An experimental drug, AMPI-109, shows promise as an immunotherapy that sensitizes triple-negative breast cancer cells, enhancing the effectiveness of the drug.1

AMPI-109 was shown to kill cancer cells in previous studies at the University of Colorado (CU). But understanding of how the drug works was limited; such limitations could preclude the drug from further clinical testing.

In this study, researchers identified how AMPI-109 works. The drug flips the switch on PRL-3, an enzyme that puts cancer cells to senescence, leading to cell death. When PRL-3 is active, cancer cells survive; when it is inactivated, the cancer cells senesce and eventually die.

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Immunotherapies are designed to teach the immune system to recognize and attach tumor tissue. Cancer cells can, however, hide and continue to thrive. As a result, the goal for immunotherapies is to keep the cancer in check, treating it as a chronic condition.

These studies suggest that inhibiting PRL-3 activity could result in a 2-hit strategy: the drug exposes cancer cells to the immune system, and then allows the immune system to fight the cancer, explain the researchers.

The researchers are working toward funding for drug safety studies. “If results remain promising, AMPI-109 could become an important tool in an oncologist’s kit to target triple-negative breast cancer with immunotherapy.”


1. Study uncovers molecular switch that may sensitize triple-negative breast cancers to immunotherapy [news release]. University of Colorado Cancer Center. August 29, 2016. Accessed September 5, 2016.