ArticleAllergy, asthma & immunology research2025
Therapeutic Efficacy of YH35324 on FcεRIα-Mediated Mast Cell/Basophil Activation.
Article in Allergy, asthma & immunology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Chronic Spontaneous Urticaria in the Era of Targeted Therapy: From Pathogenic Mechanisms to Precision Medicine.Pharmaceutics · 2026Review
- Review
- Targeting immune dysregulation in chronic spontaneous urticaria: beyond antihistamines.The Korean journal of internal medicine · 2026Review
- Immunological Basis of Chronic Spontaneous Urticaria: Immunoglobulin E and Beyond.Yonsei medical journal · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
purposeImmunoglobulin E (IgE) induces mast cell/basophil activation by binding with FcεRIα and contributes to the development of allergic disease, in which targeting IgE has been considered an effective therapeutic strategy. YH35324 (YH) is a new hybrid protein with an extracellular domain consisting of FcεRIα, and its pharmacodynamic effect and safety were validated. This study aimed to evaluate the therapeutic potential of YH as an anti-IgE immunomodulator compared with omalizumab (Oma).
methodsTo evaluate the
resultsThe YH-administered group exhibited significantly lower expression of FcεRIα on peripheral basophils compared to the Oma-administered group up to 14 days post-administration. YH directly suppressed FcεRIα expression on the surface of LAD2 cells, as it was bound to IgE-unbound FcεRIα and migrated into the cells by actin-dependent endocytosis, then was recycled by FcRn binding in the lysosome
conclusionsYH represents a new therapeutic agent for IgE-mediated allergic disease. Further studies are needed to evaluate its additional effects on the FcεRIα-mediated autoimmune mechanism.
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Registered trials
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