ArticleAntibody therapeutics2024
GB12-09, a bispecific antibody targeting IL4Rα and IL31Rα for atopic dermatitis therapy.
Article in Antibody therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Atopic Dermatitis: New Targets and Emerging Systemic Therapies.American journal of clinical dermatology · 2026Review
- Skin Lipid Dysregulation in Atopic Dermatitis and Related Inflammatory Skin Diseases.Allergy, asthma & immunology research · 2026Review
- Cross-Talk between Neurons and Immune Cells in Pruritus: from Mechanisms To Medicines.Current allergy and asthma reports · 2026Review
- Advancing Precision Medicine in Inflammatory Skin Disease.American journal of clinical dermatology · 2025Review
- Beyond the blockade: unmet needs in systemic targeted atopic dermatitis therapy.Frontiers in immunology · 2025Review
- Targeting the IL-4/IL-4R Axis in Th2 Inflammatory Diseases: A Review of Clinical Efficacy and Safety.Journal of inflammation research · 2025Review
- Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin condition characterized by dysregulated immune responses. The key mediators of AD pathogenesis are T helper 2 (TH2) cells and TH2 cytokines. Targeting interleukin 4 (IL4), IL13 or IL31 has become a pivotal focus in both research and clinical treatments for AD. However, the need remains pressing for the development of a more effective and safer therapy, as the current approaches often yield low response rates and adverse effects. In response to this challenge, we have engineered a immunoglobulin G-single-chain fragment variable (scFv) format bispecific antibody (Ab) designed to concurrently target IL4R and IL31R. Our innovative design involved sequence optimization of VL-VH and the introduction of disulfide bond (VH44-VL100) within the IL31Rα Ab scFv region to stabilize the scFv structure. Our bispecific Ab efficiently inhibited the IL4/IL13/IL31 signaling pathways
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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.