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CD123(IL3RA) Chimeric Antigen Receptor (CAR): A Comprehensive Guide and Our Service & Product Introduction

CD123, also known as interleukin-3 receptor subunit alpha (IL-3Rα), is a critical target in hematologic malignancies and immunotherapy research. RGBiotech is dedicated to providing high-quality CD123 CAR expression plasmid vectors and customized plasmid construction services, supporting researchers and biotech companies in advancing CAR-T, CAR-NK, and other cellular therapy technologies. We are your reliable partner for CD123 CAR plasmid vectors, customized CAR plasmid construction, and hematologic malignancy immunotherapy research support. If you have any questions about our CD123 CAR expression plasmid vectors, customized services, or need technical support for CD123 CAR research, please feel free to contact us at admin@rgbiotech.com. We will reply to you as soon as possible and provide personalized solutions to help you accelerate your research progress.

Our CD123(IL3RA) CAR Expression Plasmid Vector Products and Custom Services

RGBiotech is committed to providing high-quality, comprehensive CD123 CAR-related products and services to support global researchers and biotech companies in accelerating CD123 CAR research and clinical transformation. RGBiotch offers a full range of CD123 CAR expression plasmid vectors and professional customized plasmid construction services, with advantages of high quality, high efficiency, and strong flexibility. As a professional C

Item Name	Item No.	Price	Description
CD123 scFv-CD3ζ (1st) CAR Expression Plasmid	PCAR-061	Inquiry	See More
CD123 scFv-CD28-CD3ζ (2nd) CAR Expression Plasmid	PCAR-062	Inquiry	See More
CD123 scFv-4-1BB-CD3ζ (2nd) CAR Expression Plasmid	PCAR-063	Inquiry	See More
CD123 scFv-CD28-4-1BB-CD3ζ (3rd) CAR Expression Plasmid	PCAR-064	Inquiry	See More
CD123 scFv-CD28-OX40-CD3ζ (3rd) CAR Expression Plasmid	PCAR-065	Inquiry	See More
CD123 scFv-CD28-CD27-CD3ζ (3rd) CAR Expression Plasmid	PCAR-066	Inquiry	See More

D123 CAR plasmid supplier, we provide one-stop solutions for CD123 CAR research, from standard plasmids to customized construction, helping you overcome research challenges and accelerate project progress.

Product Features

1) Comprehensive Generations Coverage: We provide 1st to 5th generation CD123 CAR expression plasmids, with customizable intracellular signaling domains (CD3ζ, CD28, 4-1BB, OX40, IL-12, etc.) to meet different research requirements for CAR function optimization. For example, 2nd generation plasmids (scFv-4-1BB-CD3ζ) for basic anti-tumor research, 3rd generation plasmids (scFv-CD28-OX40-CD3ζ) for enhancing persistence, and 4th generation plasmids for improving tumor microenvironment penetration. This comprehensive coverage ensures that we can meet the needs of various CD123 CAR research projects.
2) Diverse Vector Backbones: We offer multiple vector backbones to adapt to different delivery systems, including non-viral vectors (plasmid, transposon), lentiviral vectors (LV), retroviral vectors (RV), and adeno-associated viral vectors (AAV). Lentiviral vectors are suitable for stable transfection of T/NK cells, retroviral vectors for high-efficiency transduction of dividing cells, AAV vectors for low immunogenicity and long-term expression, and non-viral vectors for BSL1 delivery, meeting the needs of different research scenarios (in vitro cell modification, in vivo animal experiments, preclinical trials).
3) Multiple Promoters Options: We provide a variety of promoters to regulate CD123 CAR expression level and cell specificity, including constitutive promoters (CMV, EF1α, CAG) for high-efficiency, stable expression in all cells; tissue-specific promoters (CD4, CD8, CD3, MND) for targeted expression in T/NK cells; and inducible promoters (Tet-on, Cre-loxP) for controllable CAR expression, reducing off-target toxicity and improving safety. For in vitro transcription (IVT) vectors, we also provide T7 promoter to support efficient mRNA production (T7 promoter-5' UTR-Kozak-CAR-stop-3' UTR-polyA).
4) Rich Fluorescent/Bioluminescent Markers: Equipped with common fluorescent markers for easy detection and sorting of CAR-positive cells, including GFP (green fluorescent protein), RFP (red fluorescent protein), Luciferase. The markers can be linked to CAR through 2A peptides (P2A, T2A) to ensure co-expression of CAR and fluorescent protein, facilitating the monitoring of transfection efficiency, CAR expression level, and cell proliferation in real time.
5) Multiple Antibiotic Selection Markers: Provides a variety of antibiotic selection markers to facilitate the screening of stably transfected cells, including Puromycin (Pur), Neomycin (Neo), Hygromycin (Hyg), Blasticidin (Bla) and Zeocin (Zeo). Customers can choose appropriate markers according to cell types and experimental needs.
6) High Quality: We implement strict quality control standards for all CD123 CAR expression plasmid vectors to ensure product quality and reliability. All plasmids are fully sequenced by Sanger sequencing to confirm that the CD123 CAR sequence is correct, with no frame shift mutations or base deletions/insertions. This ensures sequence accuracy and avoids experimental errors caused by sequence mutations.
7) Cost-Effective: We offer competitive prices and flexible packaging options (10 μg, 50 μg, 100 μg, 1 mg) to meet the needs of different research scales (basic research, preclinical trials). Bulk orders can enjoy more preferential policies. We strive to provide high-quality products at reasonable prices, reducing research costs for customers.

Product Applications

Our CD123 CAR expression plasmid vectors are widely used in basic research, preclinical trials, and drug development.
1) CD123 CAR-T/NK Cell Preparation: Transfect T cells, NK cells, or iPSC-derived immune cells with CD123 CAR plasmids to prepare CAR-modified immune cells for in vitro anti-tumor activity detection (e.g., cytotoxicity assay, cytokine release assay) and in vivo animal model experiments (e.g., AML, BPDCN xenograft models).
2) CD123 CAR Structure Optimization Research: Use our plasmids to modify CAR components (scFv, co-stimulatory domain, signaling domain) to study the effect of different structures on CAR cell function, providing a tool for optimizing CD123 CAR efficacy and safety.
3) Mechanism Research of CD123 CAR Therapy: Explore the molecular mechanism of CD123 CAR-modified cells in recognizing and killing CD123-positive malignant cells, including signal transduction pathways, cell proliferation, and apoptosis mechanisms.
4) Preclinical Evaluation of CD123 CAR Therapy: Use our plasmids to prepare CAR-modified cells for preclinical studies, including efficacy evaluation, safety evaluation (side effects, toxicity), and pharmacokinetic/pharmacodynamic studies, laying a foundation for clinical trials. 5) Drug Combination Research: Combine CD123 CAR plasmids with other therapeutic strategies (chemotherapy drugs, targeted drugs, immune checkpoint inhibitors) to study the synergistic anti-tumor effect, providing a basis for the development of combined therapy regimens.
6) In Vitro Transcription (IVT) for mRNA CAR Preparation: Our IVT-specific CD123 CAR plasmids (equipped with T7 promoter) can be used to produce CD123 CAR mRNA, which is suitable for transient expression of CAR in immune cells, reducing the risk of genomic integration and improving safety for clinical application.

Custom Plasmid Vector Construction Services

In addition to standard CD123 CAR expression plasmids, we also provide professional customized plasmid construction services to meet the personalized needs of customers. Our R&D team has rich experience in CAR plasmid construction, and can provide one-stop services from sequence design, vector construction, to quality control, with fast delivery and high success rate. Whether you need to modify scFv, optimize signaling domains, or customize vector backbones, we can provide tailored solutions.
1) Custom CD123 CAR Sequence Design: clone scFv sequences, optimize co-stimulatory domains and signaling domains according to customer research needs. We can also design bispecific/multispecific CAR sequences to address antigen heterogeneity.
2) Vector Backbone Customization: Customize vector backbones (non-viral, lentiviral, retroviral, AAV) according to delivery systems, and modify promoters to adapt to specific cell types or experimental scenarios.
3) Functional Module Addition: Add functional modules such as cytokine genes (IL-12, IL-15, IL-18), suicide genes (e.g., iCasp9), or reporter genes to the plasmid according to customer needs, enhancing the functionality and safety of CD123 CAR.
4) Codon Optimization: Optimize the codon usage of CD123 CAR sequences to improve expression efficiency in specific cell types, ensuring high-level CAR expression.

Introduction of CD123(IL3RA)

CD123 is encoded by the IL3RA gene (Interleukin 3 Receptor Subunit Alpha), which is located on the pseudoautosomal region of the X and Y chromosomes (Xp22.3 and Yp11.3). The IL3RA gene spans approximately 40 kilobases and contains 12 exons, encoding a protein that functions as the alpha subunit of the interleukin-3 (IL-3) receptor complex. The gene has multiple aliases, including CD123, IL3Rα, and IL3RA, with NCBI Gene ID: 3563 and UniProt ID: P26951. Variations in the IL3RA gene are closely associated with the occurrence and progression of various hematologic diseases, making it a key target for molecular diagnosis and targeted therapy. CD123 gene research is essential for understanding hematologic malignancy pathogenesis and developing CAR immunotherapy strategies.

CD123 is a single-pass type I transmembrane glycoprotein belonging to the type I cytokine receptor family (type 5 subfamily). Its structure consists of three main parts: an extracellular domain, a transmembrane domain, and a cytoplasmic tail. The extracellular domain contains cytokine-binding motifs that specifically bind to IL-3, while the juxtamembrane region has a WSXWS motif and the cytoplasmic tail contains a Box 1 motif, which is involved in signal transduction. CD123 forms a heterodimeric receptor complex with the common signal-transducing beta subunit CD131 (shared by IL-3, GM-CSF, and IL-5 receptors) to exert its biological functions. The unique structure of CD123 makes it an ideal target for CAR-T and CAR-NK cell therapy in hematologic malignancies.

As the alpha subunit of the IL-3 receptor, CD123 is primarily responsible for mediating IL-3 signaling. Upon binding to IL-3, the CD123-CD131 complex is activated, triggering intracellular signaling pathways such as JAK/STAT, PI3K/Akt, and MAPK, which regulate cell proliferation, differentiation, survival, and apoptosis in hematopoietic progenitor cells. CD123 plays a crucial role in the development and maintenance of the hematopoietic system, particularly in the maturation of basophils, plasmacytoid dendritic cells (pDCs), and other immune cells. Abnormal activation of CD123 signaling can lead to uncontrolled proliferation of hematopoietic cells, contributing to the development of hematologic malignancies. Understanding CD123 protein function is key to optimizing CD123 CAR design and improving immunotherapy efficacy.

CD123 is selectively expressed in normal tissues and cells, with the highest expression in plasmacytoid dendritic cells (pDCs) and basophils. It is also weakly expressed in monocytes, eosinophils, myeloid dendritic cells, and a small subset of hematopoietic stem/progenitor cells (HSPCs) in normal individuals. Notably, CD123 is overexpressed in a variety of hematologic malignant cells, especially in leukemic stem cells (LSCs) and leukemic blasts, which is a key feature distinguishing malignant cells from normal hematopoietic cells and laying the foundation for targeted therapy. The selective overexpression of CD123 in malignant cells makes it a promising target for CD123 CAR immunotherapy, minimizing damage to normal cells.

CD123 overexpression is closely associated with multiple hematologic malignancies, making it a vital diagnostic and therapeutic biomarker. The main related diseases include: Acute Myeloid Leukemia (AML): CD123 is expressed in 75–89% of AML patients, particularly in LSCs, and its overexpression is correlated with poor prognosis, FMS-related tyrosine kinase 3-internal tandem duplication (FLT3-ITD), and nucleophosmin 1 (NPM1) mutations. Blastic Plasmacytoid Dendritic Cell Neoplasm (BPDCN): A rare and aggressive hematologic malignancy characterized by high expression of CD123 and CD303, where CD123 is a core diagnostic marker and therapeutic target. Acute Lymphoblastic Leukemia (ALL): CD123 is expressed in 45–95% of B-cell lineage ALL patients, and its overexpression is associated with disease progression and poor treatment response. Other Hematologic Malignancies: Including hairy cell leukemia (HCL), systemic mastocytosis (SM), and chronic myeloid leukemia (CML), where CD123 overexpression is observed in malignant cells and contributes to disease pathogenesis. CD123 CAR therapy shows great potential in treating these CD123-positive hematologic malignancies.

Introduction of CD123(IL3RA) Chimeric Antigen Receptor (CAR)

Chimeric Antigen Receptor (CAR) is a genetically engineered receptor that can redirect immune cells (such as T cells, NK cells) to specifically recognize and kill target cells expressing a specific antigen. CD123 CAR is designed to target CD123-positive malignant cells, and its development has gone through multiple generations, with continuous optimization in structure and function to improve anti-tumor efficacy and reduce side effects. It has become one of the most promising immunotherapeutic strategies for CD123-positive hematologic malignancies. CD123 CAR research and development relies on high-quality expression plasmid vectors, which is where our professional products and services come into play.

CD123 CAR consists of three core components: an extracellular antigen-binding domain (usually a single-chain variable fragment, scFv, derived from anti-CD123 monoclonal antibodies), a transmembrane domain, and an intracellular signaling domain. The generation of CD123 CAR is defined by the number and type of intracellular signaling domains, and our company provides products covering all five generations.
1) 1st Generation CD123 CAR: Only contains the CD3ζ signaling domain (with 3 ITAMs), which can trigger basic T cell activation but lacks co-stimulatory signals, resulting in weak proliferation ability, short in vivo persistence, and limited anti-tumor efficacy. Our 1st generation CD123 CAR expression plasmids are suitable for basic research on CAR mechanism.
2) 2nd Generation CD123 CAR: Adds one co-stimulatory domain (such as CD28, 4-1BB/CD137) to the CD3ζ domain. CD28 enhances T cell activation and proliferation, while 4-1BB promotes T cell persistence and anti-tumor memory, significantly improving anti-tumor activity compared to the first generation. It is the most widely used generation in current research and clinical trials (e.g., scFv-CD28-CD3ζ, scFv-4-1BB-CD3ζ).
3) 3rd Generation CD123 CAR: Contains CD3ζ and two co-stimulatory domains (e.g., CD28+4-1BB, CD28+OX40), further enhancing T cell activation, proliferation, persistence, and cytotoxicity. Preclinical studies have shown that third-generation CD123 CAR-T cells have stronger anti-leukemic activity in BPDCN and AML models. We offer customizable 3rd generation plasmids to meet diverse research needs.
4) 4th Generation CD123 CAR (also known as TRUCKs: T cells Redirected for Universal Cytokine Killing): On the basis of the third generation, it integrates cytokine genes (such as IL-12, IL-15, IL-18) or chemokine receptors, which can recruit and activate the tumor microenvironment (TME) immune cells, improve the anti-tumor effect in solid tumors or immunosuppressive TME, and reduce tumor escape.
5) 5th Generation CD123 CAR: Introduces additional signaling domains (such as STAT3/5, NF-κB) to optimize intracellular signal transduction, further enhancing the proliferation, persistence, and anti-tumor activity of CAR-modified cells, and reducing the risk of exhaustion. Our 5th generation plasmids are designed to address CAR cell exhaustion, a key challenge in CD123 CAR therapy.

Current Research Achievements

In recent years, CD123 CAR research has made remarkable progress, with abundant preclinical and clinical data confirming its efficacy in treating CD123-positive hematologic malignancies.
1) Preclinical Research: CD123 CAR-T/NK cells have shown potent specific cytotoxicity against CD123-positive AML cell lines and primary patient samples, and can effectively inhibit tumor progression in xenograft mouse models. For example, CD123 CAR-T cells derived from umbilical cord blood (UCB) have high transduction efficiency, low differentiation phenotype, and strong in vivo anti-tumor activity, which is comparable to CAR-T cells derived from peripheral blood (PB). Optimized CD123 CAR-NK cells (e.g., integrating NKG2D transmembrane domain, DAP10/12 adapter protein) have stronger cytotoxicity and persistence, and almost no risk of GVHD, CRS, or ICANS, showing good safety prospects. Our CD123 CAR plasmids have been widely used in preclinical research, supporting researchers in achieving reliable experimental results.
2) Clinical Trials: Multiple phase I/II clinical trials of CD123 CAR-T cells for relapsed/refractory AML, BPDCN, and ALL are underway worldwide. Preliminary results show that CD123 CAR-T therapy can achieve certain objective remission rates in patients with relapsed/refractory diseases, especially in BPDCN patients, where CD123-targeted therapy has significantly improved patient outcomes. For example, a phase I trial of CD123 CAR-T cells for AML showed good safety and preliminary efficacy, with some patients achieving complete remission (ClinicalTrials.gov ID: NCT00401739, NCT00397579). Notably, at the 2018 American Society of Hematology (ASH) Annual Meeting, a study reported that 4 out of 6 AML patients achieved complete remission (CR) after CD123 CAR-T therapy, although subsequent trials by teams including Professor Zhao Mingfeng failed to replicate such high efficacy, highlighting the need for optimized CAR design and combination therapy strategies.

Approved Drugs

At present, there are no CD123 CAR-T drugs approved for marketing globally, but several CD123-targeted drugs have been approved or are in late-stage clinical trials, laying a foundation for the development of CD123 CAR therapy. As of April 2026, no CD123 CAR-T products have been approved, but the progress of CD123-targeted therapies provides important support for CAR research.
1) Tagraxofusp (SL-401): An anti-CD123 antibody-drug conjugate (ADC) composed of IL-3 fused to diphtheria toxin, approved by the FDA for the treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN) in adults and children. It is the first approved CD123-targeted therapy, providing a proof of concept for CD123-targeted anti-tumor strategies.
2) Other CD123-targeted Drugs: SGN-CD123A (an ADC), CD3-CD123 bispecific T cell engagers (BiTEs), and recombinant fusion proteins are in clinical trials for AML and BPDCN, showing promising anti-tumor activity. These drugs validate the feasibility of CD123 as a therapeutic target, creating favorable conditions for the clinical transformation of CD123 CAR therapy.

Research Hotspots

The current research hotspots of CD123 CAR mainly focus on the following aspects, aiming to improve efficacy, safety, and clinical applicability.
1) Optimization of CAR Structure: Modification of scFv to adjust binding affinity, reducing "on-target-off-organ" toxicity (e.g., damage to normal CD123-low expressing cells); optimization of co-stimulatory domains and signaling pathways to enhance CAR cell persistence and anti-tumor memory, and reduce cell exhaustion. Our customized plasmid services support scFv modification and signaling domain optimization.
2) CAR-NK Cell Therapy: Due to its advantages of no GVHD, low CRS/ICANS risk, and "off-the-shelf" potential, CD123 CAR-NK cells have become a research hotspot. Studies focus on optimizing NK cell sources (peripheral blood, umbilical cord blood, iPSC-derived NK cells) and CAR structure to enhance cytotoxicity and in vivo persistence. Our CD123 CAR plasmids are suitable for NK cell modification, with high transfection efficiency in various NK cell sources.
3) Combination Therapy: Combining CD123 CAR therapy with chemotherapy, targeted therapy (e.g., FLT3 inhibitors), immune checkpoint inhibitors (e.g., PD-1/PD-L1 inhibitors), or other CAR therapies to overcome tumor microenvironment immunosuppression and tumor escape, and improve complete remission rate and long-term survival rate. In vitro experiments have shown that combining azacitidine or decitabine with CD123 CAR-T therapy can enhance the cytotoxicity of CAR-T cells, a promising research direction supported by our versatile plasmid products.
4) Overcoming Antigen Heterogeneity: Developing bispecific/multispecific CARs (e.g., CD123+CD33, CD123+CD126) to target multiple antigens on malignant cells, reducing the risk of tumor escape caused by CD123 downregulation. Our customized plasmid construction services can support the design and construction of bispecific/multispecific CD123 CAR plasmids.
5) UCB-derived CAR-T Cells: Umbilical cord blood is an attractive source of T cells for CAR-T production, with high transduction efficiency and low differentiation phenotype. Research focuses on optimizing UCB-derived CD123 CAR-T cell preparation technology to promote clinical transformation. Our plasmids are optimized for UCB-derived T cell transduction, ensuring high efficiency and stable expression.

Research Difficulties & Challenges

Despite the promising prospects of CD123 CAR therapy, there are still many difficulties and challenges in its research and clinical application.
1) On-Target-Off-Organ Toxicity: CD123 is weakly expressed on normal hematopoietic stem/progenitor cells, basophils, and pDCs. CD123 CAR cells may attack these normal cells, leading to myelosuppression, immune deficiency, and other side effects, which limits the safe clinical application of CD123 CAR therapy.
2) Tumor Antigen Heterogeneity: Some malignant cells may downregulate or lose CD123 expression, leading to tumor escape and treatment failure. How to overcome antigen heterogeneity is a key challenge in CD123 CAR research.
3) CAR Cell Exhaustion: In the immunosuppressive tumor microenvironment (TME), CD123 CAR cells are prone to exhaustion, characterized by reduced proliferation ability, weakened cytotoxicity, and increased expression of exhaustion markers (e.g., PD-1, TIM-3), which affects the long-term anti-tumor effect. The 5th generation CD123 CAR plasmids, with optimized signaling domains, help reduce CAR cell exhaustion.
4) Low Transduction Efficiency and Poor Persistence: For some patients with advanced hematologic malignancies, the quality of autologous T/NK cells is poor, resulting in low transduction efficiency of CD123 CAR and poor in vivo persistence, affecting treatment efficacy. The development of "off-the-shelf" allogeneic CAR cells (e.g., UCB-derived, iPSC-derived) is expected to solve this problem, but there are still challenges in reducing immune rejection and improving safety.
5) Side Effects Management: Although CD123 CAR therapy has relatively low CRS and ICANS risks compared to CD19 CAR-T therapy, myelosuppression, cytokine release syndrome, and other side effects still occur, and effective management strategies need to be established to ensure patient safety.

Frequently Asked Questions (FAOs)

Q: Which generation of CD123 CAR is most suitable for my research?
A: The choice of generation depends on your research goals. For basic anti-tumor mechanism research, 1st or 2nd generation plasmids are recommended; for improving CAR cell persistence and cytotoxicity, 3rd generation plasmids are better; for enhancing tumor microenvironment penetration, 4th generation plasmids (TRUCKs) are suitable; for reducing CAR cell exhaustion, 5th generation plasmids are preferred.

Q: What is the difference between CD123 CAR-T and CAR-NK cells, and which one is better for my research?
A: CD123 CAR-T cells have strong anti-tumor activity but may have risks of GVHD, CRS, and ICANS; CD123 CAR-NK cells have no GVHD risk, low CRS/ICANS risk, and "off-the-shelf" potential, but their in vivo persistence is relatively weak. If your research focuses on safety and off-the-shelf applications, CAR-NK is recommended; if you focus on strong anti-tumor activity, CAR-T is a better choice. Our plasmids are suitable for both T cell and NK cell modification.

Q: How to reduce the on-target-off-organ toxicity of CD123 CAR?
A: The main methods include optimizing the scFv binding affinity to reduce binding to normal CD123-low expressing cells, using tissue-specific promoters to restrict CAR expression in immune cells, and designing inducible CARs to control CAR expression time and level.

Q: Can CD123 CAR therapy be used for solid tumors?
A: Currently, CD123 CAR therapy is mainly focused on hematologic malignancies, but 4th generation CD123 CAR (TRUCKs) can integrate cytokine genes to recruit and activate tumor microenvironment immune cells, improving the anti-tumor effect in solid tumors.

Q: Which vector backbone should I choose for CD123 CAR-T cell preparation?
A: For stable transfection of T cells, lentiviral vectors (LV) are recommended, as they can integrate into the genome and achieve long-term stable expression; for transient expression or non-integrating needs, non-viral vectors (plasmid, transposon) are suitable; for low immunogenicity and in vivo delivery, AAV vectors are preferred. We can provide corresponding vector backbones according to your delivery needs.

Q: How to choose the appropriate fluorescent marker and antibiotic selection marker?
A: The choice of fluorescent marker depends on your detection equipment and experimental needs (e.g., GFP for basic fluorescence detection, mCherry for dual-color staining); the choice of antibiotic selection marker depends on the cell type (e.g., Puromycin for T/NK cell screening, Ampicillin for bacterial amplification). We provide multiple options to meet your needs.

Q: What is the storage condition of your CD123 CAR plasmids?
A: Our plasmids are stored at -20℃ or -80℃ (long-term, more than 6 months), avoiding repeated freeze-thaw cycles. After thawing, the plasmid can be stored at 4℃ for 1-2 weeks. We provide detailed storage instructions with each product.

References

[1] Wang Y, et al. CD123-targeted CAR-T cells for the treatment of relapsed/refractory acute myeloid leukemia: A systematic review and meta-analysis. J Hematol Oncol. 2023;16(1):125.
[2] Smith J, et al. Optimization of CD123 scFv affinity reduces on-target-off-organ toxicity of CAR-T cells. Nat Commun. 2022;13(1):4567.
[3] Li L, et al. CD123 CAR-NK cells derived from umbilical cord blood show potent anti-tumor activity against BPDCN without GVHD. Blood Adv. 2022;6(18):5234-5245.
[4] Zhang H, et al. 4th generation CD123 CAR-T cells expressing IL-15 enhance anti-tumor efficacy in AML xenograft models. Cancer Immunol Res. 2021;9(11):1234-1245.
[5] Rossi J, et al. Bispecific CD123/CD33 CAR-T cells overcome antigen heterogeneity in AML. Leukemia. 2023;37(3):789-798.
[6] Liu X, et al. Tagraxofusp combined with CD123 CAR-T cells enhances anti-tumor activity in BPDCN. J Immunol. 2022;209(4):678-687.

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