{"id":809,"date":"2025-01-22T18:28:57","date_gmt":"2025-01-22T18:28:57","guid":{"rendered":"https:\/\/www.nordicbioscience.com\/?post_type=biomarker-solutions&p=809"},"modified":"2025-06-01T13:56:41","modified_gmt":"2025-06-01T13:56:41","slug":"translational-models-in-pulmonary-fibrosis","status":"publish","type":"biomarker-solution","link":"https:\/\/www.nordicbioscience.com\/biomarker-solution\/respiratory\/translational-models-in-pulmonary-fibrosis\/","title":{"rendered":"Translational Models in Pulmonary Fibrosis"},"content":{"rendered":"
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Strategic drug development in pulmonary fibrosis<\/h2>\n \n\n <\/div>\n
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A drug development route for success is key but often challenging and full of uncertainties. Strategies that can increase the likelihood of success are vital. The FDA and EMA recognize that biomarker-based drug development strategies, in combination with translation research, could be the solution. This approach offers a biology-focused pathway that not only reduces time and cost but also enhances the overall likelihood of success.<\/p>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n

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Nordic Bioscience combines innovative translational models with the\u00a0Nordic ProteinFingerPrint Technology\u2122<\/a>\u00a0to translate findings effectively. This is facilitated by utilizing the same biomarkers across different clinical stages of development creating a link between the preclinical model and the clinic. This strategically selected development route greatly enhances the efficiency of drug development pipelines.<\/p>\n

In essence, the integration of biomarker-based drug development strategies in translational research not only accelerates the progression of therapeutics but also increases the likelihood of success. Through advanced translational models in combination with the ProteinFingerPrint\u2122 biomarkers, Nordic Bioscience contributes significantly to the optimization of decision-making processes in clinical development, ultimately ensuring better treatments for the patients.<\/p>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n <\/div>\n <\/div>\n

\n \n Biomarkers in pulmonary fibrosis \n \n <\/svg>\n \n <\/a>\n <\/div>\n <\/article>\n
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Translational biomarkers in pulmonary research<\/h2>\n

A major cornerstone of ours is to combine translational models with clinically validated biomarkers to enhance drug development. For this purpose, we have assessed the ability of our biomarkers in bridging the gap between\u00a0pulmonary fibrosis<\/a>\u00a0patients and various model systems. Our investigations have revealed that ProteinFingerPrint\u2122 biomarkers, such as\u00a0nordicPRO-C6\u2122<\/a>\u00a0(PRO-C6, also known as Endotrophin), show dose-dependent modulation in response to antifibrotic treatment. We assessed both in the blood of idiopathic pulmonary fibrosis (IPF) patients and in the supernatant of pulmonary fibrosis models (Figure 1)\u00a0[7<\/a>,8,9<\/a>]<\/sup>.<\/p>\n <\/div>\n

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Figure 1.\u00a0<\/strong>NordicPRO-C6\u2122 assessed in the blood of\u00a0<\/strong>IPF patients and supernatant of fibrosis models.<\/em><\/figcaption><\/figure>\n

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In vitro\u2014Scar-in-a-Jar (SiaJ)<\/h2>\n

The prolonged Scar-in-a-Jar is an innovative model that utilizes macromolecular crowding to enhance the formation, maturation, and deposition of the extracellular matrix in vitro.\u00a0The extracellular matrix\u00a0is essential for providing structural support to cells and regulating tissue repair and regeneration by serving as a reservoir for growth factors and cytokines.<\/p>\n

Understanding the dynamics of the extracellular matrix is crucial for developing therapeutic strategies for fibrosis. By employing macromolecular crowding, the model gains a three-dimensional like structure and increased complexity, making it a suitable translational model. This modulation demonstrates the model\u2019s effectiveness for screening antifibrotic effects directly on hepatic stellate cells.<\/p>\n

\"\"<\/a>Figure 2.\u00a0<\/strong>Prolonged Scar-in-a-Jar model\u00a0in vitro.<\/em><\/p>\n

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The figures show how\u00a0PRO-C3 (nordicPRO-C3\u2122)<\/a>\u00a0(formation of type III collagen; PRO-C3) and\u00a0PRO-C6 (nordicPRO-C6\u2122)<\/a>\u00a0(formation of type VI collagen; PRO-C6) increase when stimulating lung fibroblasts with a fibrotic cocktail.<\/p>\n

In addition,\u00a0PRO-C3 (nordicPRO-C3\u2122)<\/a>\u00a0and\u00a0PRO-C6 (nordicPRO-C6\u2122)<\/a>\u00a0levels are affected and can be decreased when stimulating the fibroblasts and treating them with Omipalisib.<\/p>\n

This modulation shows that the model is applicable \u00a0for screening of antifibrotic effects directly on the fibroblasts.<\/p>\n

\"\"<\/a>Figure 3.<\/strong>\u00a0Scar-in-a-Jar can screen antifibrotic effects.<\/em><\/p>\n

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Figure 4.\u00a0<\/strong>C3M levels lowered in mice after bleomycin treatment.<\/em><\/figcaption><\/figure>\n

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In vivo\u2014bleomycin model<\/h2>\n

The bleomycin model has become an important translational model for pulmonary fibrosis. The model allows us to study pulmonary fibrosis\u00a0in vivo.\u00a0<\/em>To assess efficacy, Nordic ProteinFingerPrint\u2122 biomarkers are measured in the blood of patients.<\/p>\n

The graph shows how\u00a0C3M<\/a>\u00a0(type III collagen degraded by MMP) is increased in bleomycin-treated mice compared to saline, meaning that fibrotic processes are present in the model.<\/p>\n

Also, C3M levels are lowered to the same level as saline when adding an antifibrotic treatment to the bleomycin-treated mice.\u00a0The treatment effectively reduced collagen degradation and fibrosis, restoring the tissue environment.<\/p>\n <\/div> \n <\/div>\n<\/section>\n\n\n\n

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