• Type VI collagen formation.
  • Measures highly activated fibroblasts.
  • Biomarker of multi-organ failure and mortality.
  • Links the extracellular matrix and wound healing.
  • Special beaded filament collagen.

NordicPRO-C6™ measures the formation of type VI collagen which is connected to fibrogenesis and activated fibroblasts. This marker assesses Endotrophin, a hormone responsible for promoting profibro-inflammatory processes via signaling mechanisms.

PRO-C6 acts as a driver of fibro-inflammatory processes, providing an efficient tool in predicting outcomes (risk of cardiovascular events; mortality; disease progression) in many different fibrotic diseases affecting liver, heart, kidneys, gastrointestinal system. Endotrophin also has a major role in the development and progression of metabolic disorders and is highly correlated to angiogenesis.This allows for identifying patients suffering fromheart failure with preserved ejection fraction (HFpEF), and patients at risk of developing cardiovascular events and those who are at risk of death.

Cardiology

Fibrosis is a hallmark feature of HFpEF pathology, acting as a driver of outcome. Understanding the intricate pathways that lead to fibrogenesis, and how they ultimately impact pathogenesis, is important for understanding how to treat HFpEF. We have developed a biomarker of fibroblast activity, PRO-C6, which independently and with high precision can identify a subset of HFpEF patients with a very elevated risk of adverse outcome.

 

Click here for a detailed overview on PRO-C6 in HFpEF.

PRO-C6 and C3M in serum (sPRO-C6, sC3M) and urine (uPRO-C6, uC3M) were measured by ELISA in 663 patients with T1D ranging from normoalbuminuric to macroalbuminuric. Association of the biomarkers with mortality, CVEs, heart failure, decline in estimated glomerular filtration rate (eGFR) ≥30%, and end-stage renal disease (ESRD) were tested in Cox proportional hazards models after log2 transformation and adjusted for relevant clinical characteristics. Hazard ratios (HRs) were reported per doubling of biomarker levels. High levels of sPRO-C6 were independently associated with a higher risk of all-cause mortality (HR 2.26 [95% CI 1.31-3.87], P \u003c 0.0031). There was an association with higher risk of CVEs (n = 94) and heart failure (n = 28) but not after adjustment (P ≥ 0.58). In relation to renal outcomes, adjusted sPRO-C6 was associated with a higher risk of eGFR decline ≥30% in T1D, with eGFR \u003e45 and \u003e30 mL/min/1.73 m2, and with a higher risk of ESRD (all P ≤ 0.03). Higher uPRO-C6 was associated with a lower risk of decline in eGFR.

We examined a cohort of 49 IgAN and 47 AAV patients. A validation cohort of 85 IgAN patients was included. Endotrophin (ETP) was measured in serum (S-ETP) and urine (U-ETP/Cr) samples, taken on the same day before renal biopsy was performed, using the ELISA PRO-C6. The biopsies were evaluated for interstitial fibrosis and tubular atrophy according to the Banff and MEST-C scores. S-ETP and U-ETP/Cr levels correlated with kidney function, increased with CKD severity, correlated with the extent of interstitial fibrosis and gradually increased with increasing degree of interstitial fibrosis and tubular atrophy. ETP outperformed the known fibrosis biomarker Dickkopf-3 for discrimination of patients with high fibrotic burden. The association of S-ETP and U-ETP/Cr with the level of kidney fibrosis was confirmed in the validation cohort.

Therapeutic area
Gastroenterology, Cardiovascular diseases, Cancer, Hepatic diseases, Respiratory diseases, Renal diseases, Dermatology, Rheumatology, Metabolic dysregulation

Biomarker panels
Lung Fibrosis, COPD, FIB-NIT Panel™: Fibrosis Non-invasive Tests, Bridging Fibrosis, Tissue Fibrosis, Fibrosis / Fibroblasts, Kidney Disease Activity, Kidney Outcome, Kidney Preclinical, Heart Fibrosis, Atherosclerotic Plaque Instability, Heart Outcome, Tissue Fibrosis, Mucosal Damage Resolution, Systemic Sclerosis

Function
Pro-fibrotic signaling, ECM formation, Wound healing

Alternative names
PROC6, nordicPRO-C6™, Endotrophin