About Breast Cancer
Breast cancer is the most diagnosed cancer worldwide and the leading cause of cancer-related death in women. In the United States approximately 290,000 new cases of breast cancer are diagnosed annually. Although significant progress has been made in the treatment of breast cancer over the past few decades, breast cancer still carries a high mortality rate with an unmet need that provide a challenge to improving patient outcomes.
BET Inhibitors and Breast Cancer
BET inhibitors may help overcome resistance to current breast cancer therapies and address an unmet need in triple negative breast cancer and ER+ breast cancer. ZEN-3694 is also being evaluated in combination with of ZEN-3694 in combination with abemaciclib (CDK4/6 inhibitor) in adult and pediatric patients with metastatic or unresectable breast cancer for which standard curative or palliative measures are no longer effective (NCT05372640).
Triple Negative Breast Cancer
Triple Negative Breast Cancer (TNBC), defined as the absence of estrogen and progesterone receptors and lack of human epidermal growth factor receptor 2 (HER2) gene amplification, comprises 15% to 20% of breast cancers. TNBC’s high mortality rate is due to its aggressive behavior with a median survival of 10 to 13 months from time of metastasis. There are two ongoing National Cancer Institute sponsored clinical trials evaluating rationale combinations with ZEN-3694 to address this unmet need (NCT05111561, NCT05422794).
ER+ Breast Cancer
ZEN-3694 showed efficacy in various models of estrogen receptor (ER)+ breast cancers – including in models that are resistant to ER inhibitors – by down-regulating ER signaling, as well as several pathways associated with resistance to ER-based therapies in the clinic. These results suggest that ZEN-3694 could improve the efficacy of existing treatments for ER+ breast cancer patients.
About 70-80% of breast cancers are characterized by the expression of the ER. ER signaling helps cancer cells grow, hence the development of inhibitors that inhibit the synthesis of estrogen or the ER itself. Despite potent clinical efficacy, resistance to these inhibitors occurs frequently highlighting the need for other therapies that interfere with ER synthesis and signaling.
