Therefore, targeting MYCN protein could be crucial to the treatment of cancer . However, due to the complex structure of MYCN focusing on manipulating the proteins that interact with MYCN to indirectly regulate it can be an alternative strategy . BRD4 is one of the proteins that controls the MYCN activation by binding to a specific site of DNA and inhibiting BRD4 can directly affect the MYCN activation mitigating neuroblastoma . PROTAC were designed against cancer inducing BRD4 proteins which are eventually degraded by the E3 ligase protein, a cancer suppressor, is essential for destroying BRD4 proteins by bringing them in proximity via PROTAC. Computational tools used to understand E3-PROTAC-E3 interactions and design 10 novel PROTACs. PROTAC II showed the most favorable binding site. Findings suggest potential for developing potent, cost-effective PROTACs against cancer, aiding in reducing the disease's worldwide impact. The accuracy of molecular docking mainly depends on the initial structure and algorithm employed . Consequently, molecular dynamics simulations are necessary to further verify the docking findings.