Single‐centre experience with tralokinumab in dupilumab‐experienced and naïve patients with atopic dermatitis

Tralokinumab and dupilumab are monoclonal antibodies that target the Th2 immune response and are approved for moderate-to-severe atopic dermatitis (AD).1 Dupilumab targets the interleukin (IL)-4 receptor and blocks both IL-4 and IL-13 signalling, whereas tralokinumab specifically blocks the IL-13 receptor.1 The real-world effectiveness and safety of tralokinumab (with or without concomitant topical corticosteroids) were evaluated in this case series of 29 patients (aged 19–80 years) treated with tralokinumab for at least 6 weeks at the Department of Dermatology and Venereology, Lausanne University Hospital, Switzerland, between 8 July 2022 and 13 March 2024. Effectiveness was assessed using the Eczema Area and Severity Index (EASI) and Physician Global Assessment (PGA) scores. Most patients (n = 25, 86%) had transitioned from dupilumab to tralokinumab. These patients (15 male and 10 female) had a median age of 49 years and 80% had AD for >10 years. Previous treatments included topical corticosteroids (96%), phototherapy (68%), cyclosporine (16%) and methotrexate (16%). Dupilumab treatment had reduced the severity of their AD, with the median (interquartile range [IQR]) EASI reducing from 25.0 (22.0–35.2) to 7.0 (3.5–28.8) (Table 1). Despite these improvements, this cohort discontinued dupilumab, for reasons that included an initial lack of effectiveness (n = 3, 12%), a loss of effectiveness over time (n = 8, 32%) and adverse events (AEs; n = 8, 32%). After switching to tralokinumab, the patients continued to show improvements, with median (IQR) EASI scores of 3.6 (2.0–8.0) and 3.0 (2.0–7.0) after 12 and 24 weeks of treatment with tralokinumab, respectively. EASI and PGA responder analyses also support the effectiveness of tralokinumab (Table 1). At the data cut-off, 13 (52%) patients were continuing to receive tralokinumab with a median (IQR) treatment duration of 47.0 (35.1–55.7) weeks (Figure 1). Six patients had discontinued tralokinumab due to a lack of initial effectiveness and three had discontinued due to a loss of effectiveness after 26, 31 and 60 weeks of treatment, respectively. No patients had discontinued due to conjunctivitis and four out of five patients who had previously experienced ocular AEs on dupilumab reported that these had resolved or reduced following the switch to tralokinumab. Four patients (14%) in the study were dupilumab-naïve. Compared to patients previously treated with dupilumab, these individuals were younger (median age: 32 vs. 49 years) and had more severe AD at tralokinumab initiation (median EASI score: 29.3 vs. 7.0). All dupilumab-naïve patients were continuing to receive tralokinumab at the cut-off date, with a median (IQR) treatment duration of 67.2 (54.2–73.8) weeks. After initiating tralokinumab, the patients experienced rapid improvements in their AD, with median (IQR) EASI scores of 2.1 (0.8–5.1) and 1.1 (0.8–1.7) recorded after 12 and 24 weeks' treatment with tralokinumab, respectively. This retrospective case series included 29 patients with long-standing, heavily pretreated AD who initiated treatment with tralokinumab. Our results indicate that improvements in AD observed with dupilumab were maintained or increased after a switch to tralokinumab, with half of the dupilumab-experienced patients continuing to receive tralokinumab as of the cut-off date. Findings were consistent with results from the ECZTRA randomized controlled trial programme2-4 and other real-world studies of tralokinumab.5-9 This analysis had several limitations, including the case series design and lack of a control arm. In addition, the small number of dupilumab-naïve patients limited comparisons between dupilumab-naïve and -experienced patients. Overall, our results support the use of tralokinumab for AD irrespective of prior dupilumab treatment. We thank the patients who contributed to this study. Medical writing support was provided by Steph Carter (Lyrical Medical Writing Services Ltd) and funded by LEO Pharmaceutical Products Sarath Ltd., Switzerland. Medical writing support was funded by LEO Pharmaceutical Products Sarath Ltd., Switzerland. CF: None. EG: Consulting fees, payment or honoraria from Helsinn, KYOWA Kirin, Mallinckrodt Pharmaceuticals, Novartis, Recordati Rare Diseases, Sanofi, Stemline and Takeda, has a patent on diagnostic method for blood disease, has been involved in a leadership role for EADV and EORTC and has stock/stock options for Scailyte AG. CC: Scientific adviser and/or clinical study investigator—AbbVie, Actelion, Almirall, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli-Lilly, Incyte, Janssen, LEO Pharma, MSD, Novartis, Pfizer, Samsung, Sanofi and UCB. MG: Receipt of honoraria or speaker fees—Medimmune, Abbvie, Amgen, Celgene, Novartis, Lilly, Roche, Sanofi, Sienna Pharma, Boehringer, Bioderma, BMS, Takeda Pharma, Innate Pharma, Owkin; Royalties: Genentech, Biolegend, AVVA Pharma; Research grants: Galderma, Leo Pharma, Celgene, Abbvie, Amgen, Roche, Novartis, BMS, AVVA Pharma and Nogra Pharma. TS: Consulting or advisory role for AbbVie, LEO Pharma, Lilly, Novartis and Sanofi. Speaker's bureau for Novartis; and travel, accommodation and expenses from GlaxoSmithKline, MSD, Novartis and Pfizer. The consent was approved by the institutional review board and the local ethics committee of the Lausanne University Hospital CHUV, Switzerland, in accordance with the Helsinki Declaration and were reviewed by the ethical committee board of the canton of Vaud, Switzerland. The patients in this manuscript have given written informed consent to publication of their case details. The data that support the findings of this study are available from the corresponding author upon reasonable request. The data are not publicly available due to privacy or ethical restrictions.