Our experts at Eurofins Discovery developed the BioMAP® Fibrosis Panel to provide a robust platform to accelerate development of fibrosis therapies – from early discovery to clinical success.
Our panel utilizes human primary cells stimulated to model fibrotic disease, together with protein biomarkers relevant to matrix integrity, tissue remodeling, and chronic inflammation. Systems in this panel are comprised of human primary fibroblasts cultured alone or in co-culture with either primary renal or small airway epithelial cells to provide physiologically relevant assays capable of reporting test agent impact on tissue-specific disease environments. When you take biomarker activity profiles and compare to profiles of select clinical drugs and reference compounds in the BioMAP Reference Database, our panels help you gain insights on mechanism-of-action, efficacy, and safety.
BioMAP Systems and Stimuli Modeling Fibrosis

Figure 1. Modeling human fibrotic disease in vitro with the BioMAP Fibrosis Panel. Human primary lung fibroblasts are cultured either alone (MyoF, modeling fibrosis) or co-cultured with human small airway epithelial cells (SAEMyoF, modeling lung fibrosis) or renal proximal tubule epithelial cells (REMyoF, modeling kidney fibrotic disease). All cells are low passage and pooled from multiple healthy donors.
Fibrosis Panel Advantages
Assess how your candidate influences human biology—before entering clinical trials.
- Validated with therapies approved for treating Interstitial Lung Disease (ILD) and Idiopathic Pulmonary Fibrosis (IPF)
- Common protein biomarker readouts across REMyoF and SAEMyoF systems enable comparison of effects on tissue-specific fibrosis and inflammation models
- Pulmonary and renal models available
Drug Discovery Applications
- Measure 50+ protein-based clinical biomarkers in tissue-specific disease environments to support indication selection
- Prioritize compounds, evaluate target biology, and identify efficacy biomarkers based on comparisons to 80+ reference drugs—including approved antifibrotic therapeutics
- Advance drug repurposing efforts for fibrosis-related indications
- Reveal drug synergies or antagonisms with combination profiling
Impact of Nintedanib on Biomarkers of BioMAP Fibrosis Systems

FIgure 2. Biomarker activity profile of the standard-of-care drug nintedanib in the BioMAP Fibrosis Panel demonstrates antifibrotic, immunomodulatory, and anti-inflammatory activities in all three fibrosis models. Decreased activity of ECM-related molecules type I and III collagens, matrix metalloproteases, and PAI-1 are observed, together with decreased VCAM-1, IL-6, and IL-8 expression. Increased circulating MMPs, VCAM-1, and IL-8 correlate to poor outcomes for patients with idiopathic pulmonary fibrosis (Richards et al.). The effects on protein-based readouts (x-axis) are displayed as a log10 ratio over vehicle control (y-axis).
Trust a robust platform and work with an expert team—our comprehensive reference database, advanced analytical tools, and expertise provide actionable insights for drug development and repurposing efforts.
| BioMAP Fibrosis Panel Service | |
|---|---|
| Service |
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| Description |
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| Deliverables | Annotation of biomarker activities with respect to fibrosis-specific biological classifications, profile plots, graphical overlays of test and reference compound profiles, data tables, expert data interpretation and analysis |
| Fibrosis Systems and Translational Biomarker Readouts | |||
|---|---|---|---|
| System | Disease Biology Relevance | Cell Type | Translational Biomarker Readouts |
| MyoF: Fibrosis |
Myofibroblast development relevant for evaluating matrix deposition, tissue remodeling, and inflammation associated with fibrotic disease biology in tissues—scleroderma, systemic lupus erythematosus, psoriasis, arthritis | Lung Fibroblasts | α-SMA, bFGF, VCAM-1, Collagen-I, Collagen-III, Collagen-IV, IL-8, Decorin, MMP-1, PAI-1, TIMP-1, SRB |
| SAEMyoF: Pulmonary Fibrosis |
Pulmonary disease biology relevant for evaluating wound healing, matrix remodeling, and chronic inflammation-related responses associated with fibrotic disease biology in the lung—idiopathic pulmonary fibrosis (IPF) | Lung Fibroblasts + Small Airway Epithelial Cells | α-SMA, MCP-1, VCAM-1, Collagen-I, Collagen-III, IP-10, I-TAC, E-Cadherin, EGFR, M-CSF, MMP-1, MMP-9, N-Cadherin, PAI-I, sIL-6, sIL-8, SRB, sVEGF, TIMP-1, uPA |
| REMyoF: Renal Fibrosis |
Renal disease biology relevant for evaluating wound healing, matrix remodeling, and chronic inflammation-related responses associated with fibrotic disease biology in the kidney—chronic kidney disease, end-stage renal failure | Lung Fibroblasts + Renal Proximal Tubule Epithelial Cells | α-SMA, MCP-1, VCAM-1, Collagen-I, Collagen-III, IP-10, I-TAC, E-Cadherin, EGFR, Ker8/18, M-CSF, MMP-1, MMP-9, N-Cadherin, PAI-I, sIL-6, sIL-8, SRB, sVEGF, TIMP-1, tPA, uPA |
