Inflammatory bowel disease (IBD) is a chronic intestinal disorder caused by a dysfunctional immune system that mistakenly attacks intestinal tissues when fighting foreign pathogens, resulting in mucosal tissue destruction and increased extracellular matrix (ECM) remodeling. Inflammatory bowel diseases are commonly divided into Crohn's disease (CD) and ulcerative colitis (UC).

Crohn's disease and ulcerative colitis are characterized by inflammation of the mucosa with increased protease activity, leading to increased remodeling of the ECM and increased deposition of collagen in the lamina propria and submucosa. Excessive collagen deposition in the intestinal mucosa and unresolved inflammation are the main causes of surgery in IBD patients due to inadequate response to treatment. Therefore, extracellular matrix markers are important for monitoring mucosal healing/intestinal healing and predicting response to treatment.

How many people have inflammatory bowel disease?
More than 7 million people are currently diagnosed with inflammatory bowel disease (IBD), with a prevalence of approximately 0.3% worldwide. Risk factors also include age, genetics, smoking status, obesity and environmental factors.

How is inflammatory bowel disease treated?
There is no cure for IBD, but the symptoms and inflammation can be treated with immunosuppressants, steroids, or synthetic or biologic medications. The type of treatment depends on the severity of symptoms, the location of the disease, and the number of years with IBD.

How is inflammatory bowel disease diagnosed?
There is no single reference standard for diagnosing Crohn's disease (CD) or ulcerative colitis (UC). Diagnosis of CD or UC is based on a combination of clinical, biochemical (CRP and fecal calprotectin), stool-based, endoscopic, imaging, and histologic studies.

The medical need for biomarkers of IBD today is twofold. First, the diagnosis of CED remains challenging because the signs and symptoms mimic those of many other diseases, including CD and UC. Therefore, distinguishing between UC and CD is difficult. Current biomarker techniques are inaccurate and have difficulty determining patients' future prognosis.

Moreover, despite great progress in the availability of new and effective drugs in recent decades, there is still a significant proportion of patients who do not respond to treatment or whose efficacy declines over time. Diagnostic and prognostic biomarkers have the potential to greatly benefit patients by assisting in the early diagnosis of disease and initiating the most appropriate treatment at the right time, as well as monitoring mucosal healing.

Tissue remodeling as a predictor of treatment response

  • Biomarkers of the mucosal basement membrane may be predictors of response.

Monitoring of treatment response

  • Biomarkers for monitoring structural effect.

Collagen fragments as surrogate markers for endoscopic remission

  • Biomarkers for mucosal healing.

Disease complication

  • Biomarkers for intestinal fibrosis and fistula development

Furthermore, the use of predictive or prognostic biomarkers to enrich or stratify patients that are more likely to achieve mucosal healing and treatment response in drug development trials, may reduce trial length, and size required to determine therapeutic efficacy.

In addition, the use of predictive or prognostic biomarkers to enrich or stratify patients more likely to experience mucosal healing and treatment response in drug development trials may reduce the duration and size of studies needed to determine therapeutic efficacy.

Inflammatory bowel disease is characterized by chronic recurrent inflammation leading to progressive mucosal destruction and remodeling of the ECM. The Protein Fingerprint biomarker technology can be used to quantify the degree of inflammation, mucosal damage, and intestinal fibrogenesis by quantifying fragments of protease-mediated degradation of essential mucosal tissue proteins, including a novel serum calprotectin biomarker (CPa9-HNE) and collagen-derived biomarkers (e.g., C3M, PRO-C3, C4M) released into the bloodstream. This serum calprotectin biomarker eliminates the need of fecal samples, greatly increasing patient compliance and ease of sampling.

The ECM of the intestinal mucosa is mainly composed of collagen, laminin and elastin. The intestinal tissue is a high turnover tissue, which means that the epithelium is replaced once a week. ECM remodeling is essential for intestinal tissue homeostasis. However, if ECM remodeling is constantly altered and out of balance, tissue homeostasis will be compromised, resulting in severe tissue destruction and ineffective healing.

In IBD, the balance of ECM remodeling is imbalanced due to high protease activity and increased deposition of ECM, leading to increased mucosal destruction and initiation of repair processes, which in turn result in scarring of the intestinal mucosa and intestinal fibrosis.

Visit our IBD biomarker portfolio and choose a panel that fits your clinical research or drug development targets!


CPa9-HNE is suppresed in IBD patients in remissions compared to IBD patients with active disease. Thus high serum levels of CPa9-HNE reflects disease activity. 

While fecal calprotectin remains one of the best diagnostic biomarkers for distinguishing IBD from IBS, the ability of fecal calprotectin and CRP to predict response to treatment is limited. Therefore, there is still a need in medicine and drug development for biomarkers that are able to characterize and quantify structural mucosal changes and predict disease progression and response to treatment.


Protein Fingerprint biomarkers measured in serum are generally increased in UC and CD patients compared to healthy subjects (HS).


Reference: Mortensen et al 2015 JCC. 

Fragment of calprotectin degraded by human neutrophil elastase (CPa9-HNE) and type III collagen turnover (C3M/PRO-C3) are both increased in UC and CD patients compared to healthy subjects.

Protein Fingerprint biomarkers measured in serum are associated with established disease activity parameters, including SES-CD (CD endoscopic score) and mMES (UC endoscopic score), generally increased in UC and CD patients compared to healthy subjects.


Correlations between baseline biomarkers concentrations and clinical disease activity parameters. 

Protein Fingerprint biomarkers measured in serum demonstrate to be associated with different CD phenotypes e.g. fistula (C3M/PRO-C3) and fibrostenotic structures (PRO-C16).


(to the left) Reference: Haaften et al 2016 AP&T
(to the right) Reference: Mortensen et al 2018 JCC.

Association of the biomarkers C3M/PRO-C3 and PRO-C16 with fistula and fibrostenotic phenotypes for Crohn's disease.

Protein Fingerprint biomarkers allow pharmacodynamic profiling of novel treatments by measuring protein degradation fragments directly in a serum sample.


Reference: Mortensen et al 2020 JCG.

Asterisks (*) depictsignificant differences from baseline. Squares (#) depictssignificant difference betweenresponders and non-responders

Early suppression in the Protein Fingerprint biomarker VICM provides and information on target engagement and monitoring of treatment response.

Low baseline serum levels of the Protein Fingerprint biomarker, C4M, predicts response to efficacious treatment. The response is defined as being in clinical remission assessed with the HBI (CD clinical disease activity score).


Reference: Haaften et al 2020 CTG.

Baseline prediction of anti-TNFα (IFX and ADA)  clinical response with Protein Fingerprint biomarker C4M

Please don't hesitate to contact us if you have any questions or other inquiries.

Please don't hesitate to contact us if you have any questions or other inquiries.

Are you interested in learning more about Nordic Bioscience?
Enter your information in the form and a representative will contact you shortly.

By submitting this form you agree to our terms and conditions.