The chemotherapy drug motexafin gadolinium (brand name: Xcytrin, manufactured by Pharmacyclics, Inc.) works to thwart cancer cells by disrupting key enzymes involved in cellular metabolism, according to a team of researchers led by Joseph Hacia, Ph.D., assistant professor of biochemistry and molecular biology at the Keck School of Medicine of the University of Southern California.
The cellular disruption results in increases in the amount of zinc available inside the cancer cells, and because zinc is involved in protein structure and function, leads to inhibition of enzyme activity and to the death of the cells.
A paper describing these findings was published in the May 1, 2005, issue of the journal Cancer Research.
In order to gain a better understanding of the mechanism of action of this novel chemotherapeutic agent, the researchers looked at gene expression profiles and other biochemical properties of cells from human lung, prostate and lymphoma cancer cell cultures that had been treated with motexafin gadolinium, or MGd. What they found was that the drug created oxidative stress in the tumor cells, increasing the levels of expression of the genes that produce metallothioneins.