CAR-NK cells represent the next evolution in cancer cell therapy. Discover their advantages over CAR-T cells, their proven efficacy in hematologic and solid tumors, and the clinical breakthroughs shaping the future of immunotherapy.

Beyond CAR-T.  Next-generation CAR-engineered cell therapies: CAR-NK Cells

 

Alexander Ariel Padron Gonzalez

Alexander Padron

Jose Garcia

José García

 

1. CAR-NK Cells Against Hematologic Malignancies – Preclinical and Clinical Studies

Initial studies on CAR-NK cells have focused on hematological malignancies. Anti-CD19 CAR-NKs from various cell sources and signaling domains demonstrated effective cytotoxicity against B-cell malignancies both in vitro and in vivo. Anti-CD19 CAR-NK-92 cells showed strong anti-lymphoma activity against Rituximab and Obinutuzumab-resistant B-cell lymphoma cells, utilizing granule-mediated apoptosis and IFN-γ signaling. They also secreted CCL3, recruiting NK cells, T cells, macrophages, and DCs to the TME. Augmenting anti-CD19 CAR-NK cells with the human CXCR4 gene improved their homing to the bone marrow. CRISPR-Cas9 knockout of NK cell immune checkpoints further enhanced their cytotoxicity. Bispecific CAR-NK cells targeting CD19/CD22 and BCMA/CD19 showed superior efficacy against B-cell lymphoma and multiple myeloma (MM) compared to single-antigen CAR-NKs.

 

Clinical Studies

In a phase I/II trial, anti-CD19 CAR-NK cells showed an objective response in 8 of 11 patients with CD19-positive leukemia or lymphoma. These cells expanded and persisted in patients for at least 12 months, and importantly, did not cause cytokine release syndrome (CRS), neurotoxicity, or graft-versus-host disease (GvHD).

 

AML and T-Cell Malignancies

CAR-NK cells targeting CD33, CD123, FLT3, and CD38 effectively killed AML cells in vitro and in vivo. CD38-CAR NK cells posed a fratricide risk due to CD38 expression on NK cells, which was mitigated by CD38 knockout. However, a phase I trial of anti-CD33 CAR-NK cells for relapsed/refractory AML showed no notable clinical efficacy. CAR-NK cells targeting T-lymphoid malignancies, such as anti-CD5, anti-CD7, and anti-CD4 CAR-NKs, have shown specific cytotoxicity in preclinical studies without the risk of fratricide.

 

2. CAR-NK Cells Against Solid Tumors

Preclinical Studies

CAR-NK cells targeting various solid tumor antigens, such as EGFR, HER2, Mesothelin, EpCAM, EGFRvIII, and PSCA, demonstrated potent cytotoxicity in preclinical studies. Comparative studies indicated that HER2-targeting CAR-NK cells exhibited superior cell-mediated tumor killing in vivo compared to CAR-T cells, and Mesothelin-targeting CAR-NK and CAR-T cells showed equivalent tumor reduction capabilities. CAR-NK cells have also shown potential as alternatives for therapy-resistant tumors, like triple-negative breast cancer and 5-FU-resistant colorectal cancer.

 

Clinical Studies

CAR target NK cell source Cancer type Phase NCT number
CD19 UCB Hematological malignancies I/II NCT03056339
CD19 UCB B-cell NHL I NCT05472558
CD19 UCB Hematological Malignancies I NCT04796675
CD19 iPSC B-cell Malignancies I NCT05379647
CD19 iPSC Hematological Malignancies I NCT05336409
CD19 HPCs B-cell lymphoma I/II NCT05654038
CD19 Not disclosed B-cell NHL I NCT04887012
CD19 Not disclosed Hematological Malignancies I NCT05645601
CD19 Not disclosed Hematological Malignancies I NCT05410041
CD19 Not disclosed Hematological Malignancies I NCT05020678
CD19 Not disclosed ALL I NCT05563545
CD19/CD70 UCB B-cell NHL I/II NCT05842707
CD19/CD70 UCB B-cell NHL I NCT05667155
CD33 iPSC AML I NCT05665075
CD33 iPSC AML I NCT05601466
CD33 Not disclosed AML I NCT05008575
CD70 UCB Hematological Malignancies I/II NCT05092451
CD70 UCB Solid Tumors I/II NCT05703854
NKG2D NK92 Solid Tumors I NCT05528341
NKG2D Not disclosed Colorectal cancer I NCT05213195
PD-L1 NK92 GEJ cancers or HNSCC II NCT04847466
DLL3 NK92 Extensive-stage SCLC I NCT05507593
BCMA iPSC Multiple myeloma I NCT05182073
HER2 NK92 Glioblastoma I NCT03383978
Claudin6 PBMCs Reproductive system tumors I/II NCT05410717
NKG2D ligands Not disclosed Hematological Malignancies I NCT04623944

 

3. CAR-NK vs. CAR-T therapies(safety, efficacy, cost)

Aspect CAR-T Therapy CAR-NK Therapy
Safety 1. High risk of CRS/ICANS: Severe cytokine release syndrome (CRS) and neurotoxicity in 20-50% of patients.
2. GVHD risk: Allogeneic use requires immunosuppression.
3. Tumor lysis syndrome: Reported in high-tumor-burden cases.
1. Lower toxicity: Minimal CRS/ICANS (<13%) grade 1-2; severe cases rare)
2. No GVHD: MHC-independent killing avoids graft rejection.
3. NO IL-6 release: Reduces CRS drivers
Efficacy 1. High response in hematologic cancers: 70-90% CR in B-ALL/DLBCL
2. Long-term persistence: CAR-T cells survive years, enabling durable remission.
3. Limited solid tumor success: Poor infiltration and TME suppression.
1. Strong in indolent lymphomas: 83-100% CR in CD19+ lymphomas.
2. Activity against resistant tumors: Effective in 38% of CAR-T resistant lymphomas.
3. Solid tumor potential: Dual targeting (e.g., NKG2D + CAR) enhances efficacy.
Cost & Logistics 1. Autologous production: 3-6 weeks manufacturing, costing $400,000-500,000 per dose.
2. Complex infrastructure: Requires specialized facilities.
3. Patient-specific: Limits scalability
1. Off-the-shelf availability: Pre-made doses reduce cost ($100,000-150,000).
2. Rapid production: 2-3 weeks using iPSCs or NK cell lines.
3. Scalability: One donor serves multiple patients.

 

Advantages: CAR-NK cells offer several advantages over CAR-T cells. They can be derived from various sources, are HLA-independent, and can be used allogeneically without the risk of GvHD. NK cells' innate ability to recognize tumor cells via native receptors makes them resistant to antigen escape. Clinical trials have shown CAR-NK cells have a lower risk of adverse effects like neurotoxicity and CRS compared to CAR-T cells. Their ability to distinguish between healthy and malignant cells reduces off-target toxicity. Additionally, safety mechanisms like the caspase-9-based suicide gene allow controlled elimination of NK cells if necessary.

Challenges and Solutions: CAR-NK cells face challenges such as limited persistence without cytokine support. Solutions include expressing membrane-bound IL-15, using IL-15 receptor fusion constructs, or genetically engineering NK cells to produce IL-15. Overcoming the immunosuppressive TME involves using decoy-resistant IL-18, dominant-negative TGF-β receptors, or knocking out TGF-β-induced miR-27-5p. Enhancing CAR-NK cell trafficking to tumors involves arming them with chemokine receptors like CCR7 and CXCR2

CAR-NK cells recognize cancer cells via their CAR and activating NK cell receptors. They induce anti-tumor toxicity through granzyme B/perforin secretion and death receptor-mediated killing (FasL, TRAIL), participate in ADCC and activate T cells through cytokine secretion

 

References

1. Marr B, Jo D, Jang M, Lee SH. Cytokines in focus: IL-2 and IL-15 in NK adoptive cell cancer immunotherapy. Immune Netw. 2025;25(2):e17.
2. Qiu Z, Li Z, Zhang C, Zhao Q, Liu Z, Cheng Q, Zhang J, Lin A, Luo P: NK Cell senescence in cancer: from molecular mechanisms to therapeutic opportunities. aging dis 2025.
3. Taveirne S, Wahlen S, Van Loocke W, Kiekens L, Persyn E, Van Ammel E, et al. The transcription factor ETS1 is an important regulator of human NK cell development and terminal differentiation. Blood. 2020;136(3):288–98.
4. Guia S, Fenis A, Baudesson De Chanville C, Galluso J, Medjouel H, Escaliere B, et al. Genome-wide CRISPR/Cas9 screen reveals factors that influence the susceptibility of tumor cells to NK cell-mediated killing. J Immunother Cancer. 2025;13(3):e010699.
5. Wang M, Krueger JB, Gilkey AK, Stelljes EM, Kluesner MG, Pomeroy EJ, et al. Precision enhancement of CAR-NK cells through non-viral engineering and highly multiplexed base editing. J Immunother Cancer. 2025;13(5):e009560.
6. Zhu W, Fan C, Zhao Y, Li W, Niu J, Dong S, Yang Z, Zhou W. The role of NK cells in regulating tumorimmunity: current state, challenges and future strategies. Cancer Cell Int. 2025 Oct 17;25(1):360. doi: 10.1186/s12935-025-03980-y. PMID: 41107895; PMCID: PMC12535086.

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