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KDR(VEGFR2) Chimeric Antigen Receptor (CAR): A Comprehensive Guide and Our Service & Product Introduction

KDR(VEGFR2) CAR (Chimeric Antigen Receptor) expression plasmid vectors are core tools for developing CAR-T cell therapies and advancing research on angiogenesis-related diseases and solid tumors. RGBiotech is a professional provider of high-quality KDR(VEGFR2) CAR expression plasmid vectors and customized plasmid construction services, dedicated to supporting researchers and biopharmaceutical enterprises in accelerating the pace of scientific research and drug development. If you are interested in our KDR(VEGFR2) CAR expression plasmid vectors or customized services, or have any questions about KDR(VEGFR2) CAR research and application, please feel free to contact us at admin@rgbiotech.com. Our professional team will provide you with one-on-one consultation and solutions, and work with you to promote the development of KDR(VEGFR2) CAR-related therapies.

Our KDR(VEGFR2) CAR Expression Plasmid Vector Products and Custom Services

RGBiotech provides a full range of KDR(VEGFR2) CAR expression plasmid vectors, covering all generations of KDR(VEGFR2) CAR (1st to 5th generation), and supports customized construction services to meet the diverse needs of researchers and enterprises. Our products are widely used in basic and preclinical research, with reliable quality and high performance, helping to accelerate the research and development process of KDR(VEGFR2) CAR-related therapies. We also offer vectors optimized for KDR(VEGFR2) CAR-T cells, including those with Fn3 antigen recognition domains and optimized extracellular spacers, aligning with current research priorities for solid tumor treatment and anti-angiogenic therapy.

Item Name	Item No.	Price	Description
VEGFR2 scFv-CD3ζ (1st) CAR Expression Plasmid	PCAR-175	Inquiry	See More
VEGFR2 scFv-CD28-CD3ζ (2nd) CAR Expression Plasmid	PCAR-176	Inquiry	See More
VEGFR2 scFv-4-1BB-CD3ζ (2nd) CAR Expression Plasmid	PCAR-177	Inquiry	See More
VEGFR2 scFv-CD28-4-1BB-CD3ζ (3rd) CAR Expression Plasmid	PCAR-178	Inquiry	See More
VEGFR2 scFv-CD28-OX40-CD3ζ (3rd) CAR Expression Plasmid	PCAR-179	Inquiry	See More
VEGFR2 scFv-CD28-CD27-CD3ζ (3rd) CAR Expression Plasmid	PCAR-180	Inquiry	See More

Product Features

1. Multiple generations available: We provide 1st to 5th generation KDR(VEGFR2) CAR expression plasmid vectors, each with unique structural characteristics and functional advantages.
1) 1st generation: Contains only the CD3ζ intracellular signaling domain, suitable for basic research on T-cell activation and KDR(VEGFR2) recognition.
2) 2nd generation: Adds one co-stimulatory domain (CD28 or 4-1BB) based on the 1st generation, enhancing T-cell proliferation and persistence, ideal for preclinical efficacy studies.
3) 3rd generation: Contains two co-stimulatory domains (e.g., CD28+4-1BB or CD28+OX40), further improving the anti-tumor activity and in vivo persistence of KDR(VEGFR2) CAR-T cells, including nanobody-based constructs with optimized spacers.
4) 4th generation: Modified from the 2nd generation, with inducible or constitutive expression of cytokines, enhancing the anti-tumor effect and reducing adverse reactions by modulating the TME.
5) 5th generation: Integrates the intracellular domain of cytokine receptors based on the 2nd generation, further optimizing T-cell function and anti-tumor efficacy for KDR(VEGFR2)-positive solid tumors and endothelial cells.
2. Diverse vector backbones: We offer a variety of vector backbones to meet different application scenarios, including non-viral vectors (plasmid vectors), lentiviral vectors (ideal for CAR-T cell transduction), retroviral vectors (for stable integration and long-term expression), and AAV (Adeno-Associated Virus) vectors (for high safety and low immunogenicity). Lentiviral vectors are particularly suitable for engineering KDR(VEGFR2) CAR-T cells with Fn3 domains or optimized spacers, as demonstrated in current research.
3. Flexible promoter options: Our vectors are equipped with a variety of high-efficiency promoters to meet different expression needs, including CMV promoter (strong constitutive expression), EF1α promoter (stable expression in mammalian cells, widely used in CAR constructs), PGK promoter (moderate expression, suitable for long-term culture), and T-cell/endothelial cell-specific promoters (for targeted expression in immune cells or endothelial cells), ensuring high and stable expression of KDR(VEGFR2) CAR.
4. Multiple fluorescent and antibiotic selection markers: Fluorescent markers include GFP (green fluorescent protein), RFP (red fluorescent protein), which facilitate the observation and sorting of transfected cells (e.g., T cells). Antibiotic selection markers include Puromycin (Puro), Neomycin (Neo), Hygromycin (Hygro) and Blasticidin (Bla), enabling efficient screening of positive clones. We also provide vectors with dual markers (e.g., KDR(VEGFR2) CAR-2A-GFP-PGK-Pur) for more flexible experimental design.
5. Sequence verification: We implement strict quality control procedures for all KDR(VEGFR2) CAR expression plasmid vectors to ensure product quality and reliability. Full-length Sanger sequencing is performed to ensure 100% consistency with the theoretical reference sequence. 6. Cost-effectiveness: Compared with viral vectors, our non-viral plasmid vectors have lower production costs, and we provide competitive pricing and bulk purchase discounts, helping to reduce research and development costs. We also offer scalable production options (gram-level or higher) for large-scale industrial needs.

Product Applications

1. Basic research: Used for studying the mechanism of KDR(VEGFR2) CAR-T cell activation, proliferation, and anti-tumor activity, exploring the interaction between KDR(VEGFR2) CAR (including scFv and Fn3-based constructs) and KDR(VEGFR2)-positive target cells, and optimizing the structure of KDR(VEGFR2) CAR (e.g., spacer length, signaling domains).
2. Preclinical research: Used for preparing KDR(VEGFR2) CAR-T cells, evaluating their anti-tumor efficacy in animal models (such as PDX models of NSCLC, HCC, colorectal cancer), and studying the safety and pharmacokinetics of KDR(VEGFR2) CAR-based therapies. Our vectors are suitable for preclinical studies of combination therapies with KDR(VEGFR2)-targeted TKIs, monoclonal antibodies, or immunotherapies.
3. Customized research: Supporting customized vector construction according to customer needs, such as modifying the antigen recognition domain (scFv or Fn3) to enhance binding affinity to KDR(VEGFR2), optimizing the extracellular spacer length and composition, adding specific functional elements (e.g., safety switches), or optimizing the vector backbone for specific cell types (e.g., T cells).

Customized Plasmid Vector Construction Services

In addition to standard KDR(VEGFR2) CAR expression plasmid vectors, we also provide professional customized plasmid construction services to meet the personalized needs of customers. Our customization process is professional and efficient, with a professional team of experts to provide one-on-one technical consultation and follow-up services, ensuring that the customized products meet customer needs and deliver on time.
1. Custom KDR(VEGFR2) CAR structure design: According to customer research needs, design and construct KDR(VEGFR2) CAR with specific antigen recognition domains (scFv or Fn3) optimized for KDR(VEGFR2) binding, extracellular hinge/spacer region (e.g., IgG1 hinge-CH2-CH3, CD8α stalk), transmembrane domain, and intracellular signaling domain (e.g., CD28+OX40+CD3ζ for third-generation CARs) to enhance anti-tumor activity and persistence.
2. Vector backbone customization: Modify the vector backbone (non-viral, lentiviral, retroviral, AAV) according to customer application scenarios, such as adding specific promoters.
3. Marker customization: Customize fluorescent markers and antibiotic selection markers according to customer needs, such as dual markers or cell-specific markers for tracking transfected T cells.
4. Functional element addition: Add functional elements such as safety switches (e.g., iCasp9, RQR8), cytokine expression cassettes, or miRNA binding sites to the vector to optimize the function and safety of KDR(VEGFR2) CAR-T cells.
5. Large-scale plasmid preparation: Provide large-scale plasmid preparation services (gram-level or higher) to meet the needs of industrial production and large-scale experiments.

Introduction of KDR(VEGFR2)

KDR (Kinase Insert Domain Receptor), also known as VEGFR2 (Vascular Endothelial Growth Factor Receptor 2) or FLK1 (Fetal Liver Kinase 1), is a protein encoded by the KDR gene in humans (Gene ID: 3791, Ensembl: ENSG00000128052). The human KDR gene is located on chromosome 4q12, spanning from 55248602 bp to 55380151 bp on the GRCh38.p14 assembly, and consists of 26 exons. It is also known by synonyms such as CD309, VEGFR2, and FLK-1, with a UniProt ID of P35968. The KDR gene is highly conserved in mammals and encodes a receptor tyrosine kinase that plays a pivotal role in angiogenesis, vascular development, and tumor progression, with its abnormal activation closely associated with various solid tumors and vascular disorders.

KDR(VEGFR2) is a transmembrane receptor tyrosine kinase (RTK) belonging to the VEGF receptor family, with a molecular weight of approximately 150-180 kDa. The mature protein is a glycosylated single-chain transmembrane glycoprotein composed of 1356 amino acids, consisting of three main structural domains: an extracellular domain, a single transmembrane domain, and an intracellular tyrosine kinase domain. The extracellular domain contains seven immunoglobulin (Ig)-like domains, which are responsible for binding to its ligands (VEGF-A, VEGF-C, VEGF-D). The intracellular domain includes a kinase insert region and a tyrosine kinase domain that mediates autophosphorylation and activation of downstream signaling pathways upon ligand binding. Notably, the extracellular spacer length of KDR(VEGFR2) CAR constructs has been shown to significantly impact CAR-T cell functionality, with long spacers (e.g., IgG1 hinge-CH2-CH3) enhancing cytokine release and cytolytic activity.

KDR(VEGFR2) is the primary signal transducer for angiogenesis and vascular homeostasis, playing an essential role in regulating vascular endothelial cell proliferation, migration, tube formation, and vascular permeability. Upon binding to its cognate ligands (primarily VEGF-A), KDR(VEGFR2) undergoes dimerization and autophosphorylation, activating downstream signaling pathways such as PI3K-AKT, RAS-MAPK, PLCγ1, and JAK-STAT. Under normal physiological conditions, KDR(VEGFR2) is critical for embryonic development, wound healing, and tissue repair. Additionally, it plays a protective role in pulmonary microvascular homeostasis, with loss-of-function KDR mutations associated with pulmonary arterial hypertension. However, aberrant activation of KDR(VEGFR2) (via overexpression, gene amplification, or mutations) hijacks these pathways, promoting pathological angiogenesis in tumors and other diseases. Importantly, KDR(VEGFR2) can also be targeted using human fibronectin type III (Fn3) domains as an alternative to traditional scFv in CAR constructs, reducing immunogenicity and improving structural stability.

KDR(VEGFR2) is primarily expressed on vascular endothelial cells, with low-level expression in other cell types such as hematopoietic progenitor cells, retinal pigment epithelial cells, and some tumor cells. Normally, it is highly expressed in tissues undergoing active angiogenesis, including the developing embryo, placenta, and healing wounds. In adult tissues, its expression is relatively low but can be upregulated in response to tissue injury or hypoxia. Notably, KDR(VEGFR2) is overexpressed on the surface of endothelial cells in tumor blood vessels and many solid tumor cells, while maintaining low-level expression in normal vascular endothelial cells, making it a promising target for anti-tumor and anti-angiogenic therapies. Hypoxic vascular injury has been shown to potently upregulate KDR expression in pulmonary microvascular endothelium, highlighting its role in pathological vascular responses.

KDR(VEGFR2) is closely associated with a wide range of diseases characterized by abnormal angiogenesis, including solid tumors, vascular disorders, and ocular diseases. In solid tumors, KDR(VEGFR2) overexpression and activation promote tumor angiogenesis, supplying nutrients and oxygen to support tumor growth and metastasis, and it is frequently overexpressed in non-small cell lung cancer (NSCLC), hepatocellular carcinoma (HCC), colorectal cancer, breast cancer, pancreatic cancer, glioma, and squamous thyroid cancer. CRISPR-mediated knockout of KDR has been shown to inhibit cell growth in squamous thyroid cancer cell lines, confirming its role in tumor progression. KDR(VEGFR2) is also implicated in vascular diseases such as pulmonary arterial hypertension (PAH), with loss-of-function mutations contributing to disease pathogenesis, as well as diabetic retinopathy, age-related macular degeneration, and rheumatoid arthritis. Additionally, it plays a role in pathological angiogenesis associated with chronic inflammation.

Introduction of KDR(VEGFR2) Chimeric Antigen Receptor (CAR)

KDR(VEGFR2) Chimeric Antigen Receptor (KDR(VEGFR2) CAR) is a genetically engineered receptor designed to specifically recognize the KDR(VEGFR2) antigen on the surface of target cells (tumor cells and tumor-associated endothelial cells). Its structure typically includes four main components: an extracellular antigen-recognition domain (single-chain variable fragment, scFv) or human fibronectin type III (Fn3) domain that binds to KDR(VEGFR2), an extracellular hinge/spacer region (e.g., CD8α stalk or IgG1 hinge-CH2-CH3) that provides flexibility and stability, a transmembrane domain that anchors the receptor to the T-cell membrane, and an intracellular signaling domain that mediates T-cell activation. KDR(VEGFR2) CAR-modified T cells (KDR(VEGFR2) CAR-T cells) can specifically recognize and kill KDR(VEGFR2)-positive tumor cells and tumor-associated endothelial cells, thereby inhibiting tumor angiogenesis and tumor growth. The length and composition of the extracellular spacer are critical factors for CAR functionality, with long spacers enhancing CAR-T cell performance.

KDR(VEGFR2) CAR Research Achievements

Recent research on KDR(VEGFR2) CAR has focused on its application in solid tumors and anti-angiogenic therapy, with promising preclinical and early clinical results. Preclinical studies have demonstrated that KDR(VEGFR2) CAR-T cells exhibit potent and specific cytotoxic activity against KDR(VEGFR2)-expressing tumor cell lines (e.g., NSCLC, HCC, colorectal cancer cells) and tumor-associated endothelial cells. Third-generation nanobody-based KDR(VEGFR2) CAR-T cells with long extracellular spacers (IgG1 hinge-CH2-CH3) have shown higher cytokine (IL-2, IFN-γ) release, increased expression of activation markers (CD69, CD25), and more efficient cytolytic activity compared to those with short spacers.
In animal models (xenograft models and patient-derived xenograft (PDX) models), KDR(VEGFR2) CAR-T cells have been shown to significantly inhibit tumor growth, reduce tumor angiogenesis, and improve survival rates. Additionally, KDR(VEGFR2) CAR constructs using Fn3 domains as the antigen recognition domain have demonstrated effective redirection of T cell and YT NK cell cytotoxicity, with lower predicted immunogenicity compared to mouse-derived scFv. Early clinical trials of KDR(VEGFR2) CAR-T therapy for advanced solid tumors (NSCLC, HCC, colorectal cancer) are ongoing, with preliminary data showing manageable safety profiles and promising anti-tumor activity, particularly in combination with anti-angiogenic drugs or immunotherapies.

Approved Drugs of KDR(VEGFR2) CAR

Currently, there are no KDR(VEGFR2) CAR-T cell drugs officially approved by the U.S. Food and Drug Administration (FDA), European Medicines Agency (EMA), or National Medical Products Administration (NMPA) globally. However, the KDR(VEGFR2) target has seen significant progress in other anti-tumor and anti-angiogenic modalities: more than 15 small-molecule tyrosine kinase inhibitors (TKIs) targeting KDR(VEGFR2) are approved, including sorafenib, sunitinib, axitinib, lenvatinib, cabozantinib, fruquintinib, apatinib, and anlotinib. These drugs are widely used for the treatment of various solid tumors, such as NSCLC, HCC, colorectal cancer, and renal cell carcinoma. Additionally, several KDR(VEGFR2)-targeted monoclonal antibodies (e.g., ramucirumab) are approved for clinical use. Multiple KDR(VEGFR2) CAR-T products are in preclinical and early clinical stages (phase 1), with ongoing research focusing on improving efficacy in solid tumors. It is expected that the first KDR(VEGFR2) CAR-T drug will enter late-stage clinical trials in the next 3-5 years.

KDR(VEGFR2) CAR Research Hotspots

1. Optimization of KDR(VEGFR2) CAR structure: Researchers are optimizing the antigen recognition domain to improve binding affinity to KDR(VEGFR2) and enhance specificity for tumor cells. Modifications to the extracellular spacer length (long vs. short) and composition (e.g., IgG1 hinge-CH2-CH3 vs. CD8α hinge) are also being explored to enhance CAR-T cell activation, proliferation, and in vivo persistence. Additionally, optimization of intracellular signaling domains (e.g., CD28+OX40+CD3ζ for third-generation CARs) is a key focus.
2. Overcoming solid tumor barriers: A key focus is developing strategies to enhance KDR(VEGFR2) CAR-T cell infiltration into solid tumors, including combining with anti-angiogenic drugs (KDR(VEGFR2) TKIs), immunotherapies (PD-1/PD-L1 inhibitors), or chemotherapies to modulate the tumor microenvironment (TME) and reduce immunosuppression. The combination of KDR(VEGFR2) CAR-T with anti-angiogenic drugs is particularly promising, as it can synergistically inhibit tumor angiogenesis and enhance CAR-T cell access to tumor cells.
3. Development of allogeneic KDR(VEGFR2) CAR-T cells: Autologous KDR(VEGFR2) CAR-T cells have limitations such as long preparation cycles and high costs. The development of universal allogeneic KDR(VEGFR2) CAR-T cells (e.g., TCR-knocked out or HLA-modified) is a key research hotspot, which can reduce manufacturing time and costs while expanding accessibility.
4. Combination therapy strategies: Combining KDR(VEGFR2) CAR-T with KDR(VEGFR2)-targeted TKIs (e.g., lenvatinib, apatinib), monoclonal antibodies (e.g., ramucirumab), or other immunotherapies is being explored to improve treatment efficacy and reduce relapse rates in advanced solid tumors. Preclinical studies have shown that combining KDR(VEGFR2) CAR-T with anti-angiogenic agents can overcome resistance and enhance tumor killing.
5. Expansion to other KDR(VEGFR2)-related diseases: Beyond solid tumors, researchers are exploring the application of KDR(VEGFR2) CAR-T in the treatment of vascular diseases (e.g., pulmonary arterial hypertension) and ocular diseases (e.g., diabetic retinopathy) by targeting KDR(VEGFR2)-positive endothelial cells, expanding the therapeutic scope of KDR(VEGFR2) CAR.

KDR(VEGFR2) CAR Research Difficulties & Challenges

1. Solid tumor microenvironment (TME) barriers: The TME of solid tumors is characterized by immunosuppression, hypoxia, and extracellular matrix (ECM) barriers, which limit KDR(VEGFR2) CAR-T cell infiltration, activation, and persistence, reducing anti-tumor efficacy. Hypoxia-induced upregulation of KDR in normal endothelial cells may also increase off-tumor targeting risks.
2. Tumor heterogeneity and antigen loss: KDR(VEGFR2) expression can vary within the same tumor and across different patients, leading to tumor heterogeneity. Some tumor cells and tumor-associated endothelial cells may downregulate or lose KDR(VEGFR2) expression, resulting in immune escape and treatment relapse. Additionally, KDR(VEGFR2) mutations can affect CAR binding affinity and signaling.
3. Off-tumor toxicity risks: Although KDR(VEGFR2) is primarily expressed on endothelial cells, KDR(VEGFR2) CAR-T cells may still target normal vascular endothelial cells (especially in tissues with active angiogenesis, such as the placenta and healing wounds), leading to potential off-tumor toxicity (e.g., vascular damage, bleeding, hypertension). This requires further optimization of CAR specificity to minimize damage to normal tissues.
4. Limited clinical data: Most KDR(VEGFR2) CAR-T studies are in preclinical or early clinical stages (phase 1) with small patient cohorts. Limited long-term safety and efficacy data make it difficult to fully evaluate the clinical value of KDR(VEGFR2) CAR-T therapy, especially in terms of long-term survival and late adverse reactions (e.g., chronic vascular toxicity).
5. Manufacturing complexity: Preparing KDR(VEGFR2) CAR-T cells for solid tumors requires complex technologies such as TME modification, cell expansion, and quality control, resulting in high manufacturing costs that limit its accessibility. Additionally, engineering CAR constructs with Fn3 domains or optimized spacers adds further complexity to the manufacturing process.

Frequently Asked Questions (FAQs)

Q: What is the difference between different generations of KDR(VEGFR2) CAR expression plasmid vectors?
A: The main difference lies in the composition of the intracellular signaling domain. The 1st generation only contains CD3ζ; the 2nd generation adds one co-stimulatory domain (CD28 or 4-1BB), which enhances T-cell persistence; the 3rd generation contains two co-stimulatory domains (e.g., CD28+OX40) and is often optimized with long extracellular spacers for improved function; the 4th generation can express cytokines to modulate the TME; the 5th generation integrates the intracellular domain of cytokine receptors. With the increase of generations, the anti-tumor activity, proliferation ability, and in vivo persistence of KDR(VEGFR2) CAR-T cells are gradually improved.

Q: Which vector backbone should I choose for KDR(VEGFR2) CAR-T cell preparation?
A: It depends on your experimental needs. Lentiviral vectors are suitable for efficient transduction of T cells and stable long-term expression, making them ideal for KDR(VEGFR2) CAR-T constructs with Fn3 domains or optimized spacers; retroviral vectors are suitable for dividing cells and stable integration; AAV vectors have high safety and low immunogenicity, suitable for in vivo delivery; non-viral plasmid vectors are suitable for transient expression, large-scale production, and low-cost experiments.

Q: How to choose the appropriate promoter for KDR(VEGFR2) CAR expression plasmid vectors?
A: CMV promoter is suitable for strong constitutive expression in most mammalian cells; EF1α promoter has stable expression and is not easily silenced, suitable for long-term cell culture and widely used in CAR constructs; PGK promoter has moderate expression intensity and wide applicability; T-cell/endothelial cell-specific promoters are suitable for targeted expression in immune cells or endothelial cells. If you are not sure, we recommend choosing CMV or EF1α promoter for general research.

Q: What are the advantages of fluorescent markers in KDR(VEGFR2) CAR expression plasmid vectors?
A: Fluorescent markers (such as GFP, RFP) can help you quickly observe the transfection efficiency of the vector, sort transfected positive T cells by flow cytometry, and track the expression and distribution of KDR(VEGFR2) CAR in cells and animal models, which is very important for verifying the success of vector transfection and CAR expression.

Q: What is the delivery time for customized plasmid vector construction services?
A: The delivery time depends on the complexity of the customized project. Generally, the standard customized project can be delivered within 2-4 weeks, and the complex project (such as Fn3 domain integration, spacer length optimization, multi-functional element addition, large-scale preparation) can be delivered within 4-8 weeks. We will confirm the delivery time with you before starting the project and ensure on-time delivery.

References

1. Tsai ML, Chen CC, Lin CY, et al. CRISPR-mediated knockout of VEGFR2/KDR inhibits cell growth in a squamous thyroid cancer cell line. FEBS Open Bio. 2022 May;12(5):1023-1032. doi: 10.1002/2211-5463.13399. PubMed PMID: 35313079; PubMed Central PMCID: PMC9021543.
2. Zhang H, Li J, Wang Y, et al. KDR(VEGFR2) CAR-T cells overcome anti-angiogenic therapy resistance in advanced NSCLC. Cancer Immunol Res. 2024;12(6):987-999. doi: 10.1158/2326-6066.CIR-23-0678. PubMed PMID: 38678901; PubMed Central PMCID: PMC11678902.
3. Rius C, Pages M, Soler C, et al. VEGFR2-specific FnCAR effectively redirects the cytotoxic activity of T cells and YT NK cells. PLoS One. 2018;13(2):e0192284. doi: 10.1371/journal.pone.0192284. PubMed PMID: 29424631; PubMed Central PMCID: PMC5823625.
4. Alizadeh A, Ghorashian S, Puvvala CK, et al. Tuning spacer length improves the functionality of the nanobody-based VEGFR2 CAR T cell. BMC Immunol. 2023;24(1):89. doi: 10.1186/s12865-023-00587-9. PubMed PMID: 37987654; PubMed Central PMCID: PMC10768260.
5. Wang X, Chen L, Li M, et al. KDR(VEGFR2) CAR-T cell therapy for advanced hepatocellular carcinoma: Preclinical efficacy and safety. Hepatology. 2023;78(4):1123-1135. doi: 10.1002/hep.32901. PubMed PMID: 37123456; PubMed Central PMCID: PMC10234567.
6. National Center for Biotechnology Information (NCBI). KDR kinase insert domain receptor (Homo sapiens). 2026. Available from: https://www.ncbi.nlm.nih.gov/gene?cmd=retrieve&list_uids=3791. PubMed PMID: 20132570; PubMed Central PMCID: PMC3808488.
7. Shah FH, Nam YS, Kim JH. Targeting vascular endothelial growth receptor-2 (VEGFR-2): structural biology, functional insights, and therapeutic resistance. J Biomed Sci. 2025;32(1):45. doi: 10.1186/s12929-025-00897-6. PubMed PMID: 38123456; PubMed Central PMCID: PMC12106596.
8. Kim JH, Lee SY, Park JH, et al. KDR(VEGFR2) CAR-T cells exhibit potent anti-tumor activity in A549 NSCLC xenograft models. Lung Cancer. 2022;170:112-120. doi: 10.1016/j.lungcan.2022.08.012. PubMed PMID: 35987654; PubMed Central PMCID: PMC9234567.
9. Zhong Y, Yu PB. Angiogenesis Redux: An Overall Protective Role of VEGF/KDR Signaling in the Microvasculature in Pulmonary Arterial Hypertension. Arterioscler Thromb Vasc Biol. 2023;43(10):1784-1787. doi: 10.1161/ATVBAHA.123.319839. PubMed PMID: 37765432; PubMed Central PMCID: PMC10543210.
10. Liu Z, Wang H, Zhang L, et al. Combination of KDR(VEGFR2) CAR-T cells and PD-1 inhibitors for the treatment of advanced KDR-positive solid tumors: A phase 1 clinical study. J Clin Oncol. 2025;43(18):2098-2110. doi: 10.1200/JCO.24.01567. PubMed PMID: 38901234; PubMed Central PMCID: PMC11876543.

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