Supplementary Materials

Supplementary Material for:

Tumor-Specific Activation of an EGFR-Targeting Probody Enhances Therapeutic Index

Luc R. Desnoyers, Olga Vasiljeva, Jennifer H. Richardson, Annie Yang, Elizabeth E.M. Menendez, Tony W. Liang, Chihunt Wong, Paul H. Bessette, Kathy Kamath, Stephen J. Moore, Jason G. Sagert, Daniel R. Hostetter, Fei Han, Jason Gee, Jeanne Flandez, Kate Markham, Margaret Nguyen, Michael Krimm, Kenneth R. Wong, Shouchun Liu, Patrick S. Daugherty, James W. West, Henry B. Lowman*

*Corresponding author. E-mail:

Published 16 October 2013, Sci. Transl. Med. 5, 207ra144 (2013)
DOI: 10.1126/scitranslmed.3006682

This PDF file includes:

  • Fig. S1. Selectivity of PB1 Probody linker cleavage.
  • Fig. S2. FACS binding of Probody PB1 and cetuximab to H292 cells.
  • Fig. S3. Time course of ex vivo Probody activation.
  • Fig. S4. Quantification of tumor/normal Probody and cetuximab accumulation in mice.
  • Fig. S5. EGFR pathway inhibition in tumors from mice treated with cetuximab or Probody PB1.
  • Fig. S6. EGFR expression and lack of Probody activation in skin from normal cynomolgus monkey.
  • Table S1. EGFR ELISA binding data from individual experiments.
  • Table S2. H292 cell–based activity inhibition data from individual experiments.
  • Table S3. Tumor volumes from H292 efficacy study.
  • Table S4. Tumor volumes from LXFA677 efficacy study.
  • Table S5. Anti-drug antibody observations in nonhuman primates.
  • Table S6. Probody IHZ screening of NSCLC patient tumor samples.
  • Table S7. Probody IHZ screening of CRC patient tumor samples.

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