| Quantity: | |
|---|---|
Clinically relevant – Recapitulates human PN with IgE-mediated inflammation, chronic pruritus, and papulonodular skin lesions.
Mechanism-driven – IgE and Th2 cytokine (IL-4) mediated inflammation drives persistent scratching and fibrotic changes.
Comprehensive endpoints – Body weight, itch events (scratching behavior), serum IgE, skin IL-4, histopathology (HE, Masson trichrome), RNA-sequencing data.
Translational value – Ideal for testing anti-IgE biologics, JAK inhibitors, IL-4/13 antagonists, and anti-pruritic agents.
IND-ready data packages – Studies can be conducted in accordance with GLP principles.
OVA&OXA Induced BALB/c PN Model
• Efficacy testing of anti-IgE biologics (omalizumab), JAK inhibitors (tofacitinib, upadacitinib), and IL-4/13 antagonists (dupilumab)
• Evaluation of anti-pruritic agents (antihistamines, neurokinin-1 receptor antagonists)
• Target validation for IgE-mediated chronic itch and fibrosis pathways
• Biomarker discovery (IgE, IL-4, itch-associated mediators)
• IND-enabling pharmacology and toxicology studies
Parameter | Specification |
Species/Strain | BALB/c mouse |
Induction method | OVA sensitization (intraperitoneal, with alum) + repeated topical OXA challenge on shaved back skin |
Study duration | 4–8 weeks (sensitization + challenge phases) |
Key endpoints | Body weight, itch events (scratching behavior), serum IgE (ELISA), skin IL-4 levels (ELISA), histopathology (HE scoring for epidermal hyperplasia and inflammation, Masson trichrome scoring for fibrosis), RNA-sequencing data, optional: immunohistochemistry, flow cytometry |
| Positive control | Corticosteroids (e.g., prednisolone) or anti-IgE antibody available as reference compounds |
Data package | Raw data, analysis reports, behavioral data, ELISA results, histology slides, RNA-seq data, bioinformatics (optional) |
Q: How does OVA and OXA induce prurigo nodularis in mice?
A: OVA sensitization induces IgE and Th2 immunity. Repeated OXA challenge on the skin triggers a delayed-type hypersensitivity that, combined with IgE-mediated inflammation, leads to persistent scratching, papulonodular lesion formation, and fibrosis, mimicking human PN pathogenesis.
Q: What are the key similarities with human prurigo nodularis?
A: The model exhibits intense scratching, elevated IgE, Th2 cytokine (IL-4), epidermal hyperplasia, dermal fibrosis (Masson trichrome), and papulonodular lesions, closely mirroring human PN pathology.
Q: Can this model 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 OVA/OXA doses, treatment timing)?
A: Absolutely. Our scientific team tailors sensitization protocols, challenge schedules, and endpoint analyses to your specific drug candidate.
Q: What is the typical timeline for a pilot efficacy study?
A: Studies typically run 6–8 weeks, including sensitization, multiple OXA challenges, treatment, and endpoint analysis.
