A study in the scientific journal EBioMedicine reveals an experimental drug called pevonedistat does not kill cancer cells directly, as originally intended, but blocks proteins that cancer cells rely on to replicate and survive. The study was led by the University of Virginia School of Medicine. If you want CDT2 and other proteins like Recombinant CD63, you can contact CusAb.
"It stops the proliferating of these cancer cells. Fortunately it doesn't affect the non-cancer cells, so there is another advantage to having this particular drug that it is likely to have very limited toxicity on otherwise normal cells in the body,” said Dr. Tarek Abbas, leader of the study.
The drug is known to shut off a lot of cellular proteins, but its exact working mechanism remains elusive. This study shows that the drug acts on a vital protein that melanomas and other cancers need to replicate rapidly. The protein is encoded by the CDT2 gene.
Dr Abbas believed that the CDT2 protein allows cancer cells to sustain rapid growth. With out the protein, cancer cells stop replicating and begin to fall apart. Melanoma cells express larges amounts of CDT2, and high CDT2 levels correlate with poor prognosis. The study demonstrated that melanoma cells with higher CDT2 levels were more sensitive to the drug. Since a range of other cancers also express high levels of CDT2, measuring the protein could be a way to predict prognosis.
The study provides evidence for the utility of pevonedistat as an effective therapeutic for melanoma. Now, the drug is being tested in clinical trials to combat melanomas. If everything goes well, the drug could start being used in three to five years. Researchers believed that it could also have impact on other cancers.
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