The project, titled “Novel Cancer-Specific Therapy Exclusively Targeting Oncogenic TGFβ Signaling”, focuses on developing a fully human, affinity-matured therapeutic antibody that blocks oncogenic TGFβRI (ALK5) signaling; a key molecule in the oncogenic TGFβ signaling pathway. This pathway is known to drive tumor invasiveness and metastasis as well as resistance to immunotherapies such as PD-1 inhibitors (refs 1+2).
During the first phase, MetaCurUm successfully demonstrated that its therapeutic antibody binds to TGFβRI with high sub-nanomolar affinity across multiple species, providing critical insights for selecting appropriate animal models for preclinical studies. The antibody, produced from a stable cell line, showed binding properties nearly identical to those observed in transient expression systems, confirming its robustness and scalability.
Preparing for clinical trials
With these milestones achieved, MetaCurUm is now ready to initiate toxicology studies to show that our approach targeting only oncogenic TGFβ signaling avoids the side effects seen with other TGFβ inhibitors that have been discontinued due to side effects and a negative benefit-risk ratio.
“We are extremely happy for the continuation of the funding for our project and the support we receive from Vinnova to move our project forward towards the possibility to perform clinical trials,” says Maarten de Château, CEO of MetaCurUm AB.
Maximum 4 million SEK
MetaCurUm’s work builds on the research of Professor Maréne Landström at Umeå University, targeting a specific oncogenic TGFβ signaling pathway that cancer cells exploit to spread. By blocking this pathway, MetaCurUm aims to prevent tumor progression and metastasis in prostate cancer and other solid tumors.
The Vinnova program aims to accelerate the commercial development of deep tech companies by reducing risk and enhancing market opportunities. Over three years, companies can receive up to 4 million SEK across all project phases.
Refs 1+2
https://pubmed.ncbi.nlm.nih.gov/34671117/
TGFβ biology in cancer progression and immunotherapy – PubMed