LEO Pharma presents two late-breaking abstracts for temtokibart reporting positive Phase 2b efficacy, safety and biomarker results in moderate-to-severe atopic dermatitis at the 2025 EADV Annual Meeting in Paris

BALLERUP, Denmark, SEPTEMBER 17^th, 2025 – LEO Pharma A/S, a global leader in medical dermatology, today presented two late-breaking presentations showcasing the results of a Phase 2b dose finding trial evaluating the efficacy and safety of investigational agent temtokibart in adults with moderate-to-severe atopic dermatitis (AD). The trial met its primary endpoint for the three highest doses, further supported by biomarker results showing broad dampening of markers for activated immune pathways in AD. Results were shared in two LEO Pharma late breaker oral presentations at the 2025 European Academy of Dermatology and Venereology (EADV) Annual Meeting.^1,2 Temtokibart (also called LEO 138559) is an investigational agent that is not approved by any health authority.  It’s safety and efficacy have not yet been established and are subject to further larger trials.

The Phase 2b study was a randomized, double-blind, placebo-controlled, multi-site, parallel-group, dose-finding trial to evaluate the efficacy and safety of different doses of subcutaneously administered temtokibart, in adult subjects with moderate-to-severe AD.^1,3 

Temtokibart is an investigational monoclonal antibody for the treatment of moderate-to-severe AD, which blocks the IL-22RA1 receptor subunit thereby inhibiting the effect of the interleukin-22 (IL-22) cytokine (known to be elevated in pathway with atopic dermatitis), and also the effects of IL-20 and IL-24 signaling.^4–6

Phase 2b efficacy and safety late breaking abstract presented by Professor Stephan Weidinger

The results from the Phase 2b trial in 262 adult patients showed that temtokibart demonstrated significant improvement in the primary endpoint of percentage change in EASI from baseline for 600 mg (−61.2%, p<0.01), 450 mg (−57.1%, p<0.05), and 300 mg (−64.3%, p<0.01) treatment arms compared with placebo (−41.7%) at Week 16.¹ Significant improvement was observed in percentage change in EASI as early as Week 1 for 450 mg (−22.3%; p<0.01) and 300 mg arms (−19.6%; p<0.05), and as early as Week 2 with 600 mg (−35.0%; p<0.05) compared with placebo (Week 1: −8.0%, Week 2: (−22.7%).¹ These significant improvements were maintained up to Week 32 in 600 mg (−59.1%; p<0.05) and 300 mg (−60.6%; p<0.05) arms, despite no treatment used after Week 14.¹ Temtokibart was well-tolerated with no dose-dependent AEs, low incidence of conjunctivitis, and no signal for herpes.¹ AEs leading to permanent drug discontinuation or withdrawal were reported in 2.4% and 3.8% of patients in the temtokibart and placebo groups, respectively.¹

“These results are promising, as they provide further evidence of the value of targeting the IL-22 pathway in AD, via IL-22RA1 , offering a potential novel approach to the currently existing therapies used to treat atopic dermatitis” said Professor Stephan Weidinger, Professor and Chair for Dermatology at the Christian-Albrechts-University, Director of the Department of Dermatology and Allergy at the University Hospital Schleswig-Holstein, Germany, and the International Coordinating Investigator for the Phase 2b trial. “Patients with moderate-to-severe atopic dermatitis still face numerous unmet needs, so we welcome any new options that could improve their disease while limiting burdensome side effects” 

Phase 2b biomarker late breaking abstract, presented by Professor Emma Guttman-Yassky

Biomarker results from the Phase 2b trial were also presented as a late breaker at EADV 2025 which showed that temtokibart-treated patients (pooled-temtokibart data; n=22 at baseline, n=14 at Week 16) demonstrated an overall 97% improvement in immune gene expression by Week 16.² Expression of epidermal barrier-related genes were significantly restored by Week 16.² Correlation analysis revealed that reductions in EASI and SCORAD were significantly associated with reductions in Th2 and Th17/22 markers (p≤ 0.05), and DLQI and POEM correlated with reductions of key T-cell, Th2, Th17/Th22 markers (p≤ 0.05).²

“Atopic dermatitis is a complex and heterogenous disease, and there remains a significant need for further understanding the effect of targeting different pathways. By investigating biomarkers in the clinical programs we are increasing our understanding of the disease, moving us closer to a more tailored approach of treating AD via different mechanisms of action.” said Professor Emma Guttman-Yassky, Waldman Professor of Dermatology and Immunology and the Health System Chair of the Department of Dermatology at the Icahn School of Medicine at Mount Sinai, USA, Investigator and senior author of the Phase 2b biomarker abstract. “These results provide further evidence that the IL-22 pathway is a key driver of disease activity in AD and that there is a strong correlation between clinical effects and dampening of several immune pathways of importance in AD, when targeting the IL-22RA1 subunit.”

“We are encouraged by these Phase 2b results which further add to the potential clinical value of temtokibart in moderate-to-severe atopic dermatitis,” said Professor Jacob Pontoppidan Thyssen, Chief Scientific Officer & Executive Vice President, Science, Search & Innovation at LEO Pharma.

About the Phase 2b trial

The temtokibart phase 2b trial (NCT05923099) is a randomized, double-blind, placebo-controlled, multi-site, parallel-group, dose-finding trial, evaluating efficacy and safety of different doses of subcutaneously administered temtokibart in adult patients with moderate-to-severe atopic dermatitits.¹ Patients were randomized to receive one of four doses of temtokibart or placebo.¹ The primary endpoint is percent change in EASI from baseline to Week 16.³ The key secondary endpoint is number of treatment-emergent adverse events from baseline to Week 16 per subject.³ 

About atopic dermatitis 

Atopic dermatitis is a chronic, inflammatory skin disease characterized by intense itch and eczematous lesions.⁷ Atopic dermatitis is the result of skin barrier dysfunction and immune dysregulation, leading to chronic inflammation.⁸ Type 2 and IL-22 pathways play an important role in the key aspects of atopic dermatitis pathophysiology.^9–12

About investigational temtokibart 

Temtokibart is an investigational monoclonal antibody that targets the IL-22RA1 receptor subunit, currently in Phase 2 development for the potential treatment of moderate-to-severe atopic dermatitis.^3,4 It blocks the IL-22RA1 subunit and thereby inhibits the effects of the IL-22 cytokine, and also the effects of IL-20 and IL-24 signaling.^5,6 Temtokibart does not bind to the IL-22 cytokine itself.^5,6 LEO Pharma has obtained a worldwide exclusive license to develop and commercialize temtokibart from argenx.

About argenx

LEO Pharma and argenx, a global immunology company, formed a strategic alliance in 2015 to develop innovative antibody-based solutions for the treatment of chronic inflammation that underlies many skin conditions. LEO Pharma and argenx jointly developed temtokibart under this research agreement and LEO Pharma has subsequently obtained the exclusive license to develop and commercialize temtokibart.

References:

1. Weidinger S, et al. Presented at European Academy of Dermatology and Venereology 2025 Annual Meeting, Paris, September 17–20.
2. Del Duca E, et al. Presented at European Academy of Dermatology and Venereology 2025 Annual Meeting, Paris, September 17–20.
3. NCT05923099. Available at: clinicaltrials.gov/study/NCT05923099. Accessed September 2025.
4. Bangert C, et al. Presented at European Academy of Dermatology & Venereology (EADV) 2024 Annual Meeting, Amsterdam, 25–28 September 2024.
5. Thaçi D, et al. Presented at American Academy of Dermatology (AAD) 2023 Annual Meeting, New Orleans, 17–21 March 2023.
6. Thaçi D, et al. Presented at European Academy of Dermatology and Venereology (EADV) 2023 Annual Meeting, Berlin, 11–13 October 2023.
7. Weidinger S, et al. Lancet 2016;387:1109–1122.
8. Boguniewicz M, et al. Immunol Rev 2011;242:233–246.
9. Tubau C, Puig L. Immunotherapy 2021;13:327–344.
10. Bieber T. Allergy 2020;75:54–62.
11. Gittler JK, et al. J Allergy Clin Immunol 2012;130:1344–1354.
12. Nograles K, et al. J Allergy Clin Immunol 2009;123:1244–1252.

MAT- 85573 September 2025