New therapies that target mutations of genes such as p53 represent a promising approach compared to conventional organ-specific cancer treatments. These important results from a world-class scientist in a global centre of excellence in cancer research confirm and extend our understanding of the mechanism of action (“MOA”) of COTI-2. While previous internal research indicated that COTI-2’s effectiveness was related to the p53 mutation status of the tumor, the quality and amount of scientific data provided by Dr. Mills are definitive and answer the remaining MOA questions posed by potential licensing partners who are waiting for these results.
- Dr. Wayne Danter, President & CEO
The p53 gene is a tumor suppressing gene. It codes for a protein that inhibits the development and growth of tumors. However, if the p53 gene is mutated, cancers can develop and grow without control. Mutations of the p53 gene are the most common genetic alterations in human cancers, occurring in a wide range of cancers, including ovarian, lung, colorectal, breast, liver, bladder and other cancers.
Our patented drug compound, COTI-2, has a major mechanism of action in human cancer cells that is dependent on p53 gene mutation status. This is important as drug treatment for p53 mutations represents a novel therapy and would be a first in class treatment for the drug company bringing COTI-2 to market.
Unlike nearly every other cancer treatment in existence today, COTI-2 is non-genotoxic. Conventional chemotherapy involves the killing of all growing and dividing cells in the body (cancer or otherwise), which often leads to significant toxic side effects in patients. By contrast, COTI-2 specifically targets and primarily destroys tumor cells.
COTI-2 is currently in final two-species toxicity studies prior to FDA filing enabling human trials.
p53: The most frequently altered gene in human cancers
The New York Times | Drugs aim to make several types of cancer self-destruct