References

WNTs and their downstream effectors regulate various processes that are important for cancer progression, including tumor initiation, tumor growth, cell senescence, cell death, differentiation and metastasis. Targeting the Wnt pathway in cancer has been an attractive therapeutic approach. ß-catenin (CTNNB1) is a subunit of the cadherin protein complex and acts as an intracellular signal transducer in the Wnt signaling pathway. As a proto-oncogene, mutations of ß-catenin are commonly found in a variety of cancers, including primary hepatocellular carcinoma, colorectal cancer, ovarial carcinoma, breast cancer, lung cancer and glioblastoma. It has been estimated that approximately 10% of all tissue samples sequenced from all cancers display mutations in the CTNNB1 gene. However, targeting this signaling pathway and ß-catenin have proven to be challenging, as evidenced by several years of research. WntRx Pharmaceuticals is dedicated to use cutting edge technology to develop safe, non-toxic, oncogenic specific, selective, novel inhibitors of ß-catenin. 

About Us

Photo: Rick Berk (2014)

Therapeutics

Source: J Clin Onco, 2008
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Market

Erbitux survival rate increases from 19 to 23 months

Colorectal cancer (CRC) has the fastest growing population among all developed and developing countries. In the US alone, 170K+ patients are diagnosed with CRC per year, and the one-year prevalence rate lies at nearly 140K patients; in combination, over 300K patients are in need of treatment for CRC annually. Furthermore, existing targeted therapies in metastatic CRC (mCRC) are far from covering all patient needs. Several of the most popular treatments include biologic therapies such as Erbitux and Avastin, of which research has shown limited benefits (see figures below). Most importantly, targeted therapies (Cetuximab, Bevacizumab, Panitumumab, etc.) have not shown a proportional improvement effect on patients in comparison with traditional chemotherapies, and new biologic therapies will provide physicians with more factors to evaluate prognosis, giving them more selections after patients show tumor recurrence or resistant to treatment.

WntRx Pharmaceuticals is building upon the premise of Wnt signaling by applying its unique capabilities to discover and develop non-toxic, selective drugs for the treatment of patients with critical unmet medical needs. Our company focuses on the development of novel, safe, oncogenic-specific inhibitors of Wnt signaling, a pathway aberrantly activated in a multitude of cancers. WntRx is located in Boston, MA and is based on technology initially developed at the Dana-Farber Cancer Institute with Harvard University.

1. Klaus, A. & Birchmeier, W. Wnt signalling and its impact on development and cancer. Nature reviews. Cancer 8, 387-398 (2008). 
2. Clevers, H. & Nusse, R. Wnt/beta-catenin signaling and disease. Cell 149, 1192-1205 (2012). 
3. Morin, P.J., et al. Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC. Science 275, 1787-1790 (1997). 
4. Scholer-Dahirel, A., et al. Maintenance of adenomatous polyposis coli (APC)-mutant colorectal cancer is dependent on Wnt/beta-catenin signaling. Proceedings of the National Academy of Sciences of the United States of America 108, 17135-17140 (2011). 
5. Clevers, H. Wnt/beta-catenin signaling in development and disease. Cell 127, 469-480 (2006). 
6. Emami, K.H., et al. A small molecule inhibitor of beta-catenin/CREB-binding protein transcription [corrected]. Proceedings of the National Academy of Sciences of the United States of America 101, 12682-12687 (2004). 
7. Polakis, P. Drugging Wnt signalling in cancer. The EMBO journal 31, 2737-2746 (2012). 
8. Anastas, J.N. & Moon, R.T. WNT signalling pathways as therapeutic targets in cancer. Nature reviews. Cancer 13, 11-26 (2013). 
9. Comprehensive molecular characterization of human colon and rectal cancer. Nature 487, 330-337 (2012). 
10. Tetsu, O. & McCormick, F. Beta-catenin regulates expression of cyclin D1 in colon carcinoma cells. Nature 398, 422-426 (1999). 

Avastin survival rate increases from 19 to 21 months