ArticleJournal of cellular and molecular medicine2025
FT538, iPSC-derived NK cells, enhance AML cell killing when combined with chemotherapy.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Allogeneic CD56 + cell infusion as a bridge to hematopoietic stem cell transplantation in relapsed/refractory acute myeloid leukemia: a phase I clinical trial.Cancer immunology, immunotherapy : CII · 2026Article
- iPSC-derived CAR-NK extracellular vesicles for non-small cell lung cancer: evidence, engineering, and translational barriers.Frontiers in immunology · 2026Review
- Mapping the global clinical landscape of NK cell therapies for solid tumors: an analysis based on the ClinicalTrials.gov for the 2005-2024 period.Journal of cancer research and clinical oncology · 2025Article
- CD33Journal for immunotherapy of cancer · 2025Article
- FT538, iPSC-derived NK cells, enhance AML cell killing when combined with chemotherapy.Journal of cellular and molecular medicine · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Induced pluripotent stem cell (iPSC)-derived natural killer (NK) cells offer an opportunity for a standardized, off-the-shelf treatment with the potential to treat a wider population of acute myeloid leukaemia (AML) patients than the current standard of care. FT538 iPSC-NKs express a high-affinity, noncleavable CD16 to maximize antibody dependent cellular cytotoxicity, a CD38 knockout to improve metabolic fitness, and an IL-15/IL-15 receptor fusion preventing the need for cytokine administration, the main source of adverse effects in NK cell-based therapies. Here, we sought to evaluate the potential of FT538 iPSC-NKs as a therapy for AML through their effect on AML cell lines and primary AML cells. We observed that FT538 iPSC-NKs induce effector-to-target cell ratio dependent apoptosis in cell lines and primary AML cells, including cells from high-risk patients. Flow cytometric analysis revealed that FT538 iPSC-NKs induce AML cell death when combined with the AML therapies: cytarabine, venetoclax and gilteritinib. Moreover, cytarabine did not affect FT538 iPSC-NK viability, suggesting that iPSC-derived NK therapies and chemotherapy may be a promising treatment combination. This study provides the basis for further study of iPSC-derived NK cell therapies as a treatment option for high-risk AML patients, particularly those with disease resistant to standard therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.