Intestinal Fibrosis

NordicIBDTrace™

During chronic inflammation, immune cells secrete pro-inflammatory cytokines that activate tissue-resident fibroblasts, the primary producers of ECM proteins such as collagen. This fibro-inflammatory process leads to progressive tissue stiffening and, ultimately, stricture formation.

Fibrostenotic Crohn’s disease has been associated with non-response to therapeutics, with approximately 50% of patients developing fibrotic complications during their disease course.

In ulcerative colitis, fibrosis is increasingly being recognized as a clinically relevant complication that impacts long-term disease management.

The NordicIBDTrace™ biomarker panel offers a means to quantify intestinal fibro-inflammation, providing valuable insights that can support the development of antifibrotic therapies aimed at preventing or treating fibrostenotic complications.

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NordicPRO-C6™: A marker of intestinal fibrosis

The nordicPRO-C6™ biomarker measures endotrophin, a bioactive fragment with both inflammatory and fibrotic properties. Elevated nordicPRO-C6™ levels have been observed in patients with stricturing Crohn’s disease (B2, Montreal classification) and those with MRE-confirmed strictures. Furthermore, patients who experience stenotic disease progression exhibit higher levels of nordicPRO-C6™ than those who do not progress, highlighting its potential as a biomarker for identifying high-risk patients, monitoring fibrosis progression, and assessing the impact of anti-fibrotic therapies in clinical trials.

NordicPRO-C6™ levels are elevated in patients with stenosis, as well as those who experience stenotic disease progression compared to those who do not progress

Collagen formation biomarkers for tissue fibrosis

Biomarkers of collagen formation, including type III (nordicPRO-C3™), V (PRO-C5) VI (nordicPRO-C6™) , XI (PRO-C11), and XVI (PRO-C16), have been associated with stenotic Crohn’s disease and can be used to differentiate patients with fibrosis from those without.

Additionally, these biomarkers can aid in assessing changes in fibrosis in response to anti-fibrotic treatment, supporting therapeutic evaluation and internal decision making in clinical trials.

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Biomarkers associated with fibro-inflammatory signatures

The biomarkers VICM and PRO-C22, reflecting macrophage activity and remodeling of FACIT collagen type XXII, are positively associated with an inflammation-associated fibroblast (IAF) signature in UC patients. In contrast, nordicCTX-III™, which reflects MMP-mediated degradation of cross-linked type III collagen, is negatively associated with this signature.

Furthermore, elevated serum levels of PRO-C22 and VICM correlate with a molecular prediction signature that identifies non-responders to anti-IL-23 therapy, while nordicCTX-III™ shows a negative association with this signature.

These biomarkers provide insights into fibro-inflammatory pathology and fibrotic complications, supporting mode of action studies and clinical trial design. NordicCTX-III™, in particular, can be used to assess fibrosis resolution in response to anti-fibrotic treatment.

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Translational biomarkers to advance anti-fibrotic drug development

Expanding research on intestinal fibrosis is driving the development of novel treatments aimed at modulating fibrotic processes, though effective therapies remain limited. By stimulating intestinal fibroblasts with pro-fibrotic cytokines, we can model intestinal fibrosis in vitro and evaluate the efficacy of direct anti-fibrotic treatment using the Nordic ProteinFingerPrint™ biomarkers.

The nordicPRO-C3™ biomarker captures fibroblast activity by measuring the formation of type III collagen, while the nordicPRO-C6™  biomarker reflects the bioactive fragment endotrophin, which possesses both inflammatory and fibrotic properties. These biomarkers have shown to capture anti-fibrotic effects of targeted compounds, such as inhibitors of the TGFβ and JAK-STAT pathways. By integrating these biomarkers across in-vitro models, in-vivo samples, and patient cohorts with fibrotic complications, we generate actionable insights into drug-induced modulation of fibrotic pathways. This approach supports target validation, characterizes mechanisms of action, and supports internal decision-making for anti-fibrotic drug development.

NordicPRO-C3™ and nordicPRO-C6™ generate actionable insights into drug-induced modulation of fibrotic pathways

About intestinal fibrosis

  • Intestinal fibrosis is the excessive buildup of extracellular matrix (ECM) proteins, such as collagen, in the gut wall, often resulting from chronic inflammation in inflammatory bowel disease (IBD), particularly Crohn’s disease. Over time, this process leads to tissue stiffening, stricture formation, and impaired intestinal function.

  • Biomarkers like PRO-C3 and PRO-C6 measure collagen formation and help detect fibrotic activity early, before structural changes become irreversible. These non-invasive biomarkers offer real-time insights into disease progression and treatment response in patients with intestinal fibrosis

  • Early detection of fibrosis allows for timely intervention and the potential to prevent complications such as strictures or bowel obstructions. Identifying fibrosis early also helps guide therapeutic strategies and supports the development of antifibrotic treatments.

  • Yes, biomarkers such as CTX-III, PRO-C3, and PRO-C6 can help identify patients likely to benefit from antifibrotic treatments. Changes in biomarker levels can indicate whether a therapy is effectively reducing fibrotic activity, supporting clinical decision-making and trial optimization.

  • Nordic IBDTrace™ is a biomarker panel designed to quantify fibro-inflammatory activity in IBD. It includes markers that reflect collagen turnover and immune activation, offering a comprehensive tool for assessing intestinal fibrosis and supporting antifibrotic drug development.

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