DC_AC50 is a dual inhibitor of Atox1 and CCS (copper chaperones). Inhibiting intracellular copper chaperones as a means of reducing/preventing acquired chemotherapy resistance. In Vitro DC_AC50 exhibits IC 50 values of 9.88 μM, 12.57 μM, 5.96 μM and 6.68 μM in Canine Abrams, Canine D1, human HOS and human MG63) cells, respectively. ?\nDC_AC50 (0-10 μM)-treated cells are significantly less mitotically active, as demonstrated by decreased expression of phospho-histone H3 and cell cycle analysis. ?\nDC_AC50 (10 μM) potentiates carboplatin-induced apoptosis in OSA cells and decreasesclonogenic survival. ?\nDC_AC50 induces cell cycle arrest at both the 3 and 10 μM doses and? DC_AC50 induces increase S phase cells dose-independently. ?\nDC_AC50 (3 μM) inhibits the migration and of canine and human OSA cells. ?\nDC_AC50 (2.5-10 μM) is highly efficient at inhibiting cancer cell proliferation (human lung cancer H1299 cells, leukaemia cancer K562 cells, breast cancer MDA-MB-231 cells and head and neck cancer 212LN cells) in a dose-dependent manner. DC_AC50 fails to exhibit any notable inhibition of the cell proliferation of human normal epithelial lung BEAS-2B cells or breast MCF-10A cells as control cells. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Viability AssayCell Line: Canine OSA (Abrams, D1 and human OSA (HOS, MG63) cells. Concentration: 0-10 μM. Incubation Time: 72 h. Result: Dose-dependently decreased viability of OSA cells. Apoptosis AnalysisCell Line: Abrams and HOS cells. Concentration: 1, 3 and 10 μM (10 μM Carboplatin). Incubation Time: 24 h. Result: Potentiated carboplatin-induced apoptosis. Form:Solid