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. 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. ? 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. ? DC_AC50 (10 μM) potentiates carboplatin-induced apoptosis in OSA cells and decreasesclonogenic survival. ? DC_AC50 induces cell cycle arrest at both the 3 and 10 μM doses and? DC_AC50 induces increase S phase cells dose-independently. ? DC_AC50 (3 μM) inhibits the migration and of canine and human OSA cells. ? 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. 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

No numbering system information yet

No physical and chemical property information yet

No safety information yet

No production method and use information yet

No upstream information yet

No downstream information yet

No related product information yet