Author Correction: Chemically triggered drug release from an antibody-drug conjugate leads to potent antitumour activity in mice.

The original version of this Article omitted the following from the Acknowledgements: 'This work was supported by the Office of the Assistant Secretary of Defense for Health Affairs, through the Breast Cancer Research Program under Award No. W81XWH-15-1-0692. Opinions, interpretations, conclusions and recommendations are those of the author and are not necessarily endorsed by the Department of Defense'.

Chemically triggered drug release from an antibody-drug conjugate leads to potent antitumour activity in mice.

Current antibody-drug conjugates (ADCs) target internalising receptors on cancer cells leading to intracellular drug release. Typically, only a subset of patients with solid tumours has sufficient expression of such a receptor, while there are suitable non-internalising receptors and stroma targets. Here, we demonstrate potent therapy in murine tumour models using a non-internalising ADC that releases its drugs upon a click reaction with a chemical activator, which is administered in a second step.

α- Versus β-Emitting Radionuclides for Pretargeted Radioimmunotherapy of Carcinoembryonic Antigen-Expressing Human Colon Cancer Xenografts.

Pretargeted radioimmunotherapy (PRIT) with the β-emitting radionuclide Lu is an attractive approach to treat carcinoembryonic antigen (CEA)-expressing tumors. The therapeutic efficacy of PRIT might be improved using α-emitting radionuclides such as Bi. Herein, we report and compare the tumor-targeting properties and therapeutic efficacy of Bi and Lu for PRIT of CEA-expressing xenografts, using the bispecific monoclonal antibody TF2 (anti-CEA × anti-histamine-succinyl-glycine [HSG]) and the di-HSG-DOTA peptide IMP288.