| Quantity: | |
|---|---|
Clinically relevant – BLM-induced skin fibrosis recapitulates human SSc with dermal thickening, collagen accumulation, and autoantibody production.
Mechanism-driven – BLM induces DNA damage, oxidative stress, and inflammation, leading to fibroblast activation and excessive collagen deposition.
Comprehensive endpoints – Body weight, skin pull-up height (mm), hydroxyproline content (collagen quantification), histopathology (HE, Sirius Red), dermal thickness measurement.
Translational value – Ideal for testing anti-fibrotic agents (nintedanib, pirfenidone), TGF-β inhibitors, tyrosine kinase inhibitors, and immunomodulators.
IND-ready data packages – Studies can be conducted in accordance with GLP principles.
BLM Induced BALB/c SSc Model
• Efficacy testing of anti-fibrotic agents (nintedanib, pirfenidone, TGF-β inhibitors, galectin-3 inhibitors)
• Evaluation of tyrosine kinase inhibitors (imatinib, dasatinib) and immunomodulators (corticosteroids, mycophenolate)
• Target validation for fibrosis pathways (collagen synthesis, fibroblast activation)
• Biomarker discovery (hydroxyproline, collagen markers, inflammatory mediators)
• IND-enabling pharmacology and toxicology studies
Parameter | Specification |
Species/Strain | BALB/c mouse |
Induction method | Intradermal injection of bleomycin (BLM, 50–100 μL of 0.5–1 mg/mL solution) on shaved back skin, 2–3 times/week for 3–6 weeks |
Study duration | 3–8 weeks (induction + treatment phase) |
Key endpoints | Body weight, skin pull-up height (mm) as measure of skin thickness/fibrosis, hydroxyproline content (collagen quantification), skin histopathology (HE and Sirius Red staining with dermal thickness and collagen deposition scoring) |
| Positive control | Nintedanib or pirfenidone available as reference anti-fibrotic compounds |
| Data package | Raw data, analysis reports, histology slides (HE, Sirius Red), hydroxyproline assay results, bioinformatics (optional) |
High cost efficiency and throughput: It supports parallel testing of multiple drug candidates or dose groups at a lower cost, enabling rapid lead compound screening and ranking.
Stable and reproducible phenotype: The BLM-induced mouse SSc model is a gold-standard platform with well-documented protocols, delivering consistent fibrosis phenotypes for reliable efficacy comparison.
It is ideal for early target validation, preliminary efficacy screening, and mechanism-of-action studies, serving as a cost-effective stepping stone before advancing to NHP translational research.
Clinical & functional endpoints: Longitudinal body weight monitoring for safety assessment, and skin pull-up height measurement to quantify skin sclerosis severity.
Biochemical endpoints: Hydroxyproline content assay in skin tissue for quantitative collagen level detection.
Pathological endpoints: H&E staining for dermal thickness and inflammatory infiltration assessment, and Sirius Red staining for specific collagen fiber visualization and fibrosis grading.
Customized cytokine profiling and autoantibody detection assays are also available upon request.
Efficacy screening of anti-fibrotic agents targeting collagen synthesis, extracellular matrix remodeling and fibroblast activation.
Evaluation of immunomodulators, anti-inflammatory drugs and cytokine-targeted biologics for autoimmune-mediated fibrosis.
Target validation of fibrotic and autoimmune pathways, and dose-response studies to support lead compound optimization.
