ArticleDermatology and therapy2025
Lebrikizumab Rapidly Lowers Inflammatory Biomarkers with Clinical Correlations in Moderate-to-Severe Atopic Dermatitis.
Article in Dermatology and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 8 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Randomized, Double-blind, Placebo Controlled Trial to Evaluate the Efficacy and Safety of Lebrikizumab in Patients With Moderate to Severe Atopic Dermatitis
A Randomized, Double-blind, Placebo Controlled Trial to Evaluate the Efficacy and Safety of Lebrikizumab in Patients With Moderate to Severe Atopic Dermatitis.
Who cites it
8 citing papers in PubMed.
- Peripheral Immune Modulation in Atopic Dermatitis During Dupilumab or Baricitinib Treatment Is Limited, as Assessed by Proteomic, Transcriptomic, and Torque Teno Virus Analyses.International journal of molecular sciences · 2026Article
- Review
- Lebrikizumab ADvocate1 and 2 Monotherapy and ADjoin (Long-Term) Trials: Use of Topicals Therapies.Dermatology and therapy · 2026Review
- Understanding Infantile Atopic Dermatitis: A Review of Environmental, Familial, Genetic and Microbial Influences.Current allergy and asthma reports · 2026Review
- Epithelial Barrier Dysfunction in Atopic Dermatitis, Allergic Contact Dermatitis, and Chronic Spontaneous Urticaria and its Therapeutic Implications.Current allergy and asthma reports · 2026Review
- Atopic Comorbidities and Topical Steroids in Early Childhood Atopic Dermatitis: Are We Missing a Piece of the Puzzle?Clinical reviews in allergy & immunology · 2026Review
- Alopecia Areata and Atopic Dermatitis: Common Mechanisms and Emerging Therapeutics.Journal of inflammation research · 2026Review
- Chemokine ligand-receptor interactions as potential therapeutic targets for atopic dermatitis: from basic to clinical research.Frontiers in allergy · 2026Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionLebrikizumab is a novel monoclonal antibody that selectively binds to interleukin (IL)-13 with high affinity and a slow dissociation rate.
methodsWe assayed serum from select patients enrolled in ADvocate1 and ADvocate2 to determine the impact of lebrikizumab on circulating biomarkers and pathways relevant to atopic dermatitis (AD) and to assess the correlation between key biomarkers and clinical measures of improvement.
resultsAt baseline, IL-13, CC motif chemokine ligand (CCL)13, CCL17, CCL22, total immunoglobulin (Ig)E, IL-5, and periostin were elevated in patients with moderate-to-severe AD versus healthy controls (p < 0.001). Baseline Eczema and Area Severity Index (EASI) and Investigator's Global Assessment (IGA) scores were significantly correlated with IL-13, IL-5, CCL13, CCL22, and CCL26. Lebrikizumab induced rapid and progressive reductions in CCL13, CCL17, CCL22, and periostin at weeks 4, 16, and 52 compared with baseline (p < 0.05). AD-associated pathways linked to cytokine signaling were significantly improved at weeks 4 and 16. Improvements in EASI, IGA, and the Pruritus Numeric Rating Scale were correlated with reductions in CCL13, CCL17, CCL22, CCL26, and periostin across all time points. After multiple testing correction and adjusting for sex and race as covariates, we identified the chemokine CCL26 as a pharmacodynamic marker for lebrikizumab response at weeks 4 and 16.
conclusionsSelective inhibition of IL-13 with lebrikizumab monotherapy induced progressive inhibition of systemic biomarkers and pathways of type 2 inflammation, which correlated with clinical measures of improvement in patients with moderate-to-severe AD. CLINICAL TRIAL REGISTRATIONS: NCT04146363 and NCT04178967.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.