Introduction: Copper complexes can be developed as targeted agent for cancer due to increased uptake of copper by cancer cells for angiogenesis. Our previous published data showed that copper complex Cu(SBCM)2 induced apoptosis towards triple-negative MDA-MB-231 breast cancer cells. However, its effect towards other breast cancer subtype remains unknown. Current study was performed to explore the cytotoxicity of Cu(SBCM)2 towards oestrogen- receptor positive MCF-7 breast cancer cells. Methods: MTT assay was employed to study the growth inhibition of Cu(SBCM)2 towards MCF-7 breast cancer cells and human non-cancerous MCF10A breast cells. Morphological changes of Cu(SBCM)2-treated MCF-7 cells was observed under inverted light microscope. Induction of cell cycle arrest and apoptosis were accessed by flow cytometry. The expression of wild-type p53 protein was evaluated by western blotanalysis. Intracellular reactive oxygen species of MCF-7 treated with Cu(SBCM)2 was detected using DCFHDA assay. The cells were then co-treated with Cu(SBCM)2 and antioxidants to evaluate the involvement of ROS in the cytotoxicity of Cu(SBCM)2. Molecular docking study was performed to determine the interaction of Cu(SBCM)2 with DNA, DNA topoisomerase I, and human ribonucleotide reductase. Results: Cu(SBCM)2 induced G2/M phase cell cycle arrest and apoptosis in MCF-7 cells possibly via upregulation of p53 wild-type protein. Cu(SBCM)2 was less toxic towards MCF10A cells. Increased level of intracellular ROS was not detected in MCF-7 cells after treatment with Cu(SBCM)2. However, N-acetylcysteine antioxidant enhance the cytotoxicity of Cu(SBCM)2 in MCF-7 cells. Cu(SBCM)2 showed the greatest affinity for DNA topoisomerase I in comparison to DNA and human ribonucleotide reductase. Conclusions: Cu(SBCM)2 has a potential to be developed as a targeted agent for breast cancer.