CD24 Chimeric Antigen Receptor (CAR): A Comprehensive Guide and Our Service & Product Introduction

CD24 has emerged as a high-value therapeutic target in immuno-oncology, autoimmune disorders, and inflammatory diseases, owing to its unique molecular structure, broad disease-related expression profile, and critical role in immune regulation and tumor progression. CD24-targeted Chimeric Antigen Receptor (CAR) therapy has rapidly become a research hotspot in cellular immunotherapy, with growing preclinical and clinical evidence validating its therapeutic potential. For product inquiries, custom service quotes, or technical support regarding CD24 CAR plasmid vectors, please reach out to us at admin@rgbiotech.com. We offer tailored solutions for academic laboratories, biotech startups, and pharmaceutical companies.

Our CD24 CAR Expression Plasmid Vector Products and Custom Services

CD24 represents a versatile and promising therapeutic target with unmatched potential in both oncology and autoimmune disease treatment. CD24 CAR therapy is poised to address unmet clinical needs for hard-to-treat solid tumors and refractory autoimmune disorders.

To support global CD24 CAR research, RGBiotech provides a comprehensive portfolio of CD24 CAR expression plasmid vectors and flexible custom construction services, covering all CAR generations, multiple vector backbones, and versatile functional elements. Our products are designed for high expression efficiency, robust stability, and compliance with preclinical research standards, eliminating the time and cost of de novo vector construction. Partner with us to drive breakthroughs in CD24-targeted cellular immunotherapy and bring innovative treatments to patients worldwide.

Product Advantages

We offer CD24 CAR plasmids for different generations, with customizable costimulatory domains (CD28, 4-1BB, OX40, ICOS) and functional modules (suicide genes, cytokines, checkpoint inhibitors) to meet diverse research needs.

Product Applications

Custom CD24 CAR Plasmid Construction Service

Introduction of CD24

CD24 (also known as heat-stable antigen, HSA or nectadrin) is a protein-coding gene located on human chromosome 6q21. The human CD24 gene features a short open reading frame (ORF, ~0.24 kb) and a long 3’ untranslated region (UTR, ~1.8 kb) that regulates mRNA stability; three intronless pseudogenes are located on chromosomes 1, 15, and Y. Genetic polymorphisms of CD24 (e.g., P170, P1527 dinucleotide deletion) are closely linked to disease susceptibility, progression, and treatment response, particularly in autoimmune diseases and malignant tumors.

CD24 is a small, highly glycosylated glycosylphosphatidylinositol (GPI)-anchored cell surface glycoprotein with distinct structural characteristics.
1) Core peptide chain: Extremely short, only ~27–30 amino acids in mature form, with minimal intracellular domain;
2) GPI anchor: Attaches the protein to the outer leaflet of the cell membrane, enabling extracellular localization and signal transduction via membrane rafts;
3) Extensive glycosylation: Contains multiple N-linked and O-linked glycosylation sites, resulting in a molecular weight range of 35–70 kDa (varies by cell type and glycosylation level); the unique glycan structure forms a specific “glyco-code” that mediates ligand binding;
4) No transmembrane domain: Relies on GPI anchoring and interacts with Src family kinases for downstream signaling.

CD24 mediates diverse biological functions across normal physiological and pathological conditions, primarily including:
1) Immune regulation: Acts as a critical “don’t eat me” signal by binding to Siglec-10 (human) / Siglec-G (mouse), inhibiting macrophage phagocytosis and suppressing excessive immune activation; modulates T/B lymphocyte proliferation, differentiation, and immune homeostasis;
2) Cell adhesion and migration: Binds to P-selectin to promote tumor cell rolling, invasion, and distant metastasis;
3) Cell proliferation and survival: Activates MAPK/ERK, Wnt, and Arf6 signaling pathways to drive tumor cell growth, chemoresistance, and stemness maintenance;
4) Neural development: Regulates neural cell growth, differentiation, and synaptic formation in the central nervous system.

CD24 exhibits tightly regulated expression in normal tissues, with high expression in progenitor cells, immune cells (B cells, T cells, neutrophils, dendritic cells), neural cells, and epithelial stem cells, and low expression in terminally differentiated cells. Abnormally high expression is a hallmark of multiple pathological conditions, making it an ideal target for targeted therapy.

CD24 dysregulation is closely associated with a wide spectrum of human diseases, driving the development of CD24-targeted therapies.
1) Malignant Tumors
CD24 is overexpressed in nearly 20 types of solid tumors and hematological malignancies, including glioblastoma, pancreatic cancer, breast cancer, non-small cell lung cancer, hepatocellular carcinoma, ovarian cancer, urothelial carcinoma, B-cell lymphoma, and esophageal squamous cell carcinoma. High CD24 expression correlates with poor tumor differentiation, lymph node metastasis, chemoresistance, and unfavorable patient prognosis, serving as a key diagnostic and prognostic biomarker.
2) Autoimmune and Inflammatory Diseases
CD24 polymorphisms and abnormal expression are linked to systemic lupus erythematosus (SLE), multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, and autoimmune thyroiditis. It promotes pathogenic T cell proliferation and persistence in target organs, exacerbating autoimmune tissue damage.
3) Neurological Disorders
CD24 is involved in neuroinflammation and neurodegenerative processes, with potential roles in Alzheimer’s disease, Parkinson’s disease, and spinal cord injury repair.

Introduction of CD24 Chimeric Antigen Receptor (CAR)

CD24 CAR is a genetically engineered chimeric antigen receptor designed to specifically recognize the CD24 antigen on target cell surfaces, redirecting immune effector cells (primarily T cells, NK cells, or macrophages) to kill CD24-positive pathological cells. Structurally, CD24 CAR follows the classic modular CAR design, with key components including: 1) Extracellular antigen-binding domain: Single-chain variable fragment (scFv) derived from anti-CD24 monoclonal antibody, mediating specific CD24 recognition; 2) Transmembrane domain: Anchors the CAR to the effector cell membrane; 3) Intracellular signaling domain: Determines CAR generation and effector function, including costimulatory molecules and activation domains.

CD24 CAR is developed across multiple generations, with optimized signaling domains to enhance effector cell persistence, cytotoxicity, and safety.
1) First-generation CD24 CAR: Contains only CD3ζ activation domain, limited T cell proliferation and persistence, low in vivo efficacy;
2) Second-generation CD24 CAR: Integrates one costimulatory domain (CD28, 4-1BB, OX40, or ICOS) + CD3ζ, significantly improves T cell activation, proliferation, and survival, the most widely used in current research;
3) Third-generation CD24 CAR: Combines two costimulatory domains (e.g., CD28+4-1BB) + CD3ζ, further enhances effector function and persistence;
4) Fourth-generation CD24 CAR (Armored CAR): Second/third-generation backbone with transgenic cytokines (IL-12, IL-15, IL-18) or immune checkpoint inhibitors (anti-PD-L1 scFv), boosts anti-tumor activity and overcomes tumor microenvironment suppression;
5) Fifth-generation CD24 CAR: Optimized for safety and specificity, with suicide genes, conditional activation, or dual-targeting modules, reduces off-target effects and adverse events.

Research Findings and Clinical Progress

Approved Therapeutics and Market Outlook

As of 2026, no CD24 CAR cell therapy has received full regulatory approval (FDA/EMA/NMPA), but multiple candidates are in late-phase clinical development with fast-track designation potential. The unmet medical need for CD24-positive solid tumors and refractory autoimmune diseases ensures strong market demand for CD24 CAR research tools and therapeutic products.

Current Research Hotspots

Research Challenges

References

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