Natural killer (NK) cells are critical effectors of the innate immune system, capable of recognizing and eliminating pathogen-infected or malignant cells. Engineered CAR NK cells offer a promising alternative to CAR T-cell therapies, with the potential to enhance anti-tumor efficacy while minimizing the risks of cytokine release syndrome (CRS) and neurotoxicity. This study designed two CAR NK cell constructs targeting BCMA: a conventional BCMA-CAR (anti-BCMA-CD28-41BB-CD3ζ) and an advanced IL-15-secreting version, armored BCMA-IL-15-CAR, to enhance therapeutic efficacy. NK cells were expanded ex vivo using ARH77 feeder cells engineered to express membrane-bound B7H6, CD137L, IL-15, and IL-15Rα. After seven days of expansion, BCMA-CAR lentiviruses were transduced into NK cells via BaEv-TR pseudotyped lentiviral vectors. Following transduction, NK cell purity was over 90% on day 7, with transduction efficiencies of 33.5% for BCMA-CAR, and 27.7% for armored BCMA-IL15-CAR, which remained stable over 7 days. Cytotoxicity assays using K562 cells, which do not express BCMA, revealed no notable differences between groups. However, both BCMA-CAR constructs markedly increased NK cell cytotoxicity and CD107a degranulation against multiple myeloma (MM) cell lines (RPMI-8226, U266/B4, NCI-H929) compared to unmodified NK cells. Remarkably, armored BCMA-IL-15-CAR NK cells displayed significantly increased cytotoxicity against MM cells compared to BCMA-CAR NK cells alone. long-term cytotoxicity assays revealed that while both BCMA-CAR NK and BCMA-IL15-CAR NK cells effectively targeted tumor cells, BCMA-IL15-CAR NK cells demonstrated significantly prolonged cytotoxic activity. This sustained effect is likely attributed to IL-15 secretion, which enhances NK cell persistence and function. These results underscore the strong anti-myeloma activity of BCMA-CAR-NK and armored BCMA-IL-15-CAR NK cells, highlighting their potential as promising therapeutic strategies for multiple myeloma.