Fibrosis, the excessive formation of connective tissue due to injury or inflammation, plays a critical role in the progression of several chronic diseases, including liver cirrhosis, pulmonary fibrosis, and cardiac fibrosis. Fibrotic diseases arise from the abnormal differentiation of myofibroblasts, cells that are integral to tissue repair but can cause significant damage when overly activated. Despite its impact on global health, effective treatments targeting fibrosis at the cellular level remain limited. Our patented technology provides a novel approach by targeting CAPN9/CAPNS2 activity, offering a therapeutic strategy to prevent or reverse fibrotic processes associated with various pathologies.
Existing treatments for fibrotic conditions often focus on managing symptoms rather than addressing the underlying causes of fibrosis. Steroids and anti-inflammatory drugs can reduce inflammation but may not effectively halt or reverse the fibrotic process. As a result, patients with chronic fibrotic diseases often experience ongoing tissue damage, organ failure, and reduced quality of life. The lack of therapies that can directly target the abnormal differentiation of myofibroblasts—one of the key drivers of fibrosis—leaves a critical gap in the medical landscape for those suffering from these conditions.
Our patent offers a breakthrough therapeutic approach by targeting CAPN9/CAPNS2, enzymes that regulate myofibroblast differentiation. By inhibiting these enzymes, our technology interrupts the fibrotic cascade at its source, reducing myofibroblast activation and preventing the excessive tissue scarring that leads to disease progression. This mechanism has the potential to not only slow down fibrosis but also reverse some of the damage caused by abnormal tissue remodeling.
This novel approach can be applied across multiple fibrotic conditions, offering a broad spectrum of therapeutic potential. From lung fibrosis to liver disease and cardiac fibrosis, this technology provides an opportunity to address one of the most significant unmet needs in healthcare—effective treatment for fibrotic diseases.
Licensing this CAPN9/CAPNS2-targeting technology opens up new possibilities for developing treatments that directly impact the fibrotic disease process. By addressing the root causes of myofibroblast differentiation, this patent offers a path to more effective and potentially life-changing therapies for patients with chronic fibrotic conditions. This innovation has the potential to transform the future of fibrosis management.
We claim:
Targeting CAPN9/CAPNS2 activity as a therapeutic strategy for the treatment of myofibroblast differentiation and associated pathologies
David Kim, Harry C. Dietz
Johns Hopkins University
11219670
January 11, 2022
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