Dead box helicase 3, DDX3, is a potential drug target for treatment of many forms of cancer. DDX3 is involved in the B-catenin/wnt pathway by inactivating the destruction complex. Overexpression of DDX3 inactivates the destruction complex leading to unregulated cytosolic B-catenin levels. Elevated cytosolic B-catenin levels leads to over activation of the wnt target genes, which is associated with cell growth and proliferation. DDX3Y has also been identified as a possible inducer of male brain sex differentiation. A microarray of the brain of rat embryo before any effect of gonadal or adrenal hormones (E12) showed increased concentration DDX3Y in males, a fold change of 1552,15. This raises the hypothesis that DDX3Y affects brain sex masculinization. The purpose of this study is to generate inhibitors for DDX3 so further analysis can be done. 18 candidates were selected from a hit list generated from a virtual screening of the DDX3Y protein. Reduction of cell amount was used as an indicator of DDX3 inhibition. HepG2 cells were manually counted after being exposed to concentrations between 0,1µM and 10µM for 120-hours. 7 compounds had significantly reduced the cell amount when exposed to 10µM compared to their control. Compound 5, 14, 15 and 16 had reduced cell amount to below 46% of their control when exposed with 10µM. Compound 15 had 6% cell amount when exposed to 10µM, which is similar to the positive control (RK-33). RK-33 had reduced cell amount to 10% when exposed to 10µM. Given my results I argue that the next step to properly compare compound 15 and RK-33 would be to determine that compound 15 acts through the wnt/B-catenin pathway. That can be done with reporter assay for TCF-activity. Determining the DDX3X/DDX3Y binding ratio is detrimental for progression in brain sex differentiation research. Which could be done by using silencing RNAs for DDX3X and comparing those proliferation rates to the ones of this study.