Figure 2
Figure 2. Inhibition of proliferation and induction of apoptosis by carfilzomib. (A,C) IL-6–independent RPMI 8226 and IL-6–dependent ANBL-6 MM cells (2 × 104) were treated continuously (A) or pulsed for 1 hour (C) with increasing concentrations of carfilzomib. Cellular viability was determined at 24 hours using the water-soluble tetrazolium salt WST-1. (B,D) IL-6–dependent (ANBL-6, KAS-6/1) and IL-6–independent (RPMI 8226, U266) myeloma cells were continuously exposed (B) or pulsed (D) with carfilzomib for 1 hour and allowed to recover for 24 hours. Programmed cell death was then evaluated using a DNA fragmentation ELISA. Results are expressed as a fold-increase of DNA fragmentation over DMSO control, and error bars are SD.

Inhibition of proliferation and induction of apoptosis by carfilzomib. (A,C) IL-6–independent RPMI 8226 and IL-6–dependent ANBL-6 MM cells (2 × 104) were treated continuously (A) or pulsed for 1 hour (C) with increasing concentrations of carfilzomib. Cellular viability was determined at 24 hours using the water-soluble tetrazolium salt WST-1. (B,D) IL-6–dependent (ANBL-6, KAS-6/1) and IL-6–independent (RPMI 8226, U266) myeloma cells were continuously exposed (B) or pulsed (D) with carfilzomib for 1 hour and allowed to recover for 24 hours. Programmed cell death was then evaluated using a DNA fragmentation ELISA. Results are expressed as a fold-increase of DNA fragmentation over DMSO control, and error bars are SD.

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