2] Fortune Business Insights. Psoriasis Treatment Market Size, Share & Global Report (2025-2032). Last Updated September 22, 2025. Available from: https://www.fortunebusinessinsights.com/industry-reports/psoriasis-treatment-market-100600.
[3] GoodRx. 11 New Psoriasis Medications and Treatments in Development. Available from: https://www.goodrx.com/conditions/psoriasis/new-psoriasis-medications. Accessed October 8, 2025.
[4] Krueger JG, Eyerich K, Kuchroo VK, Ritchlin CT, Abreu MT, Elloso MM, Fourie A, Fakharzadeh S, Sherlock JP, Yang Y-W, Cua DJ and McInnes IB (2024) IL-23 past, present, and future: a roadmap to advancing IL-23 science and therapy. Front. Immunol. 5:1331217. doi: 10.3389/fimmu.2024.1331217
[5] Schinocca C, Rizzo C, Fasano S, Grasso G, La Barbera L, Ciccia F and Guggino G (2021) Role of the IL-23/IL-17 Pathway in Rheumatic Diseases: An Overview. Front. Immunol. 12:637829. doi: 10.3389/fimmu.2021.637829
