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Fibrosis Drug Discovery Services

Advancing anti-fibrotic therapeutics with human-relevant models and translational insight

How can you improve translational success in fibrosis drug discovery?

Fibrosis remains one of the greatest challenges in drug development. Despite promising preclinical results, many anti-fibrotic therapies fail to demonstrate efficacy in the clinic because traditional models often fail to capture the complexity of human disease. Across pulmonary fibrosis, liver fibrosis, kidney fibrosis, dermal fibrosis, endometriosis-associated fibrosis and other chronic fibrotic disorders, disease progression is driven by complex interactions between fibroblasts, epithelial cells, immune cells and the extracellular matrix. Understanding these interactions is critical for identifying effective therapies and reducing development risk.

At Concept Life Sciences, we help drug developers bridge this translational gap through human-relevant in vitro models, advanced immune-stromal co-culture systems, multicellular disease models and spatial biology technologies that generate meaningful, decision-driving data.

Our scientists work as an extension of your team, designing tailored assay strategies that provide mechanistic insight, strengthen candidate selection and support confident progression toward the clinic.

How we help you solve fibrosis drug discovery challenges

Your Challenge The Solution
Positive preclinical data fails to translate to the clinic. Human-relevant fibrosis models designed around disease biology rather than relying solely on traditional animal systems.
Uncertainty around therapeutic mechanism of action. Mechanistic assays measuring fibroblast activation, immune signaling, collagen production, and epithelial-to-mesenchymal transition (EMT).
Difficulty modeling complex disease biology. Multicellular and co-culture systems that capture immune-stromal interactions and tissue microenvironments.
Limited understanding of tissue-level therapeutic effects. Spatial biology platforms, including multiplex imaging and spatial transcriptomics.
Selecting the right candidates to progress. Translational screening strategies that generate decision-driving efficacy and mechanistic data.
Need for customized assays aligned to specific targets. Bespoke assay development tailored to your biology, modality, and program objectives.

As your scientific partner, we help clients overcome translational challenges in fibrosis drug discovery.

Improve translatability - Build confidence in your therapeutic using human primary cells, tissue-relevant disease models and translationally meaningful endpoints.

Reduce development risk - Generate robust efficacy, potency and mechanism-of-action data that supports smarter go/no-go decisions.

Understand disease complexity - Explore fibroblast activation, immune signaling, epithelial plasticity and extracellular matrix remodeling within physiologically relevant systems.

Accelerate program progression - Work with experienced scientists who design bespoke assays around your biology, modality and therapeutic objectives.

Driving your fibrosis drug discovery goals to success

Understanding fibrosis at every level - Choose the right tissue analysis approach to answer your questions.

Download the infographic

Expertise across multiple fibrosis indications

Our fibrosis discovery platforms can be tailored to investigate disease mechanisms and therapeutic responses across a wide range of organ systems.

Pulmonary Fibrosis and Interstitial Lung Disease

We support pulmonary fibrosis and interstitial lung disease research using human-relevant cell systems, including:

  • Lung fibroblasts
  • Alveolar epithelial cells (AECII)
  • Airway epithelial cells
  • Macrophage co-culture systems
Liver Fibrosis and Metabolic Dysfunction-Associated Steatohepatitis (MASH)

Our liver fibrosis and MASH capabilities include a range of physiologically relevant cellular models:

  • Hepatic stellate cells
  • Hepatocytes
  • Kupffer cells
  • 3D multicellular fibrosis models
Kidney (Renal) Fibrosis

Our renal fibrosis models include key human cell types involved in disease progression:

  • Renal fibroblasts
  • Proximal tubule epithelial cells
  • Podocytes
Dermal Fibrosis and Pathological Scarring

We provide in vitro models to investigate dermal fibrosis and pathological scarring, including:

  • Dermal fibroblasts
  • Keratinocyte co-cultures
  • Wound healing models
Endometriosis-Associated Fibrosis

Our endometriosis-associated fibrosis models support mechanistic and translational studies using:

  • Endometrial stromal cells
  • Endometriotic lesion-derived fibroblasts
  • Macrophage co-culture systems
Additional Areas of Expertise

We also support fibrosis research across a wide range of therapeutic areas, including:

  • Cardiac fibrosis
  • Intestinal fibrosis
  • Pancreatic fibrosis
  • Ocular fibrosis
  • Systemic fibrotic diseases

Although new drug candidates are emerging, a key challenge remains: how can we adapt cell‑based assays to more accurately model tissue‑specific fibrotic mechanisms and overcome the limitations inherent in animal models? Understanding how human immune cells, fibroblasts, epithelial cells and tissue microenvironments respond to treatment provides a more complete picture of therapeutic activity. We offer a suite of high-quality cell-based assays to investigate candidate drugs and our integrated fibrosis platforms combine expertise in:

This enables us to generate deeper mechanistic insights and more predictive data throughout the discovery process.

Fibroblast and Myofibroblast Assays

The activation of tissue-resident fibroblasts and their differentiation into myofibroblasts is a hallmark of fibrotic disease. Using primary human fibroblasts and tissue-specific cell systems, we evaluate the key cellular mechanisms that drive fibrosis progression.

Our assays measure:

  • Fibroblast activation
  • Myofibroblast differentiation
  • α-SMA expression
  • Collagen I and III production
  • Extracellular matrix remodeling
  • Therapeutic potency and efficacy
Mesenchymal Cell Differentiation

Our differentiation assays use TGF-β stimulation to induce fibrosis-relevant phenotypes and quantify the expression of key biomarkers, including ACTA2 and COL1A1.

This approach enables rapid assessment of anti-fibrotic activity, therapeutic potency, and pathway modulation during lead optimization.

Mesenchymal Cell Phenotyping

Using high-content imaging (HCI), we generate quantitative phenotypic data to support compound screening and lead optimization.

Our assays assess:

  • Collagen production and secretion
  • Cell morphology
  • Cell viability
  • Phenotypic responses

Learn more in our blog: Advanced Drug Discovery: What You Need to Know About HCI (High Content Imaging).

Procollagen Assays

Sensitive procollagen secretion assays provide a quantitative measure of collagen synthesis, enabling robust assessment of extracellular matrix production.

These assays support early-stage screening, candidate prioritization, and efficacy studies for anti-fibrotic therapeutics.

Immune-Stromal Biology

Fibrosis is increasingly recognized as an immune-mediated disease. Macrophages and T cells regulate fibroblast activation, extracellular matrix deposition, and tissue remodeling.

Our immunology expertise enables you to investigate how candidate therapeutics influence these disease-driving immune pathways using physiologically relevant in vitro systems.

Macrophage Assays

Human monocyte-derived macrophages can be polarized into disease-relevant phenotypes to evaluate therapeutic impact on fibrosis-associated immune responses.

Our assays evaluate:

  • Macrophage polarization
  • Cytokine production
  • Pro-fibrotic signaling
  • Fibroblast-macrophage crosstalk
T Cell Assays

Our T cell assays assess how candidate therapeutics modulate adaptive immune responses involved in fibrosis progression.

Endpoints include:

  • T cell activation
  • Th17 and Treg differentiation
  • Cytokine production
  • Immune-fibroblast communication

Assays can be performed as monocultures or integrated co-culture systems to provide greater physiological relevance.

Multicellular and 3D fibrosis models

Capture disease complexity beyond traditional cell culture

Many fibrosis pathways cannot be adequately modeled using single-cell systems.

Our multicellular and 3D models recreate key cellular interactions involved in disease progression, allowing more predictive evaluation of candidate therapeutics.

Capabilities include:

  • Fibroblast–immune cell co-cultures
  • Epithelial–stromal interaction models
  • Liver fibrosis and MASH spheroid systems
  • Custom disease-specific multicellular models

Spatial biology for fibrosis research

Visualize therapeutic effects within the tissue microenvironment

Understanding how therapies influence cells within intact tissue architecture provides critical translational insight that conventional assays cannot achieve.

Our Spatial Biology team combines:

  • Multiplex immunofluorescence
  • Spatial transcriptomics
  • Histology
  • Digital pathology
  • Advanced image analysis

to characterize:

  • Fibroblast activation states
  • Collagen deposition
  • Immune–stromal interactions
  • Tissue heterogeneity
  • Drug-induced biological changes

These technologies provide a powerful framework for mechanistic interpretation, biomarker discovery and translational decision-making.

Collagen type I deposition by human fibroblasts

3D MASH fibrosis models

Our multicellular MASH models combine hepatocytes, hepatic stellate cells and macrophages to investigate inflammatory signaling, collagen production and therapeutic responses within a physiologically relevant environment.

Selonisertib inhibits MASH disease: Hepatocytes, macrophages and hepatic stellate cells were allowed to assemble spheroids in a gel matrix prior to MASH induction in the presence or absence of candidate reference substances. The figure shows that selonisertib significantly inhibits IL-6 and procollagen production.

Epithelial-to-mesenchymal transition (EMT)

Evaluate a key mechanism of fibrosis progression

EMT contributes to tissue remodeling and fibrosis across multiple organs. Macrophages are pivotal in modulating EMT and a target for novel therapeutics targeting fibrosis. Our scratch wound assay can be adapted to include macrophages within the epithelial cell culture supporting analysis of functional changes in co-cultures treated with candidate drugs targeting fibrosis.

Our EMT full suite of assays allow you to investigate:

  • Epithelial plasticity
  • Cell migration
  • Scratch wound healing
  • Collagen deposition
  • Myofibroblast formation

Models can be enhanced through macrophage co-culture to better reflect the inflammatory environment associated with chronic fibrotic disease.

Download the poster: Epithelial to Mesenchymal Transition (EMT) can be driven by macrophages through multiple signaling pathways.

Why partner with Concept Life Sciences?

Human-relevant models - Generate data using disease-relevant systems designed around human biology rather than relying solely on traditional animal models.

Mechanism-led science - Move beyond simple activity measurements to understand how your therapeutic works and where it is most likely to succeed.

Integrated expertise - Access specialists across fibrosis biology, immunology, disease modelling, molecular biology and spatial biology through a single scientific partner.

Customized assay development - Every program is different. We design studies around your target, modality, mechanism and development objectives.

Decision-driving data - Our scientists provide clear interpretation and strategic guidance that supports candidate prioritization and reduces development risk.

Support from concept to clinic

Our fibrosis expertise is complemented by integrated capabilities across:

  • Discovery biology
  • Assay development and screening
  • Disease modeling
  • Spatial biology
  • Molecular biology
  • Medicinal chemistry
  • ADMET and DMPK
  • Toxicology

Working with a single partner helps reduce complexity, improve continuity and accelerate progression from discovery to clinical development.

Ready to advance your fibrosis program?

Whether you need targeted assay support, translational disease models, spatial biology expertise or an integrated discovery partner, our scientists are ready to help you generate the data needed to move forward with confidence.

Discuss your fibrosis program with our team today.

Fibrosis FAQs

Q: What fibrosis drug discovery services does Concept Life Sciences provide?

A: We provide end-to-end fibrosis drug discovery support, from early target validation through lead optimization and translational research. Our capabilities include human primary cell assays, fibroblast and myofibroblast models, immune-stromal co-cultures, high-content imaging, spatial biology, biomarker analysis, and bespoke assay development across multiple fibrotic diseases.

Q: Which fibrotic diseases do you support?

A: We support drug discovery programs across a wide range of fibrotic diseases, including pulmonary fibrosis, interstitial lung disease (ILD), liver fibrosis, metabolic dysfunction-associated steatohepatitis (MASH), kidney fibrosis, dermal fibrosis, pathological scarring, endometriosis-associated fibrosis, and other systemic fibrotic diseases. Our scientists can also develop customized models for specific therapeutic indications.

Q: Why use human-relevant fibrosis models instead of relying only on animal models?

A: Human-relevant in vitro fibrosis models can provide earlier insight into therapeutic efficacy and mechanism of action while improving translational relevance. By combining primary human cells, multicellular co-culture systems, and disease-relevant endpoints, our assays help generate data that better reflects human biology and supports more informed drug development decisions.

Q: Can you develop custom fibrosis assays for novel therapeutic targets?

A: Yes. We routinely develop bespoke fibrosis assays tailored to your therapeutic target, biological pathway, modality, and program objectives. Our scientific team works closely with clients to design assays that measure the most relevant cellular, molecular, and functional endpoints needed to answer specific research questions.

Q: How do your fibrosis assays help reduce drug development risk?

A: Our fibrosis assays generate mechanistic and translational data that help identify promising therapeutic candidates earlier in development. By evaluating fibroblast activation, collagen production, immune cell interactions, extracellular matrix remodeling, and tissue-level responses, we provide evidence that supports candidate selection, mechanism validation, and confident progression into later-stage studies.

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