| Quantity: | |
|---|---|
Clinically relevant – Recapitulates human CLE with photosensitive skin lesions, TLR7 pathway activation, and autoantibody production.
Mechanism-driven – TLR-7 agonist drives innate immune activation; UVB induces cellular damage and IFN-α production, synergistically inducing CLE pathology.
Comprehensive endpoints – Skin clinical score, serum anti-dsDNA antibodies, skin IFN-α levels, histopathology (HE), skin RNA-seq transcriptomics, immune cell clustering analysis.
Translational value – Ideal for testing topical and systemic immunomodulators, JAK inhibitors, anti-IFNAR biologics (anifrolumab), and TLR pathway inhibitors.
IND-ready data packages – Studies can be conducted in accordance with GLP principles.
TLR-7 Agonist+UVB Induced NHP CLE Model
• Efficacy testing of topical and systemic immunomodulators (corticosteroids, calcineurin inhibitors, JAK inhibitors)
• Evaluation of biologics targeting type I interferons (anifrolumab), TLR7/8 pathways, and B cells (rituximab)
• Target validation for photosensitive autoimmune pathways
• Biomarker discovery (anti-dsDNA, IFN-α, skin transcriptomic signatures)
• IND-enabling pharmacology and toxicology studies
Parameter | Specification |
Species/Strain | Cynomolgus macaque (Macaca fascicularis) |
Induction method | Topical TLR-7 agonist (e.g., imiquimod) application on shaved back skin + UVB irradiation (312 nm, multiple exposures) |
Study duration | 2–4 weeks (induction + treatment phase) |
Key endpoints | Skin clinical score (erythema, scaling, thickening), serum anti-dsDNA antibodies (ELISA), skin IFN-α levels (ELISA/qPCR), skin histopathology (HE scoring), skin RNA-seq transcriptomics, immune cell clustering analysis (flow cytometry/scRNA-seq) |
Data package | Raw data, analysis reports, clinical photographs, histology slides, RNA-seq data, bioinformatics analysis |
Q: Why combine TLR-7 agonist with UVB for CLE induction?
A: TLR-7 agonist activates innate immune pathways, while UVB induces cellular damage and IFN-α production. The combination synergistically recapitulates the complex pathogenesis of human CLE, including photosensitivity and type I interferon signature.
Q: What are the key similarities with human CLE?
A: The model exhibits photosensitive skin lesions, elevated anti-dsDNA antibodies, upregulation of IFN-α in skin, and histopathological changes (epidermal hyperplasia, inflammatory infiltration) mirroring human CLE.
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 TLR-7 agonist doses, UVB exposure regimens)?
A: Absolutely. Our scientific team tailors induction protocols, treatment schedules, and endpoint analyses to your specific drug candidate.
Q: What is the typical timeline for a pilot efficacy study?
A: Studies are typically completed within 4 weeks, including induction, treatment, and comprehensive endpoint analysis.