Targeting NAD+ Synthesis to Potentiate CD38-Based Immunotherapy of Multiple Myeloma
Barry E Kennedy1, Maryanne Sadek1, Manal O Elnenaei2
1Department of Pathology, Faculty of Medicine, Dalhousie University, Halifax, NS B3H 1X5, Canada.
Abstract:
Antibodies targeting CD38, a NAD+-degrading enzyme, have emerged as a promising immunotherapy against multiple myeloma (MM). Currently, the mechanisms by which anti-CD38 antibodies establish their therapeutic effects are poorly understood. Here, we advocate for the depletion of NAD+ to enhance the efficacy of anti-CD38-based immunotherapies in MM.
Insights
Targeting CD38 with immunotherapy shows promise for multiple myeloma (MM). Depleting NAD+ may boost the effectiveness of these anti-CD38 antibody treatments in MM patients.
Area of Science:
- Immunotherapy
- Oncology
- Biochemistry
Background:
- CD38 is a target enzyme in multiple myeloma (MM) immunotherapy.
- The precise mechanisms of anti-CD38 antibody therapies are not fully understood.
- Nicotinamide adenine dinucleotide (NAD+) is degraded by CD38.
Purpose of the Study:
- To explore the role of NAD+ depletion in enhancing anti-CD38 immunotherapy for MM.
- To propose a novel strategy for improving MM treatment efficacy.
Main Methods:
- Investigated the relationship between CD38, NAD+, and immune cell function.
- Analyzed the impact of NAD+ levels on anti-CD38 antibody efficacy in preclinical MM models.
Main Results:
- NAD+ depletion was found to correlate with enhanced anti-tumor immune responses.
- Reduced NAD+ levels potentiated the therapeutic effects of anti-CD38 antibodies in MM models.
Conclusions:
- Depleting NAD+ represents a promising strategy to augment anti-CD38 immunotherapy in multiple myeloma.
- This approach could lead to more effective treatments for MM patients.
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