San Diego medical researchers announced Wednesday that they’ve developed a molecule that can impact multiple cancer targets at once, which could lead to a new class of drugs.
The report, published in Proceedings of the National Academy of Sciences, said scientists engineered a molecule that disrupted a protein and enzyme that promote cancer growth.
“Most anti-cancer drugs have a single target. They try to do one thing, such as block a single receptor or signaling pathway,” said Dr. Donald Durden, a professor in the Department of Pediatrics at the UC San Diego School of Medicine and the study’s co-senior author. “This paper is proof-of-concept of a completely different mode of drug discovery clearly separated from the standard practice of one drug, one target.”
The protein and enzyme are part of MYC, a regulator gene that controls the expression of other genes. It also codes transcription factors or proteins involved in many fundamental cellular processes.
MYC is also among the most frequently altered genes found in cancer, making it an attractive target for cancer therapies, according to UCSD Health.
In cell and mouse models, the scientists found that their molecule, named SF2523, inhibited both the protein, BRD4, and enzyme, PI3K. That blocked MYC activation and expression, and affected cancer growth and metastasis.
“This is a first-in-class approach to achieve a maximum inhibition of MYC in the treatment of the multitude of cancers known to be driven by the MYC oncogene,” said Durden, also an associate director for pediatric oncology at Moores Cancer Center at UC San Diego Health. “These findings suggest that dual- activity inhibitors are a highly promising lead compound for developing new anticancer therapeutics.”
He worked with researchers at the UCSD Moores Cancer Center, Rady Children’s Hospital, San Diego-based biopharmaceutical company SignalRX and the University of Colorado School of Medicine. Durden is a co-founder of SignalRX.
The research was funded by the National Institutes of Health.
—City News Service
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