Approximately 90% of sporadic colorectal cancers contain mutations in components of the Wnt/β-catenin signaling pathway. These mutations are found in the earliest neoplasms, suggesting that this pathway is a critical gatekeeper to prevent colorectal carcinogenesis.​​
Colorectal Cancer
Small Molecule Therapeutics
Colorectal cancer (CRC) is the third most common cancer globally, accounting for about 10% of cases. Around 90% of sporadic CRCs have mutations in the Wnt/β-catenin signaling pathway, which are present in early neoplasms and suggest this pathway is crucial in preventing colorectal cancer. Most tumors have a mutation in one component of this pathway, but recent data shows multiple components can mutate together. About 85% of these mutations occur in APC, producing a truncated APC protein that fails to integrate into the β-catenin destruction complex. When the functional APC is lost, β-catenin levels rise, leading to aberrant gene expression and benign adenomas.
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MD2 targets β-catenin directly with small-molecule drugs to treat both WT and mutant cancer cells. Our inhibitors act in the cytoplasm to reduce the burden on the nucleus, offering a novel approach to treating β-catenin driven CRC.