The “Master” tumor suppressor protein p53, which induces cell-cycle arrest and apoptosis through transcriptional regulation of specific target genes, is found mutated in more than 50% of the human tumors.In addition to mutant p53 acting in a dominant-negative fashion towards wild-type p53, mutant p53 hasbeen shown to inhibit p53 family proteins p73 and p63.Consequently, p73 and p63 become incapableof exertingtheir tumor suppressive functions. p73 and p63 are transcription factors that share significantstructural homologywith p53. Similar to p53, p73 and p63 control the expressionof genes involved in cellcycle arrest and apoptosis. It hasbeen shown that p73 and p63 can functionally replace p53.Unlike p53,however, they are very rarely mutated in cancer. Therefore, restoration of the p53 pathway through its familymembers represents an attractive therapeutic approach. Currently, no cancer therapeutics directed into restoration of p53 protein activity are on the market.
Summary of the Invention
Renowned researchers from the p53 protein field at Fox Chase Cancer Center discovered compound CB002 and its analogs as p53-pathway-restoring small molecules, repressing cancer cell growth. CB002 and its derivatives are promising therapeutics that selectively induce cell death in human tumor cell lines and are safe to human normal epithelial cell lines.
Richardson C. at al., 2017, Cell Cycle, Volume 16 - Issue 18: p. 1719-1725 http://www.tandfonline.com/doi/full/10.1080/15384101.2017.1356514
- Novel therapeutics for treating various tumors based on mechanistic studies.
- Targeted and specific restoration of p53 pathway activity.
- Inexpensive small molecules.
IP Status: Patent application was published US 2019/0225613 Al.Publication file is available upon request.
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Inna Khartchenko, MS, MBA
Director, Technology Transfer and New Ventures