COTI-2 is primarily investigated for its potential in cancer therapy, particularly due to its ability to reactivate mutant forms of the p53 tumor suppressor protein. The p53 protein plays a crucial role in preventing cancer development by triggering DNA repair, initiating apoptosis, and halting cell division when DNA damage is detected. In many cancers, p53 is rendered dysfunctional due to mutations, allowing tumor cells to proliferate unchecked. COTI-2 has shown promise in restoring the normal function of certain mutant p53 proteins, thereby promoting cancer cell death and inhibiting tumor growth. It has been studied in preclinical models of various cancers, including ovarian, breast, and lung cancers, especially those with specific p53 mutations. Its mechanism involves stabilizing the correct conformation of mutant p53, enabling it to function more like the wild-type protein. Due to this targeted approach, COTI-2 is being explored as a potential therapeutic agent in personalized oncology, where treatment is tailored based on the genetic profile of a patient’s tumor. Clinical development is ongoing to evaluate its efficacy, safety, and optimal use in combination with other anticancer therapies.