Abstract
Proteasome inhibitor (PI) resistance remains a problem in multiple myeloma (MM) therapy. Metabolic reprogramming towards oxidative phosphorylation (OXPHOS) and high mitochondrial ATP supply provide proteasome inhibitor resistance (Tsvetkov, NatureChemBiol 2019). The anti-HIV drug nelfinavir (NFV) overcomes PI-resistance in combination with bortezomib. We identified the molecular targets of NFV and addressed the effect of NFV on the metabolic reprogramming of PI-resistant MM.
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