| Quantity: | |
|---|---|
Clinically relevant – Highly consistent with human Guillain-Barré syndrome in pathology, immunology, and clinical presentation.
Comprehensive endpoints – Body weight, clinical score, macrophage and CD4+ T cell infiltration, sciatic nerve histopathology (HE, LFB), pro-inflammatory cytokine analysis (TNF-α, IL-1β).
Mechanism-driven – Macrophage-mediated demyelination and phagocytosis, CD4+ T cell driven autoimmune response, closely mimicking human GBS pathogenesis.
Translational value – Ideal for testing immunomodulators (IVIG, corticosteroids), complement inhibitors, and therapies targeting T cells or macrophages.
IND-ready data packages – Studies can be conducted in accordance with GLP principles.
• Efficacy testing of immunomodulators (IVIG, corticosteroids, plasma exchange mimetics) for Guillain-Barré syndrome
• Evaluation of complement inhibitors and FcRn blockers
• Target validation for macrophage and T cell mediated peripheral nerve injury
• Biomarker discovery (cytokines, autoantibodies, nerve damage markers)
• IND-enabling pharmacology and toxicology studies
Parameter | Specification |
Species/Strain | Lewis rat |
Induction method | Immunization with SP-26 peptide (residues 53-78 of bovine P2 myelin protein) emulsified in complete Freund's adjuvant (CFA) |
Study duration | 21–35 days post-immunization (peak disease ~14-21 days) |
Key endpoints | Body weight, clinical score (0-10 scale for tail/limb weakness), sciatic nerve histopathology (HE for inflammation, LFB for demyelination), cytokine analysis (TNF-α, IL-1β by qPCR/ELISA), optional: electrophysiology (nerve conduction velocity), immunohistochemistry (macrophages, T cells), flow cytometry of nerve-infiltrating cells |
Data package | Raw data, analysis reports, clinical scores, histology slides (HE, LFB), qPCR/ELISA results, bioinformatics (optional) |
Q: How does SP-26 peptide induce EAN?
A: SP-26 corresponds to the immunodominant epitope of bovine P2 myelin protein. Immunization triggers CD4+ T cell mediated autoimmune response against peripheral nerve myelin, with macrophages serving as primary effector cells causing demyelination through direct phagocytosis and inflammatory mediator release.
Q: What are the key similarities with human Guillain-Barré syndrome?
A: EAN shares ascending paralysis, demyelinating pathology, macrophage and T cell infiltration, and response to immunomodulatory therapies with human GBS. It is the most widely accepted animal model for GBS research.
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 SP-26 doses, prophylactic vs. therapeutic dosing)?
A: Absolutely. Our scientific team tailors SP-26 dosing, treatment schedules, and endpoint analyses to your specific drug candidate.
