Peptide Therapeutic for Immune Response Activation against Metastatic Triple Negative Breast Cancer

­This invention provides compositions and methods for treating triple negative breast cancer using peptides or peptide mimics that bind to epidermal growth factor receptor (EGFR) to enhance the trafficking of EGFR to lysosomes for destruction. This mode of action induces the degradation of EGFR, loss of cancer cell survival and migratory capacity, and induces tumor regression. Efficacy experiments in a mouse model for EGFR-dependent breast cancer resulted in significant tumor regression without observable toxicity. In addition, these compound activate the immune system, exhibited by cytotoxic T lymphocytes and natural killer cells activity in the immune microenvironment, and a prognostically favorable macrophage M1/M2 ratio. Target disease indications are breast cancer, particularly triple-negative breast cancer, as well as other cancer types in which EGFR is implicated. Toxicology tests in a mouse model show favorable results.


Triple-negative breast cancer (TNBC) has long been in need of therapies that are both effective and targeted. Current drugs for TNBC such as monoclonal antibodies and PARP inhibitors have limited effectiveness and serious side effects such as nausea, fatigue, decreased white blood cell count, anemia, and upper respiratory tract infection. This invention holds the promise to make treatment of TNBC possible for more people and more effective via its unique mechanism of action, while also reducing side effects by superior targeting of the disease.


  • Pharmacological treatment of triple-negative breast cancer, including metastatic
  • Therapeutic for additional EGFR-type cancers


  • Effective pharmacological approach to treating triple negative breast cancer
  • Specific biological targeting of EGFR
  • Activates immune system to target cancer cells
  • Attractive results from animal toxicology tests


Contact Information

TTO Home Page:

Name: Laura Silva

Title: Sr. Licensing Manager, COS

Department: TLA