“CAN10 has generated strong preclinical results in models of myocarditis which is a disease with very high medical need. We are pleased that these important results are now published in an impactful scientific journal,” said Göran Forsberg, CEO of Cantargia.

The IL1RAP-binding antibody CAN10 has shown strong efficacy in various inflammatory and autoimmune disease models and is now in phase 1 clinical development. The clinical data so far indicate good safety, receptor binding and a potent pharmacodynamic effect counteracting inflammatory immune cell responses in healthy subjects. Currently, safety, pharmacokinetics and biomarker effects are investigated in participants with psoriasis in a multiple ascending dose setting. Phase 2 clinical development is planned to start H2 2025.

Myocarditis is a life-threatening disease characterized by inflammation of the heart muscle and impaired heart function. It may result from autoimmunity or as a side effect to certain pharmaceuticals (including checkpoint inhibitors), but is most commonly caused by viral infections, and rates of myocarditis increased during the COVID-19 pandemic. The data published in Circulation: Heart Failure show potent efficacy of the CAN10 mouse surrogate antibody in in vivo models of both viral and autoimmune myocarditis. Notably, CAN10 counteracted disease development in both models and the treatment effect was much stronger than blockade of IL-1 signaling only. CAN10 counteracted both inflammation in the heart muscle as well fibrosis and preserved heart function. This clearly highlights the unique and powerful function of CAN10, resulting in a broad mode of action which is beneficial in complex inflammatory and fibrotic diseases such as myocarditis. The key results have previously been reported as posters at scientific conferences.

The research has been carried out as collaborations with Prof. Daniela Cihakova at the Johns Hopkins University, Baltimore, MD, USA and Associate Prof. Alexandru Schiopu at Lund University, Sweden. The article by Diego A. Lema et al. can be accessed through the journal’s webpage www.ahajournals.org.