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. Author manuscript; available in PMC: 2013 Jun 26.
Published in final edited form as: Cancer Cell. 2013 Feb 11;23(2):139–141. doi: 10.1016/j.ccr.2013.01.018

Figure 1. ABT-199 selectively kills BCL-2 dependent tumor cells while sparing platelets.

Figure 1

(A) Navitoclax (ABT-263) binds with high affinity to both BCL-2 and BCL-XL. Since many tumors, particularly lymphoid malignancies, are addicted to BCL-2 for survival, this potently induces tumor cell apoptosis. Platelets depend primarily on BCL-XL for survival, and therefore are also destroyed by navitoclax. (B) ABT-199 is specific for BCL-2 and induces selective death of BCL-2 dependent tumor cells while sparing platelets.

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