Researchers Stumble Upon Old Antibiotic That Could Kill Dangerous Cells

At the Medical Research Council (MRC) Institute of Genetics and Molecular Medicine, scientists have found out that nifuroxazide, an old antibiotic, can kill dangerous cells within the most fatal skin cancer type called melanomas.

More Insights into the Finding of Nifuroxazide
At MRC situated in the University of Edinburgh, scientists have found out that the drug can be effectively used in existing melanoma therapies. The study was published in the journal called Cell Chemical Biology. The drug’s effect on melanoma cells was tested in mice. However to undertake further tests, scientists came to the conclusion that more research is definitely needed to determine its effectiveness.

The researchers found out that within a single tumor, there can be a variation in the properties of the cells. This is because some of the cells are more dangerous than the others, in terms of their potential to support growth or become resistant to drug treatment. Several dangerous cells in melanoma tumors an enzyme called aldehyde dehydrogenase 1 (ALDH1) in notable quantities. As per the current research, relevant processes focus a lot on blocking ALDH1. However, scientists conducted in-depth studies and found out that selective cells producing ALDH1 can be killed by using the antibiotic called nifuroxazide.

This antibiotic is activated by the enzyme called ALDH1, and this means that it only becomes toxic once it is inside cells producing the enzyme. The scientists used human melanomas implanted in mice. This was followed by monitoring the organism, which showed that the nifuroxazide therapy killed the tumor cells that produced a lot of ALDH1, without causing significant toxicity to other cells in the body.

In future, the scientists hope that this study may complement existing melanoma treatments, called BRAF and MEK inhibitors. Currently, tumours developed in some people have developed a resistance to BRAF and MEK inhibitors. Moreover, researchers found that some of these resistant tumors were high in ALDH1.