Etirinotecan pegol for the treatment of breast cancer

ABSTRACT

Introduction: Advanced breast cancer is incurable for most patients with limited therapeutic options. As such, there is a critical need for new and novel agents that lack cross-resistance and mitigate overlapping toxicities.

Areas covered: This review examines etirinotecan pegol as a promising new agent for the treatment of refractory metastatic breast cancer. Etirinotecan pegol is the first topoisomerase I inhibitor with a novel design: a long-acting polymer conjugate of irinotecan molecularly engineered to concentrate in vascularized tumors and provide sustained circulation time of SN38 for prolonged tumor cell exposure. Etirinotecan pegol pharmacology is reviewed in this paper along with safety and efficacy data from preclinical and clinical trials. In the phase II advanced breast cancer setting, etirinotecan pegol provided promising activity, which was maintained in poor prognostic subgroups, with low rates of neutropenia and neuropathy - issues plaguing our currently available agents.

Expert Opinion: Etirinotecan pegol demonstrates anti-tumor activity and improved tolerability in patients with refractory metastatic breast cancer. As a novel topoisomerase I inhibitor in breast cancer, etirinotecan pegol holds great therapeutic potential, allowing the challenge of resistance in the advanced disease setting to be addressed.

KEYWORDS:

• Advanced or metastatic breast cancer
• Chemotherapy-resistant
• Etirinotecan pegol
• Polymer-based medicine

Declaration of interest

J Cortes has received consulting fees from Roche/Genentech, Celgene; honoraria for lectures from Roche/Genentech, Celgene, Novartis, Eisai; is a member of the BEACON Steering Committee and is a stockholder from Medica Scientia Innovation Research (MedSIR). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. Writing assistance was provided by Phillips Gilmore Oncology Communications Inc., funded by Nektar Pharmaceuticals.