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Simultaneous Inhibition of Wnt, TGF beta and Hippo Signaling to Treat Cancer and Organ Fibrosis
About
Cancer is the leading cause of death worldwide, accounting for 7.5 million deaths per year and is projected to rise continually. A common cause of both cancer metastasis and resistance to therapy is a cellular process called Epithelial Mesenchymal Transition (EMT). EMT endows cancer cells with superior ability to survive drug toxicity and migrate to distant sites. Wnt, TGF beta, and Hippo signaling pathways represent the major inducers of EMT, therefore their simultaneous targeting could represent an effective way to suppress cancer progression. C19 is a promising small molecule candidate with remarkable inhibitor activity against Hippo , Wnt and TGF-beta pathways. It inhibited cancer cell migration, proliferation, and resistance to doxorubicin in vitro, and exerted strong anti-tumor activity in a mouse tumor model. By simultaneously targeting multi-EMT pathways, it provides a new class of cancer agent that have the potential to not only suppress its progression but also prevent its recurrence. C19 has completed key drug development steps including lead optimization, mechanism of action, target identification and proof of concept in animal models. Collaborations to validate its efficacy in cancer patients are awaited.
Key Benefits
- No detectable cell toxicity in-vitro and in-vivo. - Potential to suppress cancer and prevent recurrence. - Inhibits characteristic resistance of cancer cells to therapy. - Inhibits expression of pro-fibrotic markers and activates anti-obesity and anti-diabetic enzyme AMPK.
Applications
- Pan-EMT inhibitor to treat cancer and EMT-associated diseases. - Tool to facilitate study of EMT and metablolic disorders - Potential drug candidate to treat organ fibrosis and diabetes