Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that is characterized by reduced airflow and mainly affects middle-aged or older adults who smoke. COPD is a progressive disease leading to symptoms like shortness of breath, cough, and mucus production. The airflow limitation is caused by a mixture of obstructive bronchitis and fibrosis in the small airways as well as destruction of the lung parenchyma resulting in emphysema.

How many have COPD?
COPD is an underdiagnosed disease with a reported prevalence of 251 million cases worldwide. With 3.2 million deaths in 2015, COPD caused 5% of all deaths globally making it the third leading cause of death. Tobacco smoke is the primary cause of COPD, but other major risk factors include indoor and outdoor air pollution and occupational dusts or fumes.

How is COPD treated?
There is no cure for COPD, but bronchodilators are the most common type of treatment to improve lung function temporarily and reduce symptoms. The treatment regimen is based on symptoms, lung function, and risk of exacerbations.

How is COPD diagnosed?
The current diagnosis is based on spirometry with a post-bronchodilator value of forced expiratory volume in 1 second (FEV1) / forced vital capacity (FVC) ratio below 0.7. This confirms persistent airflow limitation, and together with symptoms leads to a diagnosis.

The medical need for biomarkers in COPD is to enable precision medicine. First, a diagnostic biomarker identifying distinct subtypes would be of value due to the vast heterogeneity of COPD. Second, a prognostic biomarker identifying patients at risk of rapid progression would stratify patient selection for clinical trials and guide treatment strategy. Third, a predictive biomarker to select patients likely to respond to a therapeutic drug in clinical trials may reduce the length of trials as well as the number of participants required to determine therapeutic efficacy.

During COPD, persistent exposure to cigarette smoking or other irritants are causing chronic inflammation. A normal repair response yields a balance between extracellular matrix (ECM) proteins that are broken down and rebuild to uphold tissue structure and function. However, the balance between degradation and formation is disturbed during chronic inflammation which leads to an altered tissue remodelling in COPD. The tissue derived Protein Fingerprint biomarkers can be measured in serological samples and used to accurately quantify changes in tissue turnover in the lung in the individual patient.

In the COPD field, only plasma fibrinogen has been qualified as a biomarker for trial enrichment, as elevated levels are associated with a higher risk of acute exacerbations and death. Plasma fibrinogen levels reflect systemic wound healing which occurs continuously all over the body, thus its capacity is limited. Furthermore, no biomarkers are available for subtyping or prediction of treatment response. Therefore there still is a medical- and drug development need for biomarkers that may characterize and quantify structural tissue changes and predict disease progression and treatment response. Tissue derived Protein Fingerprint biomarkers as well as neo-epitope biomarkers of wound healing are highly relevant for assessing the pathological changes occurring in the lungs of patients with COPD. Our biomarkers can be used separately or in combination to reflect aberrant lung tissue remodeling, wound healing and inflammation.  


Protein Fingerprint biomarkers measured serologically are generally increased in COPD patients compared to healthy individuals. Smoking status in healthy individuals alters the lung tissue turnover and this may also be reflected by the Protein Fingerprint biomarkers.


Lung tissue remodeling, quantified by type VI collagen formation (PRO-C6) and MMP mediated degradation (C6M) and elastin degradation mediated by neutrophil elastase (EL-NE) or proteinase-3 (ELP-3), as well as wound healing, quantified by X-FIB, are both increased in COPD as compared to smoking and even more so when compared with never-smoking healthy controls.

References: Bihlet A et al 2017 Respir Res; Rønnow SR et al 2019 SciRep; Manon-Jensen T and Langholm LL et al 2019 Respir Med

Protein Fingerprint biomarkers measured in serum are associated with subtypes of COPD, such as chronic bronchitis or emphysema.


Lung tissue degradation quantified by MMP degraded type VI collagen (C6M) is associated with the COPD subtype characterized by chronic bronchitis.

Reference: Bihlet A et al 2017 Respir Res

Protein Fingerprint biomarkers measured in serum are associated with acute exacerbations of COPD (AECOPD). AECOPD are periods of worsening of respiratory symptoms that drive disease progression. Thus, the Protein Fingerprint biomarkers are associated with disease activity in patients with COPD.


Lung tissue degradation quantified by MMP degraded type I, III, IV and VI collagen (C1M, C3M, C4M, C4Ma3, C6M), and neutrophil elastase degraded elastin (EL-NE) are all increased during hospitalized acute exacerbations of COPD as compared to baseline and 4 weeks follow-up.

References: Sand JM et al 2015 Respir Res; Stolz D et al 2017 Chest; Schumann DM et al 2018 Chest

Protein Fingerprint biomarkers measured in serum may predict disease progression as determined by decline in lung function (FEV1).


Associations are shown per increase of 1 SD in each biomarker. Protein Fingerprint biomarkers (C1M and C6M) are associated with rate of change in FEV1 to a higher degree than the standard serological biomarkers.

Reference: Leeming DJ et al 2017 BMC Pulm Med

Protein Fingerprint biomarkers measured in serum are associated with mortality in COPD and may be useful in predicting outcome and aid therapeutic decision making.


COPD patients with high baseline serum levels of Protein Fingerprint biomarkers (Q4) have increased risk of all-cause mortality.

Reference: Sand JM et al 2016 Respir Res

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