The Myc transcription factor and its associated Max protein have an essential role in developing several types of cancers, including prostate cancer. They act through the dimerization into a Myc-Max heterodimer and the binding to specific DNA sequences known as enhancer box (E-box). Disrupting the Myc- Max heterodimer interaction or its binding to canonical E-box sequences (CME) to disrupt gene transcription is a promising strategy to treat cancer. Using computational biology tools, we designed pMyc and pMax peptides from Myc and Max reference sequences and evaluated their ability to bind specifically CME through an electrophoretic mobility shift assay (EMSA). We then coupled them to AuNPs and evaluated the hemocompatibility and the cytotoxic effect in three different prostate adenocarcinoma cell lines (LNCaP, PC-3, and DU145) and a non-cancerous cell line (Vero CCL-81). The EMSA results suggest that the pMyc-pMax dimers bind to CMEs. Through UV-Vis absorption spectra, we determined peptide conjugation to the AuNPs. The hemolysis test showed little hemolytic activity for the nanosystems (NS) at the concentrations (5, 0.5, and 0.05 ng/ µL) evaluated. Cell viability assays showed mixed results depending on which cell line was being evaluated. Overall, results suggest that NS with pMyc and pMax peptides might be suitable for further research regarding Myc-driven prostate adenocarcinomas.