Off-label dermatologic uses of IL-23 inhibitors
Open accessAbstract
BACKGROUND: While IL-23 inhibitors, which include guselkumab, tildrakizumab, and risankizumab, are currently FDA-approved solely for the treatment of psoriasis, several other inflammatory skin conditions have been associated with elevated IL-23 levels. The purpose of this review is to summarize and interpret the literature surrounding the off-label uses of IL-23 inhibitors in dermatologic practice. METHODS: for clinical trials, observational studies, case series, and case reports assessing use of the three IL-23 inhibitors for non-psoriatic dermatologic conditions. RESULTS: Conditions exhibiting promising response to treatment with IL-23 inhibitors include hidradenitis suppurativa, lichen planus, pityriasis rubra pilaris, pyoderma gangrenosum, dissecting cellulitis of the scalp, congenital ichthyosiform erythroderma, lichen planus pemphigoides, acrofacial vitiligo, lichen planopilaris, frontal fibrosing alopecia, lupus erythematosus tumidus, and Stewart-Treves angiosarcoma. CONCLUSION: Current literature suggests that IL-23 inhibitors may be effective in treating these conditions due to shared pathophysiologic pathways with psoriasis. Although these results are promising, further research through large-scale, randomized clinical trials is needed to further evaluate the efficacy and safety of IL-23 inhibitors in treating these off-label conditions.
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Selective IL-23 inhibitors show high efficacy with durable responses in psoriasis, likely by disrupting the maintenance of disease-driving Th17 cells.
“selective IL-23 inhibitors have also shown high efficacy with durable responses, likely by disrupting the maintenance of disease-driving Th17 cells [29,30,31,32].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [32]
The Introduction (page unavailable) says selective IL-23 inhibitors demonstrated efficacy in phase III psoriasis trials and explains that IL-23 maintains inflammation-driving Th17 cells. It does not characterize the efficacy as high or state that responses are durable; the References list a five-year efficacy study but do not report its results. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe IL-23/Th17 axis is a central driver of psoriasis.
“The identification of the IL-23/Th17 axis as a central driver of psoriasis has led to the development of biologic therapies that selectively interrupt cytokine networks.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [32]
IL-23 is an upstream regulator of pathogenic T-cell populations in psoriasis.
“Furthermore, increasing evidence supports IL-23 as an upstream regulator of pathogenic T-cell populations; thus, selective IL-23 inhibitors have also shown high efficacy with durable responses, likely by disrupting the maintenance of disease-driving Th17 cells [29,30,31,32].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [32]
Therapies targeting IL-17, including monoclonal antibodies against IL-17A or its receptor, produce rapid and efficient clinical responses in psoriasis by suppressing keratinocyte activation and neutrophil recruitment, which are key downstream effects of Th17 immunity.
“Therapies targeting IL-17 (monoclonal antibodies against IL-17A or its receptor) have shown rapid and efficient clinical responses by directly suppressing keratinocyte activation and neutrophil recruitment, which are key downstream effects of Th17 immunity.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [32]
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Tinca, A. C., Cozac-Szoke, A. R., & Cotoi, O. S. (2026) · Dermatopathology · doi:10.3390/dermatopathology13020022 · Cited by 1 · see citing works
“Furthermore, increasing evidence supports IL-23 as an upstream regulator of pathogenic T-cell populations; thus, selective IL-23 inhibitors have also shown high efficacy with durable responses, likely by disrupting the maintenance of disease-driving Th17 cells [29–32].”
- Authors
- Porter, J., Zimmerman, L., Nickles, M., & Hoyer, S.
- Affiliations
- University of Illinois College of Medicine, Peoria, IL, USA
- University of Illinois Chicago (US)
- Corresponding author
- Porter, Justin
- Venue
- Journal of Dermatological Treatment
- Publisher
- Informa UK Limited
- Published
- 2024-12-08
- Volume
- 35
- Issue
- 1
- Pages
- 2436015-2436015
- ISSN
- 0954-6634 (ISSN-L)
- 1471-1753
- OpenAlex
- W4405154592
- Cited by
- 3
- References
- 51
- Citations by year
- 2026: 2 · 2025: 1
- FWCI
- 0.13
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- Locations
- Journal of Dermatological Treatment (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Dermatology › Cutaneous lymphoproliferative disorders research
- Keywords
- IL-23 inhibitors, off-label drug use, guselkumab, tildrakizumab, risankizumab, psoriasis, hidradenitis suppurativa, lichen planus, pityriasis rubra pilaris, pyoderma gangrenosum, dissecting cellulitis of the scalp, congenital ichthyosiform erythroderma, lichen planus pemphigoides, acrofacial vitiligo, lichen planopilaris, frontal fibrosing alopecia, lupus erythematosus tumidus, inflammatory skin diseases, shared pathophysiology
- MeSH terms
- Antibodies, Monoclonal, Dermatologic Agents, Humans, Skin Diseases, Interleukin-23, Off-Label Use, Antibodies, Monoclonal, Humanized
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