Targeting c-Myc directly has been challenging due to its role as a transcription factor and its lack of a defined enzymatic activity. However, several strategies have been explored, including small molecules that inhibit c-Myc-max dimerization, disrupting its ability to bind DNA, and antisense oligonucleotides that degrade c-Myc mRNA. Additionally, targeting upstream regulators of c-Myc, such as the PI3K/Akt/mTOR pathway, has shown promise in preclinical studies.
