Cantargia Publishes Promising Preclinical Results Highlighting CAN10's Potential to Inhibit Vascular Inflammation

• IL1RAP expression positively correlates with inflammatory markers in human atherosclerotic plaques.

• IL1RAP blocking antibodies inhibit endothelial activation and neutrophil adhesion induced by IL-1, IL-33 and IL-36.

IL1RAP targeted therapy offers a novel strategy to mitigate vascular inflammation.

LUND, SE / ACCESS Newswire / May 19, 2025 / Cantargia (Cantargia AB (publ); Nasdaq Stockholm:CANTA) today announced the publication of preclinical results from IL1RAP targeting antibodies in models of vascular inflammation. Cytokines dependent on IL1RAP strongly affect human endothelial cells to induce release of proinflammatory mediators, attract immune cells and increase vascular permeability. These changes can be potently blocked by antibodies targeting IL1RAP. Also, IL1RAP levels in human atherosclerotic lesions correlate with various inflammatory markers, indicating translational possibility into human cardiovascular diseases (CVDs). The results are published in the Journal of the American Heart Association (JAHA).

"IL1RAP and its ligands, IL-1, IL-33 and IL-36, are central for inflammation not only because of their effects on immune cells but also due to effects on other cells that respond to inflammation. The work now published show how IL1RAP-targeting antibodies can block inflammation by acting directly on endothelial cells and potentially reduce events important in several inflammatory diseases, including CVD"said David Liberg, CSO of Cantargia

Vascular inflammation is a central part of several inflammatory diseases, including atherosclerosis. The current findings revealed that IL1RAP targeting antibodies inhibit the IL-1β, IL-33 and IL-36γ induced release of inflammatory and chemotactic mediators and genes related to endothelial activation and adhesion. Concordantly, endothelial permeability and neutrophil adhesion were inhibited by antibodies blocking IL1RAP. Analysis of human atherosclerotic plaques showed a correlation between the levels of IL1RAP and several of the inflammatory markers reduced by IL1RAP blockade, including interleukin-6 and -8 (IL-6 and IL-8).