Women lose a valuable weapon against their breast tumors when the potency of hormone therapy fades. But what if there was a way to “reprogram” breast tumor cells to be receptive to hormone therapy? Waltham, MA-based Syndax Pharmaceuticals might have such a way.
Syndax has shown in a 26-patient clinical trial that its drug, entinostat, could improve the ability of hormone therapies to kill breast cancer. The biotech startup—which was co-founded by scientists from the Salk Institute for Biological Studies in La Jolla, CA in 2005—has embarked on a new human study that will give it a clearer picture than previous studies provided of how well its drug improves breast cancer treatment. Its research has been displayed in recent days at the American Society of Clinical Oncology (ASCO) annual meeting in Chicago.
The company’s new Phase II clinical trial for entinostat for breast cancer patients is a big test of the firm’s technology. The firm has raised $49 million from venture capital firms such as the San Diego venture firms Domain Associates, Avalon Ventures, and Forward Ventures as well as MPM Capital, of Boston and South San Francisco, and Pappas Ventures in Durham, NC. (Eckard Weber, a well-known partner at Domain in San Diego, co-founded and served as an early CEO of Syndax.) Joanna Horobin, the firm’s CEO, said that the startup raised its latest $9 million in venture financing this year to complete its new mid-stage clinical trial, which she hopes will yield evidence of its lead drug’s utility by early next year.
For several years Syndax has been one of the biotechs to watch in the hot field of epigentics, which involves the study chemical changes in cells that impact how genes are expressed or suppressed without changing the underlying DNA code. Epigenetics grabbed the cover of Time magazine in January. For instance, breast tumor cells can undergo epigenetic changes that make them immune to hormone therapies, which are intended to stymie the production of estrogen needed to sustain tumor survival. Syndax’s drug aims to reprogram breast tumor cells in which those detrimental epigenetic switches occur.
“The idea is that you turn off the
