Carbon Chain Length in a Novel Anticancer Aryl‐Urea Fatty Acid Modulates Mitochondrial Targeting, Reactive Oxygen Species Production and Cell Killing

Author:

Elmaghrabi Yasmin A.1,Roseblade Ariane2,Rahman Khalilur1,Rawling Tristan2,Murray Michael1ORCID

Affiliation:

1. Discipline of Pharmacology and Sydney Pharmacy School Faculty of Medicine and Health University of Sydney Camperdown NSW 2006 Australia

2. School of Mathematical and Physical Sciences Faculty of Science University of Technology Sydney Ultimo NSW 2007 Australia

Abstract

AbstractThe cancer cell mitochondrion could be a promising target for the development of new anticancer agents. 16‐([3‐chloro‐5‐(trifluoromethyl)‐phenyl]carbamoylamino)hexadecanoic acid (2) is a novel aryl‐urea fatty acid that targets the mitochondrion in MDA‐MB‐231 breast cancer cells and activates cell death. In the present study, the relationships between alkyl chain length in 2 analogues, mitochondrial disruption and cell killing were evaluated. The chain‐contracted C13‐analogue 7 c optimally disrupted the mitochondrial membrane potential (IC50 4.8±0.8 μM). In addition, annexin V‐FITC/7‐AAD assays demonstrated that 7 c was the most effective cell killing analogue and C11 BODIPY (581/591) assays demonstrated that 7 c was also most effective in generating reactive oxygen species in MDA‐MB‐231 cells. Together, carbon chain length is a key factor that determines the capacity of 2 analogues to disrupt the mitochondrial membrane, induce the production of reactive oxygen species and kill breast cancer cells. As an aryl‐urea with enhanced activity and improved drug‐like properties, 7 c may be a suitable lead molecule for entry into a program of development of these molecules as anticancer agents.

Publisher

Wiley

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