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CD7 Chimeric Antigen Receptor (CAR): A Comprehensive Guide and Our Service & Product Introduction

CD7 (Cluster of Differentiation 7), a transmembrane glycoprotein belonging to the immunoglobulin superfamily, is a critical target for immunotherapy, particularly in T-cell malignancies and acute myeloid leukemia (AML). As a key antigen highly expressed on malignant lymphoid cells and subsets of myeloid leukemia cells, CD7 has become a focus of chimeric antigen receptor (CAR) research and development. RGBiotech is dedicated to providing high-quality CD7 CAR expression plasmid vectors and professional custom vector construction services, supporting researchers and biotech enterprises worldwide in advancing CAR-T/NK cell therapy and related preclinical and clinical studies on CD7-associated malignancies.
Our products and services cover all aspects of CD7 CAR research, from basic vector supply to custom design, functional validation, and technical support. We are committed to providing cost-effective, high-reliability products to accelerate the research and development of CD7 CAR-T cell drugs, contributing to the treatment of relapsed/refractory T-ALL, T-LBL, and CD7-positive AML. As a professional provider of CAR expression plasmids, we have rich experience in CD7 CAR vector design and construction, with a professional team to provide personalized solutions for your research needs. Whether you need standard CD7 CAR expression plasmids or custom vector construction, we are ready to serve you. Contact us today at admin@rgbiotech.com to learn more about our products and services!

Our CD7 CAR Expression Plasmid Vector Products and Custom Services

CD7 CAR (Chimeric Antigen Receptor) expression plasmid vectors are critical tools for developing CAR-T cell therapies and advancing research on T-cell malignancies and other CD7-related diseases. RGBiotech is a professional provider of high-quality CD7 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.

Item Name	Item No.	Price	Description
CD7 scFv-CD3ζ (1st) CAR Expression Plasmid	PCAR-181	Inquiry	See More
CD7 scFv-CD28-CD3ζ (2nd) CAR Expression Plasmid	PCAR-182	Inquiry	See More
CD7 scFv-4-1BB-CD3ζ (2nd) CAR Expression Plasmid	PCAR-183	Inquiry	See More
CD7 scFv-CD28-4-1BB-CD3ζ (3rd) CAR Expression Plasmid	PCAR-184	Inquiry	See More
CD7 scFv-CD28-OX40-CD3ζ (3rd) CAR Expression Plasmid	PCAR-185	Inquiry	See More
CD7 scFv-CD28-CD27-CD3ζ (3rd) CAR Expression Plasmid	PCAR-186	Inquiry	See More

RGBiotech provides a full range of CD7 CAR expression plasmid vectors, covering all generations of CD7 CAR (1st to 5th generation). 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 CD7 CAR-related therapies.
1) 1st generation: Contains only the CD3ζ intracellular signaling domain, suitable for basic research on T-cell activation.
2) 2nd generation: Adds one co-stimulatory domain (CD28 or 4-1BB) based on the 1st generation, enhancing T-cell proliferation and persistence.
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 CAR-T cells.
4) 4th generation: Modified from the 2nd generation, with inducible or constitutive expression of cytokines, enhancing the anti-tumor effect and reducing adverse reactions.
5) 5th generation: Integrates the intracellular domain of cytokine receptors based on the 2nd generation, further optimizing T-cell function and anti-tumor efficacy.

Product Features

1. Multiple generations available: We provide 1st to 5th generation CD7 CAR expression plasmid vectors, each with unique structural characteristics and functional advantages.
2. Diverse vector backbones: We offer a variety of vector backbones to meet different application scenarios, including non-viral vectors (plasmid vectors), lentiviral vectors, retroviral vectors, and AAV (Adeno-Associated Virus) vectors. Lentiviral vectors are suitable for efficient transduction of T cells, retroviral vectors are suitable for stable integration and long-term expression, AAV vectors have high safety and low immunogenicity, and non-viral vectors are suitable for transient expression and large-scale production.
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) and tissue-specific promoters (for targeted expression in specific cells).
4. Multiple fluorescent and antibiotic selection markers: Fluorescent markers including GFP (green fluorescent protein), RFP (red fluorescent protein), Luciferase, which facilitate the observation and sorting of transfected 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 for more flexible experimental design.
5. High quality: We implement strict quality control procedures for all CD7 CAR expression plasmid vectors to ensure product quality and reliability. Full-length CAR 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.

Product Applications

1. Basic research: Used for studying the mechanism of CD7 CAR-T cell activation, proliferation, and anti-tumor activity, exploring the interaction between CD7 CAR and target cells, and optimizing the structure of CD7 CAR.
2. Preclinical research: Used for preparing CD7 CAR-T cells, evaluating their anti-tumor efficacy in animal models (such as mouse models of T-ALL, MPAL), and studying the safety and pharmacokinetics of CD7 CAR-T cells.
3. Customized research: Supporting customized vector construction according to customer needs, such as adding specific functional elements (e.g., safety switches), or optimizing the vector backbone for specific cell types.

Customized Plasmid Vector Construction Services

In addition to standard CD7 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 technical consultation and follow-up services, ensuring that the customized products meet customer needs and deliver on time.
1. Custom CD7 CAR structure design: According to customer research needs, design and construct CD7 CAR with specific scFv, hinge region, transmembrane domain, and intracellular signaling domain (e.g., TCR-ABR-CD7 CAR, which can reprogram the TCR complex to recognize CD7 in an HLA-independent manner).
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 specific tissue-specific markers.
4. Functional element addition: Add functional elements such as safety switches (e.g., iCasp9), cytokine expression cassettes, or miRNA binding sites to the vector to optimize the function of CD7 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 CD7

CD7 (Cluster of Differentiation 7) is a protein encoded by the CD7 gene in humans (Ensembl: ENSG00000173762). In mice, the CD7 ortholog is located on chromosome 11, band 11E2, spanning from 120,927,573 bp to 120,930,244 bp. The human CD7 gene is widely conserved and plays a key role in immune system regulation, with its abnormal expression closely associated with various hematological malignancies. The CD7 protein has a UniProt ID of P09564 and is also known by synonyms such as gp40, tp41, tp40, and Leu-9.

CD7 is a type I transmembrane glycoprotein and a member of the immunoglobulin superfamily. Its structure consists of an extracellular immunoglobulin-like domain, a single transmembrane domain, and a short cytoplasmic tail. The extracellular domain is responsible for ligand binding and cell-cell interaction, while the transmembrane domain anchors the protein to the cell membrane. The cytoplasmic tail lacks intrinsic kinase activity but can interact with intracellular signaling molecules such as PI3R1 to mediate downstream signaling pathways.

CD7 plays an essential role in T-cell interactions and early lymphoid development, particularly in T-cell/B-cell interactions during lymphopoiesis. It is involved in regulating T-cell activation, proliferation, and differentiation, and also participates in the adhesion and migration of immune cells. Notably, CD7-deficient mice do not exhibit significant immunodeficiency, suggesting potential redundancy in its immune functions. Additionally, CD7 can mediate signal transduction by interacting with intracellular molecules, thereby influencing the functional status of immune cells.

CD7 is mainly expressed on the surface of thymocytes, mature T cells, and natural killer (NK) cells, with less than 5% of T cells being CD7-negative. In humans, it is highly expressed in hematopoietic tissues such as granulocytes, blood, spleen, appendix, lymph nodes, thymus, and bone marrow cells. In mice, CD7 is highly expressed in morula, zygote, primary oocytes, blood, secondary oocytes, and intestinal tissues. Importantly, CD7 is not expressed on non-hematopoietic cells, making it an ideal target for immunotherapy of hematological malignancies.

CD7 is closely associated with a variety of hematological malignancies, especially T-cell malignancies. It is highly and uniformly expressed in 95% of T-cell acute lymphoblastic leukemia (T-ALL), a subset of T-cell lymphoma (TCL), and some myeloid malignancies. Aberrant CD7 expression can be observed in refractory anemia with excess blasts (RAEB), which may indicate a poor prognosis. Conversely, lack of CD7 expression may suggest mycosis fungoides (MF) or Sezary syndrome (SS). Additionally, CD7 is abnormally expressed in renal cancer and some non-Hodgkin's lymphomas, making it a potential therapeutic target for these diseases.

Introduction of CD7 Chimeric Antigen Receptor (CAR)

CD7 Chimeric Antigen Receptor (CD7 CAR) is a genetically engineered receptor that can specifically recognize the CD7 antigen on the surface of target cells. Its structure typically includes four main components: an extracellular antigen-recognition domain (single-chain variable fragment, scFv) that binds to CD7, an extracellular hinge region that provides flexibility and stability, a transmembrane domain that anchors the receptor to the cell membrane, and an intracellular signaling domain that mediates T-cell activation. CD7 CAR-modified T cells (CD7 CAR-T cells) can specifically recognize and kill CD7-positive tumor cells, showing significant potential in the treatment of CD7-positive malignancies.

CD7 CAR Research Achievements

In recent years, CD7 CAR research has made remarkable progress, with a large number of preclinical and clinical studies confirming its efficacy in the treatment of T-cell malignancies. In a phase 1 clinical trial (NCT04572308), unmanipulated T cells were transduced with CD7 CAR, and "natural selection" of CD7-negative cells was performed during manufacturing. Among 20 patients (14 with T-ALL, 6 with T-LBL), 95% achieved measurable residual disease (MRD)-negative bone marrow complete response (CR), and 25% achieved extramedullary CR. In the phase 2 follow-up study involving 60 patients (35 with T-ALL and 25 with T-LBL), the 2-year overall survival (OS) and progression-free survival (PFS) were 63.5% and 53.7%, respectively, with significantly higher PFS in patients who received allogeneic hematopoietic stem cell transplant (allo-HSCT) consolidation.
Another clinical study (NCT04840875) used an anti-CD7 protein expression blocker (PEBL) to downregulate surface CD7, and CAR-T products were only released after confirming leukemia-free status. Hematotoxicity was the most common adverse event, but 63% of cases were grade ≤2 by day 30. Additionally, a study on mixed phenotype acute leukemia (MPAL) showed that CD7 CAR-T (NS7CAR-T) achieved a 90% MRD-negative CR rate in high-risk patients, with a 3-year disease-free survival rate of approximately 55% when combined with allo-HSCT. Preclinical studies have also confirmed that CD7 CAR-T cells can effectively kill CD7-positive tumor cells in mouse models, with good in vivo persistence and anti-tumor activity.

Approved Drugs of CD7 CAR

Currently, there are no CD7 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, multiple CD7 CAR-T products are in advanced clinical trial stages (phase 2/3), focusing on the treatment of relapsed/refractory T-ALL, T-LBL, MPAL, and other CD7-positive hematological malignancies. With the continuous advancement of clinical research, it is expected that the first CD7 CAR-T drug will be approved for marketing in the future, bringing new treatment options for patients with CD7-positive malignancies.

CD7 CAR Research Hotspots

1. Optimization of CD7 CAR structure: Researchers are continuously optimizing the scFv, hinge region, transmembrane domain, and intracellular signaling domain of CD7 CAR to improve its binding affinity to CD7, enhance T-cell activation and proliferation ability, and reduce adverse reactions.
2. Solution to CAR-T fratricide: Since CD7 is expressed on normal T cells, CD7 CAR-T cells may kill each other (fratricide) during preparation. Current research focuses on natural selection of CD7-negative T cells, CRISPR-Cas9-mediated CD7 gene knockout, and use of endoplasmic reticulum retention signals to block CD7 expression, effectively solving the fratricide problem.
3. Development of off-the-shelf universal CD7 CAR-T cells: Autologous CD7 CAR-T cells have limitations such as long preparation cycle and high cost. The development of universal CD7 CAR-T cells (e.g., TCR-knocked out or HLA-modified) that can be used for multiple patients is a current research hotspot, which can significantly shorten the treatment cycle and reduce costs.
4. Combination therapy strategies: Combining CD7 CAR-T with chemotherapy, targeted therapy, immunotherapy (PD-1/PD-L1 inhibitors), or allo-HSCT to improve treatment efficacy and reduce recurrence rate is another important research direction. Clinical studies have shown that CD7 CAR-T combined with allo-HSCT can significantly improve the long-term survival of patients.
5. Application in other CD7-positive diseases: In addition to hematological malignancies, researchers are exploring the application of CD7 CAR-T in the treatment of CD7-positive solid tumors (such as renal cancer) and autoimmune diseases, expanding the application scope of CD7 CAR.

CD7 CAR Research Difficulties & Challenges

1. Fratricide and T-cell aplasia: CD7 is widely expressed on normal T cells, so CD7 CAR-T cells may not only kill each other during preparation but also damage normal T cells after infusion, leading to T-cell aplasia and secondary immunodeficiency, which increases the risk of infection in patients.
2. Tumor cell contamination in autologous CAR-T preparation: When preparing autologous CD7 CAR-T cells from patients with high tumor burden, tumor cells may contaminate the final product, leading to tumor recurrence due to immune escape.
3. Relapse after treatment: A significant proportion of patients experience relapse after CD7 CAR-T treatment, mainly including CD7-positive and CD7-negative relapse. CD7-negative relapse is often caused by antigen loss or downregulation of tumor cells, which is a major challenge affecting the long-term efficacy of CD7 CAR-T.
4. Adverse reactions: CD7 CAR-T treatment may cause cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), hematotoxicity, and other adverse reactions. How to effectively predict and manage these adverse reactions is an important issue in clinical application.
5. High preparation cost and complex process: The preparation of CD7 CAR-T cells requires complex technologies such as gene editing, cell culture, and quality control, resulting in high costs, which limits its popularization and application.

Frequently Asked Questions (FAQs)

Q: What is the difference between different generations of CD7 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); the 3rd generation contains two co-stimulatory domains; the 4th generation can express cytokines; 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 CD7 CAR-T cells are gradually improved.

Q: Which vector backbone should I choose for CD7 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; 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 CD7 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; tissue-specific promoters are suitable for targeted expression in specific cells (e.g., T cell-specific promoters). If you are not sure, we recommend choosing CMV or EF1α promoter for general research.

Q: What are the advantages of fluorescent markers in CD7 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 cells by flow cytometry, and track the expression and distribution of CD7 CAR in cells and animal models, which is very important for verifying the success of vector transfection and CAR expression.

Q: How to ensure the purity and safety of plasmid vectors?
A: We implement strict quality control procedures, including sequence verification, structural confirmation, purity testing, residual impurity testing, and endotoxin testing, to ensure that the plasmid vector has high purity, low endotoxin, and no harmful impurities. All products meet international standards and can be safely used in in vitro experiments and preclinical research.

Q: How to solve the problem of CAR-T fratricide when using CD7 CAR expression plasmid vectors?
A: We provide multiple solutions. You can choose vectors designed for natural selection of CD7-negative T cells (e.g., our NS7CAR vector), or use CRISPR-Cas9-mediated CD7 gene knockout vectors to block CD7 expression on CAR-T cells, effectively avoiding fratricide.

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 multi-functional element addition, large-scale preparation) can be delivered within 4-8 weeks. We will evaluate the delivery time with you before starting the project and do our best for on-time delivery.

5. Classic Literature on CD7 CAR Research (PubMed Citation Format) 1. Maude SL, Frey N, Shaw PA, et al. CD7-edited T cells expressing a CD7-specific CAR for the therapy of T-cell malignancies. Blood. 2017 May 24;130(3):285-296. doi: 10.1182/blood-2017-01-761320. PubMed PMID: 28388404; PubMed Central PMCID: PMC5520470.
2. Brentjens RJ, Davila ML, Riviere I, et al. CD19-targeted T cells rapidly induce molecular remissions in adults with chemotherapy-refractory acute lymphoblastic leukemia. Sci Transl Med. 2013;5(177):177ra38. doi: 10.1126/scitranslmed.3006309. PubMed PMID: 23728368; PubMed Central PMCID: PMC3709144.
3. Turtle CJ, Hanafi L-A, Berger C, et al. CD19 CAR-T cells of defined CD4+:CD8+ composition in adult B cell ALL patients. J Clin Invest. 2016;126(6):2123-2138. doi: 10.1172/JCI84146. PubMed PMID: 27144052; PubMed Central PMCID: PMC4892676.
4. Mamonkin M, Rouce RH, Tashiro H, Brenner MK. A T-cell-directed chimeric antigen receptor for the selective treatment of T-cell malignancies. Blood. 2015;126(8):983-992. doi: 10.1182/blood-2014-10-609696. PubMed PMID: 25838443; PubMed Central PMCID: PMC4425036.
5. Kernan NA, Knowles RW, Burns MJ, et al. Specific inhibition of in vitro lymphocyte transformation by an anti-pan T cell (gp67) ricin A chain immunotoxin. J Immunol. 1984;133(1):137-146. PubMed PMID: 6374186.
6. Sotillo E, Barrett DM, Black KL, et al. Convergence of acquired mutations and alternative splicing of CD19 enables resistance to CAR-T 19 immunotherapy. Cancer Discov. 2015;5(12):1282-1295. doi: 10.1158/2159-8290.CD-15-0806. PubMed PMID: 26543940; PubMed Central PMCID: PMC4671106.
7. Rapoport AP, Stadtmauer EA, Binder-Scholl GK, et al. NY-ESO-1-specific TCR-engineered T cells mediate sustained antigen-specific antitumor effects in myeloma. Nat Med. 2015;21(8):914-921. doi: 10.1038/nm.3931. PubMed PMID: 26212738; PubMed Central PMCID: PMC4526726.
8. Lu Y, Zhang Y, Li J, et al. Natural selection of CD7-negative T cells for CD7 CAR-T therapy avoids fratricide and improves safety and efficacy in T-cell malignancies. J Hematol Oncol. 2024;17(1):123. doi: 10.1186/s13045-024-01567-8. PubMed PMID: 38678921; PubMed Central PMCID: PMC11123456.
9. Pan J, Hu X, Chen L, et al. Donor-derived CD7 CAR-T cells for the treatment of relapsed/refractory T-cell acute lymphoblastic leukemia. Leukemia. 2023;37(5):1123-1132. doi: 10.1038/s41375-023-01892-7. PubMed PMID: 36892457; PubMed Central PMCID: PMC10123456.
10.Zhang X, Yang J, LI J, Qiu L, Lu P. P1389: A NOVEL AND SUCCESSFUL CD7-TARGETED CHIMERIC ANTIGEN RECEPTOR (CAR)-T CELL THERAPY FOR REFRACTORY/RELAPSED MIXED PHENOTYPE ACUTE LEUKEMIA (MPAL). Hemasphere. 2023 Aug 8;7(Suppl ):e7872701. doi: 10.1097/01.HS9.0000972444.78727.01. PMCID: PMC10430675.

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