DC_AC50 chemical structure
Chemical structureResearch use only
CAT. NO. DC20945Featured

DC_AC50

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TotalUS$500
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Product overview

Description & Application

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].

ParameterValue
Chemical Name3-amino-N-(2-bromo-4,6-difluorophenyl)-6,7-dihydro-5H-cyclopenta[b]thieno[3,2-e]pyridine-2-carboxamide
CAS No.497061-48-0
Synonyms3-amino-N-(2-bromo-4,6-difluorophenyl)-6,7-dihydro-5H-cyclopenta[b]thieno[3,2-e]pyridine-2-carboxamide;3-Amino-N-(2-bromo-4,6-difluorophenyl)-6,7-dihydro-5H-cyclopenta[b]thieno[3,2-e]pyridine-2-carboxamide
FormulaC17H12BrF2N3OS
M.Wt424.262488365173
SMILESFC1=CC(F)=C(NC(C2SC3=NC4CCCC=4C=C3C=2N)=O)C(Br)=C1
Purity>98%
Storage2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

Biological Activity

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]. Cell Viability Assay[1] Cell 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 Analysis[1] Cell Line: Abrams and HOS cells. Concentration: 1, 3 and 10 μM (10 μM Carboplatin). Incubation Time: 24 h. Result: Potentiated carboplatin-induced apoptosis.

In Vivo

No in vivo data are provided in the current product source. Contact us for further information.

References & source

[1]. Jordon M Inkol, et al. Inhibition of copper chaperones sensitizes human and canine osteosarcoma cells to carboplatin chemotherapy. Vet Comp Oncol. 2020 Dec;18(4):559-569.

[2]. Jing Wang, et al. Inhibition of human copper trafficking by a small molecule significantly attenuates cancer cell proliferation. Nat Chem. 2015 Dec;7(12):968-79.

DC Chemicals original product information

Published experimental findings depend on the model and assay conditions. They do not guarantee equivalent performance in every application. For laboratory research use only.

Product documentation

Refer to the certificate supplied with your lot for batch-specific release results.

Handling guide

2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

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