Figure 4.
Figure 4. Copanlisib sensitizes DLBCL cells to venetoclax. (A) Induction of apoptosis shown as percentage of viable (annexin V/PI–negative) cells after 96-hour exposure to ABT-199 (0-250 nM). Results show average viability plus or minus SEM from at least 3 biological replicates. Cell lines are ranked from the most resistant to the most sensitive to venetoclax. (B) Correlation between cytochrome c release induced by BAD peptide (BCL2 plus BCL-xL) minus that induced by the HRK peptide (BCL-xL) (BCL-2 dependency; y-axis) with induction of apoptosis after 96-hour exposure to ABT-199 (250 nM; x-axis). (C) Induction of apoptosis (percentage of viable [annexinV/PI–negative] cells) after 96-hour exposure to the combination of MCL-1 inhibitor (S63845, 0-250 nM) and ABT-199 (0-250 nM). Results show average viability plus or minus SEM from 2 biological replicates. Synergy visualized as median CI. CI < 1 indicates synergy.

Copanlisib sensitizes DLBCL cells to venetoclax. (A) Induction of apoptosis shown as percentage of viable (annexin V/PI–negative) cells after 96-hour exposure to ABT-199 (0-250 nM). Results show average viability plus or minus SEM from at least 3 biological replicates. Cell lines are ranked from the most resistant to the most sensitive to venetoclax. (B) Correlation between cytochrome c release induced by BAD peptide (BCL2 plus BCL-xL) minus that induced by the HRK peptide (BCL-xL) (BCL-2 dependency; y-axis) with induction of apoptosis after 96-hour exposure to ABT-199 (250 nM; x-axis). (C) Induction of apoptosis (percentage of viable [annexinV/PI–negative] cells) after 96-hour exposure to the combination of MCL-1 inhibitor (S63845, 0-250 nM) and ABT-199 (0-250 nM). Results show average viability plus or minus SEM from 2 biological replicates. Synergy visualized as median CI. CI < 1 indicates synergy.

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