Bifogade filer
Cantargia publishes promising preclinical results highlighting CAN10's potential to inhibit vascular inflammation
Prenumeration
Beskrivning
| Land | Sverige |
|---|---|
| Lista | Small Cap Stockholm |
| Sektor | Hälsovård |
| Industri | Bioteknik |
- 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.
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).
These data signify IL1RAP as a key regulator in vascular inflammation and in maintaining vascular integrity, which in turn implies targeting IL1RAP may have promising potential in several inflammatory diseases, including CVD.
“Inflammation is a central hallmark of atherosclerosis, and our research shows that targeting IL1RAP inhibits important inflammatory markers central in atherosclerosis. The established collaboration with Cantargia is very valuable both for us and for development of therapeutic options within CVDs” said Associate Professor Karin H Franzén, Örebro University
These data were generated in collaboration with Associate Professor Karin Franzén’s research group at Örebro University. The article, titled “IL1RAP expression in human atherosclerosis - a target of novel antibodies to reduce vascular inflammation and adhesion”, by Lindkvist et al., is available at Journal of the American Heart Associations website and at Cantargias website.