Targaprimir-96 causes programmed cell death in breast cancer animal models.
Researchers in a recent study were able to create a drug that decreased tumor cell growth in animal models of triple negative breast cancer.
"This is the first example of taking a genetic sequence and designing a drug candidate that works effectively in an animal model against triple negative breast cancer," said researcher Matthew Disney, PhD. "The study represents a clear breakthrough in precision medicine, as this molecule only kills the cancer cells that express the cancer-causing gene -- not healthy cells. These studies may transform the way the lead drugs are identified -- by using the genetic makeup of a disease."
In the study, published by Proceedings of the National Academy of Sciences, the compound targaprimir-96 caused breast cancer cells to self-destruct through programmed cell death by targeting RNA that ignites the cancer.
Researchers used a computational approach called Inforna that focuses on developing designer compounds that bind to RNA folds in order to create this molecule, according to the study.
The researchers targeted microRNA-96, which promotes cancer through discouraging programmed cell death that is designed to rid the body of cells with uncontrolled growth.
Researchers tested targaprimir-96 in animal models for 21 days and found a decreased production of microRNA-96 and increased programmed cell death. According to the study, it also reduced tumor growth.
Healthy cells were found to be unaffected by the compound, since researchers found it is highly selective in the molecules it targets unlike typical cancer therapeutic targets that are not selective.
"In the future we hope to apply this strategy to target other disease-causing RNAs, which range from incurable cancers to important viral pathogens such as Zika and Ebola," concluded study first author Sai Pradeep Velagapudi.