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Clinically relevant – Two complementary models cover allergen-induced urticaria and passive IgE-mediated anaphylaxis, closely mimicking human disease.
Quantifiable endpoints – Clinical scores, wheal size, serum IgE, blood eosinophils, skin histopathology (HE, toluidine blue), mast cell degranulation.
Mechanism-driven – HDM model reflects environmental allergen sensitization; PCA model isolates IgE/mast cell axis.
Translational value – Ideal for testing anti-IgE biologics, mast cell stabilizers, H1-antihistamines, and anti-inflammatory agents.
IND-ready data packages – Studies can be conducted in accordance with GLP principles.
Representative data from our NHP Urticaria Model:
HDM Induced NHP Urticaria Model


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HDM Induced NHP Urticaria Model

• Efficacy testing of anti-IgE biologics (omalizumab, ligelizumab), mast cell stabilizers (cromolyn), H1-antihistamines, and anti-inflammatory agents
• Target validation for IgE/FcεRI pathway and mast cell biology
• Biomarker discovery (IgE, eosinophils, mast cell mediators)
• Mechanism of action (MOA) studies for anti-allergic compounds
• IND-enabling safety pharmacology studies
Parameter | HDM Induced Urticaria Model | DNP-IgE & DNFB Induced PCA Model |
Species | Cynomolgus macaque (Macaca fascicularis) | Cynomolgus macaque (Macaca fascicularis) |
Induction method | Repeated epicutaneous or intradermal HDM extract sensitization | Intradermal injection of DNP-IgE followed by DNFB challenge (topical or intradermal) |
Study duration | 4–6 weeks (sensitization + challenge) | 1–2 weeks (passive sensitization + acute challenge) |
Key endpoints | Clinical score (wheal/flare), serum IgE, blood eosinophils, skin H&E score, toluidine blue (mast cell degranulation), eosinophil infiltration | Wheal size, clinical feature, blood eosinophils (optional), mast cell degranulation |
Data package | Raw data, analysis reports, clinical photographs, histology slides (HE, toluidine blue), bioinformatics (optional) | |
Q: What are the differences between the two urticaria models?
A: The HDM model represents allergen-induced urticaria through active sensitization, involving IgE production and eosinophil recruitment. The PCA model is a passive IgE-mediated acute reaction, directly testing mast cell/IgE axis without active sensitization.
Q: Which model is more suitable for testing anti-IgE therapies?
A: Both can be used, but the PCA model (passive sensitization) allows precise control of IgE levels and is ideal for evaluating drugs targeting IgE or its receptor. The HDM model better reflects chronic allergen exposure and associated immune responses.
Q:Can these models be used for IND-enabling studies?
A: Yes. Studies can be conducted in accordance with GLP principles for regulatory submissions (FDA, EMA).
Q: Do you offer customized study protocols (e.g., different allergens, IgE concentrations)?
A: Absolutely. Our scientific team tailors sensitization protocols, challenge schedules, and endpoint analyses to your specific drug candidate.