Webinar | Breaking down the Matrix: Autoimmunity – Nordic Bioscience

Breaking down the Matrix: The Interplay Between Fibrosis, Inflammation, and Autoimmunity

Watch our latest dermatology webinar “Breaking down the Matrix: The Interplay Between Fibrosis, Inflammation, and Autoimmunity”, to learn more about the role of the ECM in the pathogenesis of autoimmune conditions affecting both skin and joints, with a focus on systemic sclerosis and lupus.

In this webinar we will dive into the the interplay between fibrosis, inflammation, and autoimmunity.

Scientific Topics

Autoimmune skin diseases involve more than immune dysfunction—they disrupt tissue structure through early and persistent extracellular matrix (ECM) remodeling. This webinar examines the ECM’s central role in the pathogenesis of autoimmune conditions affecting both skin and joints, with a focus on systemic sclerosis and lupus.

Systemic sclerosis is characterized by immune dysregulation, vascular abnormalities, and progressive fibrosis, driven by activated fibroblasts and sustained pro-fibrotic signaling that lead to excessive ECM deposition and multi-organ involvement. In lupus, widespread inflammation and immune-mediated tissue damage also intersect with ECM remodeling, contributing to disease heterogeneity and long-term complications.

By exploring shared inflammatory and fibrotic pathways across these diseases, we highlight recent advances in targeted therapies designed to interrupt ECM-driven pathology and improve disease management.

Agenda

  • Welcome and Introduction to the Extracellular Matrix and Autoimmunity by moderator Dr. Signe Holm Nielsen
  • Systemic Sclerosis: The Vascular–Inflammatory–Fibrotic Axes and Investigating Their Role with Collagen Biomarkers in The ECM and Cellular Therapies | Prof. Dr. Dinesh Khanna
  • Do Fibroblasts Matter in Cutaneous Lupus? | Prof. Dr. J. Michelle Kahlenberg
  • Challenges in Drug Development for Systemic Sclerosis | Dr. Christina Merz-Stoeckle
  • Questions from the chat

Duration: 90 minutes

Speakers

Prof. Dr. Dinesh Khanna

  • Prof. Dr. Dinesh Khanna is a leading expert in scleroderma and related conditions, with an H-index of 107, i10-index of 485, and over 64,000 citations.
  • He directs a multidisciplinary team of clinicians, scientists, and researchers focused on advancing understanding and treatment of scleroderma.
  • His research includes the development of novel patient-reported outcome measures for scleroderma and various joint diseases.
  • Prof. Dr. Khanna has extensive expertise in clinical trial design for evaluating new treatments in scleroderma.
  • He plays a key role in leading international initiatives to establish management guidelines for scleroderma and gout.
  • His work bridges patient-centered research with evidence-based clinical practice.
  • Prof. Dr. Khanna is recognized globally for shaping therapeutic strategies in rare autoimmune and rheumatic diseases.
  • He is committed to improving quality of life and outcomes for patients through innovative research and clinical care.
  • His leadership fosters strong collaborations between academia, clinical medicine, and patient advocacy groups.
  • Prof. Dr. Khanna’s contributions have positioned him as a driving force in rheumatology and systemic autoimmune disease research.

Prof. Dr. J. Michelle Kahlenberg

  • Prof. Dr. J. Michelle Kahlenberg is Professor of Internal Medicine and Dermatology at the University of Michigan, where she also serves as Vice Chair of Research for the Department of Internal Medicine.
  • She holds an H-index of 47, i10-index of 103, and over 8,600 citations.
  • Prof. Dr. Kahlenberg earned her BS in Biology (Summa Cum Laude) at Denison University, followed by her MD, PhD, and Internal Medicine training at Case Western Reserve University, and a Rheumatology fellowship at the University of Michigan.
  • Her clinical expertise focuses on caring for complex lupus patients, particularly those with refractory skin disease.
  • She established her independent research laboratory in 2013, supported by NIH and foundation funding, integrating patient samples and murine models to investigate mechanisms driving cutaneous and systemic lupus and other autoimmune diseases.
  • She is the inaugural Giles Bole and Dorothy Mulkey Research Chair in Rheumatology at the University of Michigan.
  • Prof. Dr. Kahlenberg has received major recognitions, including the Lupus Foundation of America’s Mary Betty Stevens Award (2018), the Presidential Early Career Award for Scientists and Engineers (2018), and the American College of Rheumatology Henry Kunkel Young Investigator Award (2022).
  • In 2023, she was inducted into the Henry Kunkel Society and the American Society of Clinical Investigation.
  • She is widely recognized for her translational research bridging clinical rheumatology with mechanistic discoveries in lupus and autoimmunity.
  • Prof. Dr. Kahlenberg continues to be a national leader in advancing therapies and improving outcomes for patients with lupus and autoimmune diseases.

Christina Merz-Stoeckle

  • Dr. Christina Merz-Stöckle is a Senior Principal Scientist at Novartis Institutes for BioMedical Research (NIBR) with over 25 years of experience in autoimmune and inflammatory diseases.
  • She holds a Master’s degree from the University of Oxford and a PhD from the University of Tübingen, specializing in autoimmune diseases.
  • During her academic training, she served as Speaker of the Graduate School, highlighting her leadership and communication skills.
  • At Novartis, she is Head of Lab and Project Team Lead in Autoimmunity, Transplantation, and Inflammation.
  • Her work focuses on identifying and validating drug targets in pre-clinical and early-stage drug development.
  • Dr. Merz-Stöckle is known for effectively bridging discovery research with translational applications in drug development.
  • She has authored numerous scientific publications, with an H-index of 20 and more than 1,000 citations.
  • She is widely recognized for her expertise, leadership, and contributions to advancing therapies for autoimmune and inflammatory diseases.

This webinar was co-hosted with The Extracellular Matrix Pharmacology Congress.

The PRO-C3 Story | Webinar

Fibroblast Activity is Highly Prognostic for Outcome in Over 50 Chronic Diseases

Overview

Fibroblast activity is a major cause of 35% of deaths in the Western world. Fibroblasts are key drivers of outcome in solid tumors as well as in fibrosis of the liverlungkidneyintestineskin, and in heart failure. To alter the trajectory of organ failure and patient outcomes, we must quantify and change fibroblast activity.

One measure of fibroblast activity is PRO-C3, which was launched by Roche in May 2025 with a Context of Use (COU) as a diagnostic enrichment tool for liver fibrosis -a milestone in the field of biomarker discovery and development.

This webinar highlights the process of how an ELISA kit was advanced through CLSI validation into an RPA prototype assay with Roche, moving to IVD quality on the flagship 801 equipment, and gathering data for CE launch. At the same time, it was submitted to the FDA for: 1) a Letter of Intent, 2) qualification advice, and 3) a full qualification package under the LITMUS consortium.

This work resulted in an FDA Letter of Support—the first ever for a serological biomarker for the assessment of tumor fibrosis. This is a story of the work of hundreds of researchers and remarkable teamwork that would not have been possible without extraordinary stamina.

This webinar is a celebration of the PRO-C3 story and all the people involved. We highlight the best diagnostic, prognostic, and pharmacodynamic data, demonstrating how dangerous fibroblast activity is for patients, as well as the role of PRO-C3 in drug development across a range of indications where the extracellular matrix is a key component. From cellular mechanisms to serological assessment in patients—this is about how to quantify and control fibroblast activity.

Naturally, we also discuss weight-dependent and weight-independent approaches to modulating fibroblast activity, and the challenges and opportunities that follow.

Agenda

1. Introduction

  • Welcome and overview of webinar objectives
  • The clinical burden of fibroblast activity in chronic diseases
  • Framing fibroblast biology as a therapeutic target

2. The PRO-C3 Biomarker

  • What PRO-C3 measures: Active fibrogenesis and fibroblast activity
  • Initial development and academic validation of the ELISA
  • Translating research use into regulated diagnostics

3. Roche Collaboration and Industrialization

  • Transitioning from ELISA to RPA prototype assay
  • Validation to IVD standard on Roche 801 platform
  • CLSI validation and CE marking process

4. Regulatory Milestones

  • FDA engagement: Letter of Intent, Qualification advice, Full qualification package (under LITMUS)
  • FDA Letter of Support: First for a serological tumor fibrosis biomarker

5. Clinical and Translational Applications

  • Diagnostic, prognostic, and pharmacodynamic performance across diseases
  • Use of PRO-C3 in liver fibrosis, tumor stroma, pulmonary and renal fibrosis
  • Patient stratification and trial enrichment strategies

6. Mechanistic Insights and Modulation Strategies

  • Fibroblast activity: Weight-dependent vs. weight-independent pathways
  • Implications for therapeutic intervention design

7. Lessons from the PRO-C3 Development Journey

  • Multi-disciplinary collaboration and sustained execution
  • Integrating biomarker science, regulatory strategy, and platform scaling
  • Opportunities for other biomarkers following a similar path

8. Q&A and Closing Remarks

  • Open discussion with Dr. Morten Karsdal and Dr. Diana J. Leeming
  • Final reflections on the future of fibroblast-targeted biomarker development

Speakers

Dr. Morten Karsdal

  • Dr. Morten Karsdal joined Nordic Bioscience in 2001 and became CEO in June 2010, leading the company to significant advancements in biomarker development and disease biology.
  • Dr. Karsdal is a KOL in extracellular matrix research, with more than 700 publication and an impressive H-factor of 100.
  • Dr. Karsdal is an honorary professor of inflammation research at the University of Southern Denmark, where he continues to supervise PhD students, fostering the next generation of researchers.
  • Dr. Karsdal chairs the Extracellular Matrix Pharmacology Congress, an important forum for advancing drug development by focusing on the extracellular matrix (ECM) as a key factor in most chronic diseases. He is renowned for his deep expertise in fibrosis, rheumatology (including rheumatoid arthritis and osteoarthritis), diabetes, and other chronic conditions, particularly in relation to ECM and biomarker research.
  • Dr. Karsdal has led the development of FDA-approved and supported molecular diagnostics, as well as more than 100 commercialized biomarker assays, including ELISA assays and high precision automated platforms.
  • He has extensive experience in clinical trial design and the clinical application of biochemical markers, often serving as a consultant to major pharmaceutical companies for the use of serological biomarkers in clinical trials.
  • In 2016, he and his research team authored the first edition of “Biochemistry of Collagens, Laminins and Elastin,” published by Elsevier Science. The book, now in its 3rd edition as of 2023, is a key resource on collagens and structural proteins, with a focus on their applications in chronic diseases.

Dr. Diana Julie Leeming

  • Dr. Diana Julie Leeming is the Senior Director of Fibrosis, Hepatic, and Pulmonary Research at Nordic Bioscience.
  • She joined Nordic Bioscience in 2004 and assumed the role of Director of Fibrosis in 2010, later being promoted to Senior Director in 2024.
  • Dr. Leeming focuses on developing serologically assessed markers to evaluate extracellular matrix remodeling in patients with pulmonary or hepatic fibrosis, aiding in diagnosis and pharmacodynamic evaluation.
  • She is a principal inventor of the PRO-C3 assay, a fibrogenesis marker utilized in multiple clinical trial studies.
  • Dr. Leeming has authored over 280 peer-reviewed publications, demonstrating her extensive contributions to the field.
  • Her H-index is 61, her I10-index is 174, and her research has garnered over 11,825 citations as of March 2024.

The webinar was organized exclusively by Nordic Bioscience.

Get in touch

Are you interested in exploring collaboration possibilities?
Enter your information in the form and a representative will contact you shortly.

    Canstatin Is Associated with Mortality Risk in Advanced Atherosclerosis

    Canstatin, a type IV collagen fragment, is associated with risk of cardiovascular and all-cause mortality in patients with advanced atherosclerosis

    Introduction

    Atherosclerosis, a common underlying cause of cardiovascular disease, is defined by the formation of
    plaques in the arterial walls. Changes in the ECM composition impact the risk for plaque rupture, which may cause acute complications (i.e. stroke or myocardial infarction (MI)). Type IV collagen is primarily known as a major component of basement membranes and has previously been reported to promote plaque stability. Canstatin is the non-collagenous C-terminal domain of type IV collagen alpha 2 chain. It is not only a by-product of proteolytic activity, but also a bioactive molecule. This study investigated if canstatin was associated with adverse outcomes in patients with advanced carotid atherosclerosis.

    Poster

    Conclusion

    Higher circulating canstatin levels in patients undergoing carotid endarterectomy predicted cardiovascular mortality and all-cause mortality over 7.5 years. This suggests that canstatin is a potential novel tool for risk stratification in patients with advanced atherosclerosis, warranting further studies.

    Get in touch

    Are you interested in exploring collaboration possibilities?
Enter your information in the form and a representative will contact you shortly.

      The Brain’s Breakdown: Biomarkers and ECM in Neuroinflammation and Neurodegeneration

      In this webinar we uncovered how the brain’s extracellular matrix (ECM) and emerging biomarkers are reshaping our understanding of neuroinflammation and neurodegeneration, with a focus on their role in disease mechanisms, diagnosis, and therapeutic innovation.

      The brain is more than just neurons; it is a complex, finely tuned environment shaped by the extracellular matrix (ECM) and molecular signaling.

      This webinar examines the structure and function of the brain ECM, emphasizing its influence on neural plasticity, signaling, and repair. After establishing a foundation in ECM biology, we will explore how this network interacts with disease mechanisms and why it has become a central focus in neuroscience.

      Agenda and Speakers

      Introductions and welcome to the webinar by moderator Dr. Signe Holm Nielsen

      Fluid biomarkers for neurodegeneration and inflammation in neurological diseases – Prof. Dr. Ir. Charlotte Teunissen

      Neuroinflammation, biomarkers and upcoming treatments in Multiple Sclerosis – Prof. Dr. Tobias Sejbæk

      Should we target the Extracellular Matrix of the Brain in Drug discovery? – Dr.  Kim Henriksen

      Questions from the chat

      Scientific Topics

      A major topic will be the growing importance of biomarkers in neurodegenerative and neuroinflammatory disease research. Notably, phosphorylated tau at threonine 217 (pTau217) has emerged as a promising diagnostic marker for Alzheimer’s disease, representing a significant advance in early detection.

      However, identifying equally robust and specific biomarkers for conditions such as Parkinson’s disease and multiple sclerosis remains challenging, with unresolved issues in diagnosis, prognosis, subtyping, and assessment of drug efficacy.
      ​​​​​​​
      The webinar will conclude by examining how insights into brain ECM dynamics and disease-specific molecular profiles can drive drug discovery and therapeutic innovation, offering new opportunities to develop targeted treatments and improve clinical outcomes.

      Prof. Dr. Ir. Charlotte Teunissen

      • Prof. Dr. Ir. Charlotte Teunissen is a Full Professor of Neurochemistry dedicated to improving care for neurological disease patients through the development of body fluid biomarkers.
      • Her research spans the full biomarker development pipeline—from discovery to assay development, validation, and clinical implementation.
      • She leads the body fluid biomarker program at the Alzheimer Center Amsterdam, a key center for biomarker innovation in neurodegenerative diseases.
      • Prof. Teunissen’s work focuses on biomarkers for diagnosis, patient stratification, prognosis, and treatment monitoring in neurological conditions, particularly dementia.
      • She is an international leader in biomarker collaboration, serving as chair of the CSF Society and the Alzheimer’s Association Global Biomarker Standardization Consortium.
      • She recently co-founded the Coral proteomics consortium to advance proteomic approaches in biomarker research.
      • Prof. Teunissen coordinates the EU-funded Marie Curie MIRIADE project, training 15 early-stage researchers in dementia biomarker development.
      • Her team plays a critical role in translating biomarker research into clinical practice, with an emphasis on standardization and global accessibility.
      • She is recognized for fostering interdisciplinary and international collaborations to accelerate progress in neurodegenerative disease research.
      • Prof. Teunissen’s work is shaping the future of personalized neurology by enabling earlier diagnosis and more precise treatment of dementia and related disorders.

      Dr. Kim Henriksen

      • Dr. Kim Henriksen is the Director of Endocrinology and Neuroscience at Nordic Bioscience, where he has worked since 2002 and assumed his current leadership role in 2018.
      • He leads a team of 15 scientists and technicians focused on developing novel biomarkers for neurodegenerative diseases, particularly blood-based tools for identifying individuals in need of treatment.
      • Dr. Henriksen’s research also targets the development of peptide therapies for metabolic diseases, including obesity, NASH, and type 2 diabetes.
      • He is a key inventor behind the DACRA peptide family, with the lead molecule currently in phase 2 clinical development.
      • His earlier work led to the patenting and advancement of two peptide families—KBPs and OXMs—now progressing toward clinical use.
      • Dr. Henriksen has authored nearly 200 peer-reviewed publications.
      • He has an H-index of 65, i10-index of 158, and over 11,985 citations as of August 2024.
      • His translational research bridges biomarker science and therapeutic innovation in both endocrinology and neuroscience.
      • Dr. Henriksen is widely recognized for his contributions to precision medicine in metabolic and neurodegenerative disorders.
      • He continues to drive Nordic Bioscience’s strategy in peptide drug development and biomarker discovery for complex chronic diseases.

      Prof. Dr. Tobias Sejbæk

      • Dr. Tobias Sejbæk is Head of Research and Consultant in Neurology at Esbjerg Hospital, affiliated with the University of Southern Denmark.
      • He joined the University of Southern Denmark in 2011 and became Head of Research in 2019.
      • Dr. Sejbæk is a leading figure in clinical neurology, particularly in the field of multiple sclerosis (MS).
      • He serves as the national Principal Investigator for major MS clinical trials, including FENHANCE, GEMINI, HERCULES, and PERSEUS.
      • He has authored nearly 65 peer-reviewed publications and holds an H-index of 15.
      • Dr. Sejbæk has received multiple awards for his clinical trial presentations and contributions to advancing MS treatment.
      • He is a board member of the Danish Neurological Association, reflecting his national leadership in the neurology community.
      • His research focuses on translating clinical data into improved treatment strategies for neurological diseases.
      • He actively promotes evidence-based neurology and is committed to integrating new therapies into clinical practice.
      • Dr. Sejbæk continues to lead high-impact research and clinical initiatives that shape the future of MS care in Denmark and beyond.

      We are also excited to inform you about our upcoming in-person event, The Extracellular Matrix Pharmacology Congress, taking place in Copenhagen in June 2026. This congress will be a unique opportunity to gather with leading experts in the field and explore the latest advancements in extracellular matrix research and pharmacology.

      In the meantime, feel free to watch our previous webinars.

      The ECM Pharmacology Symposium Series is a close collaboration with our industry sponsor Nordic Bioscience.

      Get in touch

      Are you interested in exploring collaboration possibilities?
Enter your information in the form and a representative will contact you shortly.

        Investigating Type IV Collagen Biomarkers in Multiple Sclerosis

        Multiple sclerosis (MS) is characterized as an inflammatory neurodegenerative disease in the central nervous system (CNS), presenting with significant inter- and intra individual heterogeneity. The pathological hallmarks of active MS lesions are blood brain barrier (BBB) disruption, inflammation, and demyelination with axonal damage. Blood-based biomarkers reflecting tissue changes in immunology and/or neurobiology may reflect MS pathology and be easily accessible.

        Type IV collagen biomarkers in Multiple Sclerosis

        In our latest publication in “Multiple Sclerosis and Related Disorders”, we introduce nordicCANTM, a technically robust assay, which targets a fragment of the α2 chain of type IV collagen to detect canstatin (CAN) in human serum. This was evaluated as a biomarker for MS together with other type IV collagen biomarkers, and the results showed TUM to be an excellent diagnostic biomarker in MS, while CAN and PROC4 were both acceptable diagnostic biomarkers.

        To our knowledge, this is the first study to quantify fragments of type IV collagen in serum from patients with MS, and such biomarkers may be used to assess patients’ eligibility for targeted treatments and fill a part of the gap for biomarkers in clinical management and trials.

        Article: Investigation of type IV collagen biomarkers in multiple sclerosis

        Collagen Type I Degradation Biomarkers Are Associated with Risk of Mortality After STEMI

        Collagen type I degradation biomarkers are associated with risk of mortality after ST-elevated
        myocardial infarction.

        Introduction

        Following ST-elevation myocardial infarction (STEMI), there is acute degradation of type I collagen (COL1), the primary structural protein of the myocardium. This process reflects extensive extracellular matrix remodeling, which may contribute to cardiac tissue destabilization and elevate the risk of subsequent adverse events. To better understand this pathological remodeling, we aimed to quantify COL1 using specific plasma biomarkers, including a novel signaling fragment of COL1 (C1SIG) and a more established COL1 degradation marker (C1M). Additionally, we investigated the prognostic value of these biomarkers for predicting all-cause mortality following a STEMI event.

        Poster

        Conclusion

        C1M and C1SIG are independently prognostic for mortality in STEMI patients after 1 year, in a multivariate
        model based on the Framingham Score. Assessing acute extracellular matrix processing in STEMI patients
        using COL1 biomarkers could be beneficial for predicting mortality and identifying a patient subset at
        increased risk of long-term outcome.

        Get in touch

        Are you interested in exploring collaboration possibilities?
Enter your information in the form and a representative will contact you shortly.

          ACR70 Response and Its Dependence on Deep Tissue Efficacy

          Introduction

          Over the past decade, drugs developed for rheumatoid arthritis (RA) have been approved based on an ACR20 response rate of 60%. There is an increasing need for new RA drugs to achieve an ACR100 response in a significant portion of patients. Achieving ACR100 can profoundly improve patients’ quality of life by reducing pain, enhancing physical function, and decreasing fatigue.

          The key question remains: which patients are likely to achieve ACR100?

          An important aspect of RA pathogenesis involves the destruction and remodeling of bone, cartilage, and synovial tissue. Serum biomarkers that measure collagen and other extracellular matrix fragments can be used to assess disease activity at the tissue level. Examples include C1M (type I collagen destruction), C4M (type IV collagen destruction), and Osteocalcin (bone formation) [1].

          The aim of this study was to examine the demographic, clinical, and serum markers of tissue remodeling as predictors linked to ACR20, ACR50 and ACR70 responses to tocilizumab.

          Poster

          Conclusion

          While predictors of moderate response (ACR20) included clinical, demographic, and biomarker factors, predictors of significant response (ACR70) were exclusively biomarkers of extracellular matrix fragmentation. To achieve remission (ACR70 or ACR100) may require therapeutic interventions that specifically target and address tissue remodeling processes.

          Get in touch

          Are you interested in exploring collaboration possibilities?
Enter your information in the form and a representative will contact you shortly.

            Serological Extracellular Matrix Fragments May Serve as Early Kidney Damage Biomarkers

            Serological extracellular matrix fragments may serve as early kidney damage biomarkers in children with defects in Alport genes

            Introduction

            Alport syndrome is a genetic disorder caused by variants in COL4A3, COL4A4, or COL4A5, which encode type IV collagen. The α3.α4.α5(IV) collagen network is a critical structural component of the glomerular and tubular basement membranes within the kidney’s extracellular matrix (ECM). Variants in this network compromise basement membrane integrity, leading to cell injury, inflammation, and fibrotic remodeling of the surrounding interstitial matrix, which contributes to progressive kidney dysfunction.

            We aim to identify serological protease-generated fragments of the ECM as potential early biomarkers of kidney damage.

            Poster

            Conclusion

            The following biomarkers were altered in children with Alport syndrome, compared to healthy donors, before the onset of detectable proteinuria:


            These biomarkers could potentially indicate early kidney damage and enable earlier initiation of kidney-protective treatments in children with Alport syndrome.

            Get in touch

            Are you interested in exploring collaboration possibilities?
Enter your information in the form and a representative will contact you shortly.

              Hidradenitis Suppurutiva Awareness Week: Biomarkers for Hidradenitis Suppurutiva

              The Hidradenitis Suppurutiva Awareness Week is held annually to spread knowledge about the disease and how it affects patients. Affecting roughly 1% of the population, HS causes significant physical and emotional challenges that are often overlooked.

              Hidradenitis Suppurativa Awareness Week is held annually to raise awareness about this systemic skin disease

              HS is believed to result from a complex mix of genetic predisposition, lifestyle factors, and immune system dysfunction, driving a continuous cycle of inflammation. It commonly presents as painful nodules, abscesses, draining tunnels beneath the skin, and scarring.

              These symptoms often cause physical discomfort and disability, affecting quality of life, personal relationships, and career opportunities. People living with HS respond differently to treatments, and we believe that raising awareness and supporting research is key to developing tailored treatment strategies that truly address their challenges.

              Our dermatology biomarkers enable precision medicine by providing information about ongoing pathological processes, such as damage and repair, within the ECM. This can guide targeted treatments and therapies, enhancing patient outcomes and personalized medicine approaches. At the same time, our markers, supported by our long history of experience and expertise, expedite drug development by specifically identifying target populations and reducing costs, over proteomic providers’ hopes to hit the right target by chance.

              Type III and VI Collagen Have the Potential to Distinguish Between IPF and HP

              Type III and VI Collagen remodeling biomarkers have the potential to distinguish between IPF and HP

              Introduction

              IPF and HP are two ILDs with similar clinical phenotype but distinct management, making their precise separation critical. Serological biomarkers may assist in distinguishing the two. In this study we assessed the clinical value of type III and VI collagen remodeling biomarkers and their potential to act as a tool to distinguish between HP and IPF in two separate, independent cohorts.

              Poster

              Conclusion

              We conclude that nordicPRO-C3™ could distinguish between HP and IPF in the AUH-ILD cohort. Furthermore, the distinct collagen remodeling takes place in each disease. In conclusion, these findings suggest that ECM remodeling biomarkers could act as potential tools to distinguish between HP and IPF.

              Get in touch

              Are you interested in exploring collaboration possibilities?
Enter your information in the form and a representative will contact you shortly.