Esophageal Fibrosis

Esophageal fibrosis is characterized by excessive extracellular matrix deposition, primarily collagen accumulation within the lamina propria, leading to structural remodeling and impaired tissue function.

Biomarkers reflecting collagen turnover provide a non-invasive approach to assessing disease activity, monitoring fibrosis progression, and evaluating the impact of therapeutic interventions in EoE.

By capturing dynamic changes in extracellular matrix remodeling, these biomarkers support drug development efforts, offering insights into target engagement, treatment response, and disease modification.

Patients with endoscopic strictures and esophageal rings exhibited increased turnover of cross-linked type III collagen both at baseline and at end of study, as reflected by elevated nordicCTX-III™ and net fibrolysis.

These findings highlight the potential of biomarkers reflecting collagen remodeling and cross-linking to identify patients with severe fibrosis and monitor disease progression or treatment response in clinical trials, supporting biomarker-driven patient stratification.

Patients who experienced fibrosis progression throughout the study exhibited persistently elevated nordicPRO-C3™ and nordicPRO-C6™ levels, indicating sustained type III and type VI collagen formation.

These biomarkers may serve as predictive tools for identifying fibrosis progressors versus non-progressors, enabling patient stratification in clinical trials.

Integrating nordicPRO-C3™ and nordicPRO-C6™ into clinical development can enhance trial design, optimize patient selection, and support the assessment of anti-fibrotic treatment efficacy.