Murray, Michael published the artcileCarbon Chain Length Modulates MDA-MB-231 Breast Cancer Cell Killing Mechanisms by Mitochondrially Targeted Aryl-Urea Fatty Acids, Related Products of bromides-buliding-blocks, the main research area is aryl urea fatty acid preparation structure breast cancer mitochondrion; antitumor agents; apoptosis; breast cancer; fatty acids; lipid drugs.
Targeting the tumor cell mitochondrion could produce novel anticancer agents. We designed an aryl-urea fatty acid (1 g; 16({[4-chloro-3-(trifluoromethyl)phenyl]carbamoyl}amino)hexadecanoic acid) that disrupted the mitochondrion and decreased MDA-MB-231 breast cancer cell viability. To optimize the aryl-ureas the present study evaluated mitochondrial targeting by 1 g analogs containing alkyl chains between 10-17 carbons. Using the dye JC-1, the C12-C17 analogs efficiently disrupted the mitochondrial membrane potential (IC50s 3.5±1.2 to 7.6±1.1μM) and impaired ATP production; shorter analogs were less active. 7-Aminoactinomycin D/annexin V staining and flow cytometry showed that these agents activated the killing mechanisms of necrosis and apoptosis to varying extents (7-aminoactinomycin D/annexin V staining ratios 4.3-6.0). Indeed, 1 g and its C17 analog preferentially activated necrosis and apoptosis, resp. (ratios 2.1 and 16). Taken together, alkyl chain length is a determinant of mitochondrial targeting by aryl-ureas and can be varied to develop analogs that activate apoptosis or necrosis in a regulated fashion.
ChemMedChem published new progress about Antiproliferative agents. 55099-31-5 belongs to class bromides-buliding-blocks, name is Ethyl 10-bromodecanoate, and the molecular formula is C12H23BrO2, Related Products of bromides-buliding-blocks.
Referemce:
Bromide – Wikipedia,
bromide – Wiktionary