“These new exciting results provide an important mechanistic context supporting the clinical results obtained with nadunolimab. The data also provide new opportunities to follow biomarkers during treatment. More speculatively, these results may also provide important tools for Cantargia’s second clinical program CAN10 which is designed to treat inflammation and fibrosis in autoimmune diseases,” said Göran Forsberg, CEO of
One factor that significantly contributes to the poor treatment response in PDAC is the high abundance of tumor-supporting stroma, driven by the excessive activity of cancer-associated fibroblasts (CAFs). Pro-C3 is a biomarker for that activity which also correlates with aggressive disease and short survival. The new data demonstrate that IL-1α and IL-1β, that are upregulated in PDAC, induce formation of type III collagen in cancer-associated fibroblasts as measured by pro-C3. The data also show that when PDAC cancer cells and CAFs are cultured together, pro-fibrotic genes and the production of pro-C3 are upregulated. Notably, addition of nadunolimab to these cultures inhibited the formation of pro-C3. Thus, the new data highlight the potential for nadunolimab to counter the detrimental, fibrotic microenvironment in PDAC tumors and this effect may be documented by measuring the biomarker pro-C3.
These findings support the promising clinical data previously presented at the ASCO Annual Meeting 2022, at the AACR annual meeting in 2023 and at the AACR special conference on pancreatic cancer in 2023. In over 70 PDAC patients evaluated in the phase IIa part of the clinical trial CANFOUR, nadunolimab in combination with chemotherapy results in efficacy well above historical controls for chemotherapy alone. Currently,
The data was generated in collaboration with
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