Cantargia AB (publ) announced that the Good Laboratory Practice (GLP) toxicity study for its anti-inflammatory IL1RAP-binding antibody CAN10 has been concluded. Data from the study show that CAN10 was well tolerated when administered over six weeks. Cantargia plans to initiate the phase I clinical trial for CAN10 during the first half of 2023. In the present GLP toxicity study, CAN10 was given intravenously once weekly for six weeks at doses up to 50 mg/kg, which is well above the intended clinical dose levels. CAN10 was also administered subcutaneously at 5 mg/kg. There were no adverse findings associated with the intravenous or subcutaneous administrations of CAN10. No safety signals were detected in body weight, or on respiratory, cardiovascular or neurological functions, attributed to the administration of the antibody. There were also no changes in clinical pathology (e.g. hematology, serum chemistry, coagulation, and urinalysis), anatomic pathology, or microscopic evaluation of selected tissue. Completion of the GLP toxicity study is required by regulatory authorities prior to initiation of clinical trials. As a next step in the development of CAN10, once additional administrative procedures have been finalized, Cantargia plans to submit an application to regulatory authorities to start the phase I clinical trial. The study start is dependent on timelines for regulatory review, but treatment of healthy volunteers could be initiated shortly following approval of the application, as early as the first half of 2023. CAN10 is Cantargia's second development program and extends the reach of Cantargia's IL1RAP platform beyond oncology to inflammatory and autoimmune disease, with initial focus on systemic sclerosis and myocarditis. During 2022, Cantargia
presented preclinical data demonstrating strong treatment effects of a CAN10 surrogate antibody in several different in vivo disease models. For example, the CAN10 surrogate antibody was shown to reduce skin and lung fibrosis and affect relevant proinflammatory markers in models of systemic sclerosis. It also reduced inflammation and disease severity in models of viral and autoimmune myocarditis. These effects are a consequence of the broad and specific mechanism by which CAN10 modifies the activity of the target molecule IL1RAP.