The study suggests that, while brostallicin is more effective in cells with normal p53 status, cells with abnormal or missing p53 are also killed when treated. P53 is a protein that regulates the cell cycle and acts as a tumor suppressor.
The study examined brostallicin’s effect on cell viability, cell cycle modulation, and the initiation of cell death in cancer cell models with either normal (also referred to as wild-type) or abnormal (mutated or absent) p53 tumor suppressor. These results were supported through tests in animal models, where brostallicin demonstrated a statistically significant effect on suppressing tumor growth.
Jeffrey Jacob, CEO of Systems Medicine, said: “The results of this study support the further clinical development of brostallicin. They also provide deeper insight into brostallicin’s context of vulnerability concerning different types of p53 protein, and where it is most effective.”