In spite of the advances accomplished in treating ErbB2 breast cancer, the ErbB2 cancer challenge still remains an unmet need. Also, mTORC1 is activated in up to 80% of human cancers [56], while current mTOR inhibitors are of limited clinical efficacy due to resistance invoked by de-suppression of mTOR feedback networks and due to worrisome side effects. If proved in future clinical studies, the bifunctional activity of MEDICA in abrogating ErbB receptors and inhibiting mTORC1 activity (Fig. 7f) may offer a novel treatment mode for mTORC1-driven cancers in general and ErbB2 breast cancer in particular.

Treatment of ErbB2 breast cancer by mitochondrial targeting