Supplementary Materials

Supplementary Material for:

Exploiting selective BCL-2 family inhibitors to dissect cell survival dependencies and define improved strategies for cancer therapy

Joel D. Leverson,* Darren C. Phillips, Michael J. Mitten, Erwin R. Boghaert, Dolores Diaz, Stephen K. Tahir, Lisa D. Belmont, Paul Nimmer, Yu Xiao, Xiaoju Max Ma, Kym N. Lowes, Peter Kovar, Jun Chen, Sha Jin, Morey Smith, John Xue, Haichao Zhang, Anatol Oleksijew, Terrance J. Magoc, Kedar S. Vaidya, Daniel H. Albert, Jacqueline M. Tarrant, Nghi La, Le Wang, Zhi-Fu Tao, Michael D. Wendt, Deepak Sampath, Saul H. Rosenberg, Chris Tse, David C. S. Huang, Wayne J. Fairbrother, Steven W. Elmore, Andrew J. Souers

*Corresponding author. E-mail: joel.leverson{at}abbvie.com

Published 18 March 2015, Sci. Transl. Med. 7, 279ra40 (2015)
DOI: 10.1126/scitranslmed.aaa4642

This PDF file includes:

  • Materials and Methods
  • Fig. S1. BCL-XL–selective inhibitor A-1155463 kills Mcl-1−/− MEF cells but not Bak−/− Bax−/− MEFs.
  • Fig. S2. Navitoclax synergizes with docetaxel to kill breast cancer cell lines.
  • Fig. S3. Navitoclax-docetaxel combination kills breast cancer cell lines by inducing apoptosis.
  • Fig. S4. Selective BCL-XL inhibition suffices for synergy with docetaxel in ovarian cancer cell lines.
  • Fig. S5. BCL-XL–selective inhibitor A-1331852 kills Mcl-1−/− MEF cells but not Bak−/− Bax−/− MEFs.
  • Fig. S6. Relationship between exposure and platelet reduction is similar for navitoclax with or without docetaxel.
  • Table S1. Plasma exposures and platelet effects of navitoclax-docetaxel combinations.
  • References (4951)

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