ATRAG Mechanism of Action in IPF
We are motivated by patients in exploring the protection, resolution and repair system of the AT2-receptor and science is leading us in unlocking the full potential of our drug candidates, angiotensin II type 2 receptor agonists (ATRAGs).
AEC1 cells – gas exchange. AEC2 cells – repair function
IPF develops in lung alveoli – tiny air-filled sacks where the exchange of oxygen and carbon dioxide takes place. The inner surface of the alveoli is covered by type 1 and type 2 epithelial cells. Type 1 epithelial cells are important for the gas-exchange in the lungs. With time, they get damaged and continuously need to be replaced. Type 2 epithelial cells divide and differentiate into new type 1 epithelial cells, thereby maintaining alveolar integrity to keep the lungs healthy and functioning properly.
Lung fibrosis development
Dysfunctional AEC2 cells – trigger for fibrosis
In IPF, type 2 alveolar epithelial cells become dysfunctional and lose their ability to repair and maintain alveolar integrity. The loss of integrity is a starting point for scarring, leading to release of profibrotic mediators stimulating fibroblasts to produce excessive collagen fibers causing fibrosis.
C21 stimulates AEC2 cells and alveolar repair
Vicore is developing a new class of drugs called ATRAGs, angiotensin II type 2 receptor agonists. AT2 receptors are highly expressed on the type 2 epithelial cells in the alveoli. In IPF, ATRAGs bind to and activate the AT2 receptor of the type 2 epithelial cell.
The receptor activation triggers protective signalling pathways, promoting alveolar repair and maintenance of alveolar integrity. The fibrosis formation is reduced, disease stabilized and lung capacity increased.
Learn more about how ATRAGs promotes alveolar repair by viewing the animation: Mode of Action in IPF