Unlike adult cancers, childhood cancers are not caused by aging or environmental factors, but arises from malfunctions in developmental biology. One example is neuroblastoma, which originates from precursor cells of the sympathetic nervous system. Depending on the developmental stage at which the cancer cells occur, different neuroblastoma subtypes can emerge. The earlier in development the tumor arises, the more aggressive it tends to be. The most aggressive form, high-risk neuroblastoma, primarily affects infants under one year of age. Although, current therapies have improved survival, they are associated with high toxicity and long-term side effects. To circumvent these, there is a strong need for the development of targeted therapeutic strategies. While initial responses to a targeted drug are often very promising, patients will develop resistance and therefore combination therapies are being explored as a strategy to increase patient survival while minimizing side-effects. Previous research from the host lab demonstrated that dual inhibition of RRM2 and CHK1, both implicated in the replication stress response pathway, is effective in high-risk neuroblastoma. However, earlier inhibitors such as 3-AP and prexasertib were limited by high toxicity and poor target selectivity. This study aims to investigate whether new inhibitors targeting the same pathway can achieve comparable or improved results, while reducing toxicity. This will be done using zebrafish models in which neuroblastoma cells are injected. These in vivo experiments aim to generate strong pre-clinical data to support clinical translation, and to prioritize one of the two drug combinations for further testing in mouse models.