An already approved cancer drug called Carfilzomib may help restore the effectiveness of CAR-T cell therapy in advanced multiple myeloma cases. Technical University of Munich researchers have discovered a molecular mechanism that causes cancer cells to evade treatment and have shown that blocking it can make immunotherapy work again in some patients.
CAR-T cell therapy involves removing a patient’s T cells, genetically altering them in the laboratory, and reintroducing them so they can recognize and attack cancer cells. For multiple myeloma, these engineered cells target a molecule known as BCMA, which appears on diseased plasma cells. The approach can extend survival, sometimes by years, but it rarely eliminates the disease entirely.
Unfortunately, the therapy loses impact over time, steadily becoming less effective as patients continue to use the therapy. Cancer cells that carry less BCMA on their surface are more likely to survive, while those with high levels are destroyed. This evolutionary pressure allows resistant cells to multiply, gradually weakening the treatment’s effect. CAR-T cell therapy is currently used only after other options have failed.
The Technical University of Munich Department of Internal Medicine III Director Florian Bassermann says BCMA is an attractive target because it is largely restricted to cancerous plasma cells. At the same time, he notes that immunotherapy can drive rapid changes within tumors, allowing them to adapt under pressure.
The research team investigated why BCMA disappears from the surface of some cancer cells. Study lead author Leonie Rieger says the group found that the ubiquitin-proteasome system plays a key role. This system regulates which proteins are broken down inside cells. The researchers demonstrated that it can also remove BCMA from the cell membrane, a process that had not been clearly understood before.
Carfilzomib, a proteasome inhibitor that has already received approval for multiple myeloma, blocks part of this degradation machinery. In laboratory and animal models, the drug prevented the loss of BCMA. The team then tested the strategy in 10 patients whose previous CAR-T therapy had failed. After receiving Carfilzomib, all 10 patients showed renewed BCMA expression on their cancer cells. Six patients who still had sufficient CAR-T cells in circulation experienced a renewed therapeutic response.
Department of Internal Medicine III Cellular Immunotherapy Head Judith S. Hecker says the findings could open a new option for patients who have exhausted standard CAR-T cell approaches. She cautions that the study group was small, and it remains difficult to predict which patients will respond best. Bassermann notes that larger studies are planned and that researchers are exploring whether the drug might be given earlier in treatment to prevent resistance from emerging.
These findings offer hope that the use of CAR-T treatments could be broadened, and it comes at a time when many enterprises like Calidi Biotherapeutics Inc. (NYSE American: CLDI) are also investing heavily in developing novel immunotherapy treatments for cancer. A time is coming when immunotherapy could be the go-to therapy for cancer patients.
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