DC_AC50

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^[1].
In Vitro: DC_AC50 exhibits IC₅₀ 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^[1].
DC_AC50 (0-10 μM)-treated cells are significantly less mitotically active, as demonstrated by decreased expression of phospho-histone H3 and cell cycle analysis^[1].
DC_AC50 (10 μM) potentiates carboplatin-induced apoptosis in OSA cells and decreasesclonogenic survival^[1].
DC_AC50 induces cell cycle arrest at both the 3 and 10 μM doses and DC_AC50 induces increase S phase cells dose-independently^[1].
DC_AC50 (3 μM) inhibits the migration and of canine and human OSA cells^[1].
DC_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^[2].