Fig. 7

Schematic representation of CDC20 inhibition strategies tested in hematological malignancies. A The small molecule Apcin prevents the substrate recognition capacity of APC/C^CDC20 leading to the stabilization of CDC20 substrates that could result in mitotic arrest or mitotic slippage based on intracellular SAC activity. B Pro-Tame binds in a competitive manner the APC/C core complex preventing its association with CDC20 that results in mitotic arrest through stabilization of CCNB1. C The compound 9f, like Apcin, inhibits CDC20 downstream activity leading to mitotic arrest. It has also been shown that 9f inhibits tubulin polymerization and compromises microtubule network organization, causing cell cycle arrest and inducing apoptosis