Multi-Target Investigational Drug Class Effectively Kills Cancer Cells
SF2523 can dually inhibit a protein and an enzyme associated with cancer.
In the past, the MYC regulator gene became a target for cancer research, since this gene controls the expression of other genes, and codes for proteins involved with cellular processes.
While MYC has been shown to be an optimal target, it has been elusive. However, in a study published by the Proceedings of the National Academy of Sciences, the authors created a novel class of drugs observed to inhibit multiple molecular targets simultaneously.
This new drug was observed to increase both the efficacy and the safety of cancer treatment.
“Most anti-cancer drugs have a single target. They try to do one thing, such as block a single receptor or signaling pathway,” said study co-senior author Donald L. Durden, MD, PhD. “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.”
Through molecular modeling and nuclear magnetic resonance imaging, the investigators created SF2523. They discovered that this small molecule compound was able to disrupt 2 important MYC-mediating factors that promote cancer cell growth, the enzyme PI3K, and the BRD4 protein, according to the study.
In both in vivo and in vitro models, the investigators found that SF2523 was able to simultaneously inhibit the PI3K and BRD4 targets. This action was observed to stop MYC activation and expression, which significantly impeded cell growth and metastasis.
This compound was also seen to be more efficient and less toxic to the host, according to the study.
Since the drug is able to block multiple cancer cell processes at 1 time, patients would be less likely to experience adverse events seen from taking multiple drugs. Additionally, immunotherapy techniques tend to elicit less side effects, compared with traditional chemotherapy or radiation.
SF2523 could also reduce drug costs, since it takes action against multiple targets rather than 2 drugs to address them separately.
“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,” Dr Durden concluded. “These findings suggest that dual-activity inhibitors are a highly promising lead compound for developing new anticancer therapeutics.”