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Cantargia publishes preclinical data on the potential of CAN10 in systemic sclerosis in a leading scientific journal
Prenumeration
Beskrivning
| Land | Sverige |
|---|---|
| Lista | Small Cap Stockholm |
| Sektor | Hälsovård |
| Industri | Bioteknik |
Cantargia (Cantargia AB; Nasdaq Stockholm: CANTA) today reported publication of preclinical results obtained with CAN10 in systemic sclerosis in one of the leading rheumatology journals, ‘Annals of the Rheumatic Diseases’. CAN10 reduces both lung and skin fibrosis in multiple preclinical models of systemic sclerosis. The results are strengthened by the target of CAN10, IL1RAP and its signaling systems (IL-1, IL-33, and IL-36) being upregulated and disease-promoting in systemic sclerosis patient skin. CAN10 is an antibody in phase I clinical development.
“We are really pleased that the important results supporting CAN10 development in systemic sclerosis is recognized in a leading scientific journal. With phase I clinical studies ongoing, we are already now preparing for phase II clinical development in this life-threatening disease” said Göran Forsberg, CEO of Cantargia.
Systemic sclerosis is a life-threatening autoimmune disease resulting in fibrosis in the skin, lung, and other internal organs. Patients often have a severely impacted quality of life and there are no effective treatments today. Systemic sclerosis is one of the lead indications in the CAN10 development program.
The published data demonstrate that the target for CAN10, IL1RAP, and the IL1RAP-dependent signaling molecules IL-1, IL-33 and IL-36, are upregulated in skin from systemic sclerosis patients and that IL-1, IL-33 and IL-36 have profibrotic effects on skin fibroblasts from systemic sclerosis patients, which can be reduced by CAN10. Moreover, therapeutic treatment with a surrogate of CAN10 (mCAN10) in three different preclinical models of systemic sclerosis potently reduced both skin and lung fibrosis. Gene expression analysis indicated a broad mode of action of mCAN10, which normalized the expression of a majority of the genes commonly dysregulated in systemic sclerosis. In summary, the published data show that CAN10 targets central processes important for systemic sclerosis and that CAN10 provides a novel and promising opportunity to treat this disease. The publication in this high-impact journal (impact factor 27.4) reflects the scientific significance of the data.
This work was performed in collaboration with a world-leading research group headed by Prof. Dr. Jörg Distler at the Heinrich-Heine University, Düsseldorf, Germany. Key data from these studies were recently presented as a poster at the Systemic Sclerosis World Congress March 14-16, 2024.
“Systemic sclerosis patients have a very high need for new treatments. The published data provide strong evidence that signaling via IL1RAP regulates disease development in systemic sclerosis. The use of both patient samples and three different preclinical models strengthens the translational aspect of the data and indicates an effect of CAN10 on key signaling pathways in this disease. I am very much looking forward to following the clinical development of CAN10, which has the potential of becoming a novel, targeted treatment for systemic sclerosis patients.” said Prof. Dr. Jörg Distler.
The article, titled “Combined inhibition of IL-1, IL-33 and IL-36 signaling by targeting IL1RAP ameliorates skin and lung fibrosis in preclinical models of Systemic Sclerosis”, is authored by Grönberg et al. and is available via this link.