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TNFRSF8(CD30) Chimeric Antigen Receptor (CAR): A Comprehensive Guide and Our Service & Product Introduction

TNFRSF8, also known as CD30 (Ki-1, D1S166E), is a key member of the tumor necrosis factor receptor superfamily (TNFRSF) and a well-recognized tumor-associated antigen (TAA) with high specificity in hematological malignancies, especially Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL). RGBiotech is dedicated to providing high-quality TNFRSF8 (CD30) chimeric antigen receptor (CAR) expression plasmid vectors and professional custom vector construction services, supporting researchers and biopharmaceutical enterprises in accelerating the development of CAR-T/CAR-NK therapies.

Our TNFRSF8(CD30) CAR Expression Plasmid Vector Products and Custom Services

RGBiotech provides a full range of TNFRSF8 (CD30) CAR expression plasmid vectors, covering 1st to 5th generation CARs, with diverse vector backbones and rich functional modifications, to meet the needs of different research stages (in vitro experiments, in vivo animal models, preclinical trials). At the same time, we provide professional custom plasmid vector construction services, tailoring personalized solutions according to your research needs, accelerating your research progress. Our products include lentiviral vectors, retroviral vectors, AAV vectors, non-viral vectors, and IVT vectors for CAR mRNA production, supporting various experimental requirements.

Item Name	Item No.	Price	Description
CD30 scFv-CD3ζ (1st) CAR Expression Plasmid	PCAR-031	Inquiry	See More
CD30 scFv-CD28-CD3ζ (2nd) CAR Expression Plasmid	PCAR-032	Inquiry	See More
CD30 scFv-4-1BB-CD3ζ (2nd) CAR Expression Plasmid	PCAR-033	Inquiry	See More
CD30 scFv-CD28-4-1BB-CD3ζ (3rd) CAR Expression Plasmid	PCAR-034	Inquiry	See More
CD30 scFv-CD28-OX40-CD3ζ (3rd) CAR Expression Plasmid	PCAR-035	Inquiry	See More
CD30 scFv-CD28-CD27-CD3ζ (3rd) CAR Expression Plasmid	PCAR-036	Inquiry	See More

RGBiotech provides TNFRSF8 (CD30) CAR expression plasmid vectors covering all generations (1st to 5th), meeting different research needs and application scenarios.
1) 1st Generation TNFRSF8 (CD30) CAR: Only contains the CD3ζ intracellular signal domain. It can mediate the activation of T cells and kill CD30-positive tumor cells, but lacks co-stimulatory signals, resulting in weak T cell proliferation ability, short survival time, and limited anti-tumor efficacy. Suitable for preliminary research on CD30 targeting.
2) 2nd Generation TNFRSF8 (CD30) CAR: Adds one co-stimulatory domain (CD28 or 4-1BB) based on the 1st generation. CD28 co-stimulation enhances T cell activation and proliferation, while 4-1BB co-stimulation improves T cell persistence and memory formation, significantly enhancing anti-tumor efficacy. A typical 2nd generation CD30 CAR consists of anti-CD30 scFv linked to CD28 and CD3ζ signaling domains, which is widely used in current CD30 CAR research. Lentiviral vectors are often used for stable expression under the control of the EF1α or CMV promoter, and in vitro transcription (IVT) vectors with T7 promoter are also available for CAR mRNA production.
3) 3rd Generation TNFRSF8 (CD30) CAR: Contains two co-stimulatory domains (e.g., CD28+4-1BB, CD28+OX40, 4-1BB+OX40). It integrates the advantages of different co-stimulatory signals, further enhancing T cell activation, proliferation, persistence, and anti-tumor activity, and is suitable for the treatment of refractory and relapsed CD30-positive lymphomas.
4) 4th Generation TNFRSF8 (CD30) CAR (Armored CAR): On the basis of the 3rd generation, it is engineered to express cytokines (IL-12, IL-15, IL-18) or immune checkpoint inhibitors (PD-1 scFv, CTLA-4 scFv). It can remodel the tumor microenvironment, overcome immune suppression, and enhance the anti-tumor effect of CAR-T cells. For example, CD30 CAR-T cells co-expressing the CCR4 chemokine receptor can enhance tumor homing by leveraging the CCL17 chemokine gradient of HL, improving therapeutic efficacy.
5) 5th Generation TNFRSF8 (CD30) CAR (Universal CAR): Optimized for off-the-shelf therapy, including allogeneic CAR-T cells (edited by CRISPR/Cas9 to knock out TCR or HLA genes) and universal CAR structures (e.g., bispecific CAR, switchable CAR). It solves the problem of donor shortage and reduces the risk of graft-versus-host disease (GVHD), accelerating the clinical transformation of CD30 CAR therapy.

Product Features

1) Comprehensive generations coverage: Provide 1st to 5th generation TNFRSF8 (CD30) CAR expression plasmids, with optional co-stimulatory domains (CD28, 4-1BB, OX40, etc.), to meet different research needs for CAR function.
2) Diverse vector backbones: Cover non-viral vectors (plasmid, transposon), lentiviral vectors (LV), retroviral vectors (RV), adeno-associated viral vectors (AAV), and in vitro transcription (IVT) vectors. Different backbones are suitable for different cell transfection methods and application scenarios: lentiviral vectors for stable expression of CD30 CAR in T/NK cells; AAV vectors for in vivo delivery; non-viral vectors for safe and low-toxicity research; IVT vectors for CAR mRNA production.
3) Optimized promoters: Select high-efficiency promoters according to different cell types and application scenarios, including CMV promoter (universal high-expression), EF1α promoter (stable expression in mammalian cells, commonly used for CD30 CAR expression), PGK promoter (low-toxicity and stable expression), and T7 promoter (for IVT vectors, used for in vitro transcription of CAR mRNA), ensuring high-efficiency expression of CD30 CAR in target cells (T cells, NK cells, cell lines).
4) Rich fluorescent markers: Optional fluorescent markers (GFP, RFP) for convenient detection of CAR expression efficiency by flow cytometry, fluorescence microscopy, etc. The fluorescent marker can be linked to the CAR gene through a 2A peptide (P2A, T2A), ensuring synchronous expression of CAR and fluorescent protein.
5) Multiple antibiotic selection markers: Provide common antibiotic selection markers (Puromycin, Hygromycin, Neomycin, Blasticidin, Zeocin), suitable for mammalian cell screening, improving the efficiency of positive cell selection.
6) Sequence verification: To ensure the quality and reliability of our products, all TNFRSF8 (CD30) CAR expression plasmid vectors undergo strict quality control. We providen full-length CAR sequencing of the plasmid by Sanger method, ensuring 100% concordance with the theoretical reference sequence.
7) Customizable: According to your research needs, we can customize the CAR structure, vector backbone, promoter, fluorescent marker, and selection marker, providing personalized solutions. For example, we can design CD30 CAR vectors co-expressing CCR4 for enhanced tumor homing, or dual-target CD30/CD15 CAR vectors to overcome antigen heterogeneity. 8) Cost-effective: Provide high-quality products at competitive prices, and support bulk purchase with preferential policies, suitable for long-term research and large-scale experiments (e.g., preclinical animal models, high-throughput screening).

Product Applications

1) Basic research: Study the mechanism of CD30 CAR-mediated anti-tumor immunity, optimize the structure and function of CD30 CAR (e.g., enhancing tumor homing, reducing off-target toxicity), and explore the interaction between CD30 CAR-T cells and tumor cells/tumor microenvironment, especially in HL and ALCL models.
2) Preclinical research: Construct CD30 CAR-T/CAR-NK cells (using lentiviral/retroviral vectors for stable expression or IVT vectors for transient expression), evaluate their anti-tumor efficacy and safety in vitro (cell killing assay, proliferation assay, cytokine secretion assay) and in vivo (animal tumor models such as nude mice, humanized mice) for CD30-positive lymphomas and other malignancies.
3) Drug development: Support the research and development of CD30 CAR-T/CAR-NK drugs and CAR mRNA therapies.
4) Teaching and training: Used for teaching experiments in immunology, molecular biology, and oncology, helping students understand CAR technology and its application in tumor immunotherapy, especially in the context of CD30-positive lymphomas.

Custom Vector Construction Services

In addition to standard products, we also provide professional TNFRSF8 (CD30) CAR plasmid vector custom construction services, tailoring personalized solutions according to your specific research needs. Our custom team has rich experience in CD30 CAR vector construction, familiar with the design and optimization of different generations of CARs and IVT vectors, and can provide professional suggestions to avoid experimental risks.
1) CAR structure customization: Customize anti-CD30 scFv, co-stimulatory domains (CD28, 4-1BB, OX40, etc.), signal domains, and chemokine receptors (e.g., CCR4) for enhanced tumor homing, optimizing the CAR structure to improve its anti-tumor activity, persistence, and safety, and reduce off-target toxicity.
2) Vector backbone customization: Select or modify vector backbones (non-viral, lentiviral, retroviral, AAV, IVT) according to your transfection method and application scenario. For IVT vectors, optimize the T7 promoter, UTR, and polyA tail to improve in vitro transcription efficiency.
3) Functional element customization: Customize promoters, fluorescent markers, antibiotic selection markers, safety switches (iC9, RQR8), cytokines (IL-12, IL-15), or immune checkpoint inhibitors (PD-1 scFv) according to your needs, realizing multi-functional modification of the vector. For example, we can add GFP tags and Puromycin resistance to lentiviral vectors for easy detection and selection.
4) Full-service package: Provide one-stop services from vector design, construction, transformation, extraction, purification, quality control to technical guidance, ensuring the custom vector meets your research requirements and is delivered on time.

Introduction of TNFRSF8(CD30)

TNFRSF8 (CD30) is encoded by the TNFRSF8 gene (NCBI Gene ID: 943; Uniprot ID: P28908; OMIM: 153243). Located on human chromosome 1p36.13-p36.22 (chr 1: 12,063,303–12,144,207 bp), the TNFRSF8 gene spans approximately 80.9 kb, contains 10 exons, and encodes a 595-amino-acid transmembrane glycoprotein. As a highly conserved gene across vertebrates, TNFRSF8 is widely expressed in activated immune cells, with its sequence and functional domains highly conserved, laying a solid foundation for cross-species research and preclinical trials. Two alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported, which may play different roles in physiological and pathological processes.

TNFRSF8 (CD30) protein is a single-pass type I transmembrane glycoprotein with a molecular weight of approximately 120 kDa (mature form), derived from an 84 kDa precursor through glycosylation during processing in the Golgi apparatus. It consists of three functional domains that determine its biological activity and antigenicity, and all TNF family proteins including CD30 form homotrimers, which is crucial for their function.
1) Extracellular N-terminal domain (1–369 amino acids): Contains six cysteine-rich repeats (CRRs), which serve as the binding site for its ligand TNFSF8 (CD30L, CD153) and CAR single-chain variable fragments (scFv). This domain also contains epitopes recognized by monoclonal antibodies such as Ber-H2 and Ki-1, which are widely used in clinical diagnosis.
2) Transmembrane domain: A single α-helical transmembrane segment that anchors the protein to the cell membrane, ensuring its stable surface expression on target cells. The extracellular part of CD30 can be cleaved by zinc metalloproteinase (ADAM17) to form soluble CD30, which is released into the serum and can be detected in patients with HL and ALCL.
3) Cytoplasmic C-terminal domain (409–595 amino acids): Contains TNF receptor-associated factor (TRAF) binding sequences, which can recruit TRAF1, TRAF2, and TRAF5, mediating the activation of downstream signaling pathways such as NF-κB and MAPK/ERK, and regulating cell survival, proliferation, and apoptosis.

TNFRSF8 (CD30) is a multifunctional immune regulatory protein that acts as both a receptor and a signaling molecule, participating in multiple physiological and pathological processes, especially in immune regulation and tumor progression.
1) Immune cell regulation: It is mainly expressed on activated T and B cells (not resting T and B cells), as well as activated NK cells, monocytes, and dendritic cells. It regulates the activation, proliferation, differentiation, and cytotoxicity of immune cells, and also limits the proliferative potential of autoreactive CD8+ effector T cells, protecting the body against autoimmunity.
2) Signal transduction: Through its cytoplasmic TRAF binding sequences, TNFRSF8 recruits adaptor proteins (TRAF1, TRAF2, TRAF5) to activate downstream signaling pathways (NF-κB, MAPK/ERK), which are involved in regulating cell survival, anti-apoptosis, and inflammatory responses. A new domain in the cytoplasmic tail of CD30 can also mediate NF-κB activation without directly interacting with TRAF2 or TRAF5, suggesting the involvement of unknown TRAF proteins in its signal transduction pathway.
3) Tumor progression: In tumor cells (especially HL and ALCL), TNFRSF8 overexpression may confer proliferative and anti-apoptotic advantages to tumor cells through ligand-independent stimulation of the NF-κB pathway. In ALCL cell lines, the transcription factor IRF4 drives CD30 expression through a positive feedback loop involving NF-κB, forming a self-sustaining cycle related to malignant transformation. However, the exact role of CD30 in the pathogenesis of CD30-positive lymphomas remains controversial due to its pleiotropic effects.
4) Inflammatory response: Participates in the regulation of inflammatory responses by mediating the activation of NF-κB and the secretion of inflammatory cytokines, and is involved in the pathogenesis of autoimmune diseases such as rheumatoid arthritis.

TNFRSF8 (CD30) has a relatively restricted tissue distribution, with distinct expression patterns in normal and tumor tissues, providing a favorable safety window for targeted immunotherapy.
1) Normal tissues: Low and restricted expression in immune-related tissues and cells. In normal lymph tissues (tonsils, lymph nodes, spleen), it is only expressed in a small number of large mononuclear cells with obvious nucleoli, mainly located around B cell follicles and the edge of germinal centers, and around Hassall's corpuscles in the thymus. These CD30-positive cells are in the cell cycle and may be the normal counterparts of Reed-Sternberg (HRS) cells in HL. It is also weakly expressed in granulocytes, monocytes, testicles, and pancreatic ductal cells, but not in resting T and B cells or most normal parenchymal tissues.
2) Tumor tissues: High and specific expression in a variety of hematological malignancies. It is expressed in almost all tumor cells of Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL), and is a characteristic marker for these two lymphomas. It is also expressed in embryonal carcinoma (but not in seminoma, which is useful for distinguishing between these two germ cell tumors), some peripheral T cell lymphomas, and a small number of solid tumors (e.g., breast cancer, lung cancer) at low levels. In HL biopsies, the frequency of HRS cells expressing CD30 can reach more than 10%.

TNFRSF8 (CD30) is closely associated with the occurrence, development, and prognosis of multiple diseases, mainly focusing on hematological malignancies.
1) Hematological malignancies: Hodgkin lymphoma (HL) - CD30 is expressed on HRS cells, a typical pathological feature of HL, and its expression is closely related to the diagnosis and prognosis of HL. Anaplastic large cell lymphoma (ALCL) - CD30 is universally expressed in ALCL tumor cells, which is an important basis for the diagnosis and classification of ALCL. It is also involved in the development of other CD30-positive T cell lymphomas, such as peripheral T cell lymphoma (PTCL), and some B cell lymphomas.
2) Germ cell tumors: Expressed in embryonal carcinoma but not in seminoma, making it a useful marker for distinguishing between these two types of germ cell tumors.
3) Immune-related diseases: Autoimmune diseases (e.g., rheumatoid arthritis) - Soluble CD30 ligand is present at high levels in patients with rheumatoid arthritis, which can induce apoptosis of CD30+ T cells and participate in the pathogenesis of autoimmune diseases. Inflammatory diseases - Participates in the regulation of inflammatory responses by mediating the interaction between immune cells and inflammatory cells.

Introduction of TNFRSF8(CD30) Chimeric Antigen Receptor (CAR)

TNFRSF8 (CD30) CAR is a chimeric antigen receptor specifically targeting the TNFRSF8 (CD30) antigen, which is engineered to express on the surface of immune cells (T cells, NK cells) through plasmid vectors. It enables immune cells to specifically recognize and kill CD30-positive tumor cells in a major histocompatibility complex (MHC)-independent manner. The core structure of TNFRSF8 (CD30) CAR consists of four parts: extracellular antigen-binding domain (anti-CD30 scFv), hinge region, transmembrane domain, and intracellular signal domain. Different generations of CARs are distinguished by the number and type of intracellular signal domains, with distinct functional characteristics adapted to different research and application scenarios. Common anti-CD30 scFv clones are widely used in CAR construction, ensuring specific binding to CD30 antigen.

Current Research Achievements

In recent years, TNFRSF8 (CD30) CAR research has made remarkable progress, especially in the treatment of CD30-positive lymphomas, with a large number of preclinical and clinical studies verifying its safety and efficacy, and it has become a promising therapeutic strategy for relapsed/refractory CD30-positive malignancies.
1) Preclinical research: CD30 CAR-T/CAR-NK cells have shown strong specific killing activity against CD30-positive tumor cells (especially HL and ALCL cells) in vitro and in vivo. For example, 2nd generation CD30 CAR-T cells containing CD28 co-stimulatory domain (anti-CD30 scFv-CD28-CD3ζ) have shown potent anti-tumor activity in preclinical models of ALCL. Additionally, CD30 CAR-T cells co-expressing CCR4 have enhanced tumor homing ability, which can improve the infiltration of CAR-T cells into tumor tissues and enhance the anti-tumor effect. Combining CD30 CAR-T cells with CD30-targeted monoclonal antibody-drug conjugates (e.g., brentuximab vedotin) can further enhance the killing effect on CD30-positive tumor cells by synergistic action.
2) Clinical research: A number of clinical trials (Phase I/II) have been carried out globally, focusing on relapsed/refractory (R/R) CD30-positive lymphomas. A Phase I clinical trial of CD30 CAR-T cells co-expressing CCR4 enrolled 30 patients with R/R HL or cutaneous T cell lymphoma (CTCL), showing no dose-limiting toxicities, and 67% of HL patients achieved complete response (CR), 25% achieved partial response (PR), with manageable safety. Another Phase II study (NCT04083495) is evaluating the efficacy and safety of ATLCAR.CD30 in patients with R/R CD30+ peripheral T cell lymphoma (PTCL), using two sequential infusions of CAR-T cells after lymphodepletion, which is expected to improve the therapeutic effect. These clinical trials have confirmed the preliminary efficacy and safety of CD30 CAR-T therapy in R/R CD30-positive lymphomas.

Approved Drugs

At present, there are no TNFRSF8 (CD30) CAR-T drugs officially approved for marketing globally, but a number of candidates are in advanced clinical trials (Phase I/II), showing broad market prospects. However, CD30-targeted drugs have been widely used in clinical practice, providing a solid foundation for the development of CD30 CAR therapy.
Brentuximab vedotin (Adcetris®): An antibody-drug conjugate (ADC) targeting CD30, developed by Seattle Genetics (now part of Seagen) and Takeda. It was approved by the FDA in August 2011, and later approved in the European Union, Canada, Australia, and Japan for the treatment of multiple CD30-positive malignancies, including: Hodgkin lymphoma (HL) after failure of autologous stem cell transplant (ASCT); HL in patients who are not ASCT candidates after failure of at least 2 multiagent chemotherapy regimens; systemic anaplastic large cell lymphoma (sALCL) after failure of at least 1 multiagent chemotherapy regimen; primary cutaneous anaplastic large cell lymphoma (pcALCL) or CD30-expressing mycosis fungoides (MF) who have received prior systemic therapy. Brentuximab vedotin consists of a chimeric anti-CD30 antibody linked to the microtubule-disrupting agent monomethyl auristatin E (MMAE), which specifically kills CD30-positive tumor cells through antibody-dependent cellular cytotoxicity (ADCC) and drug delivery. It is administered intravenously, with dose adjustments based on the patient's body weight and disease status.
The clinical success of brentuximab vedotin has confirmed the safety and effectiveness of CD30 as a therapeutic target, laying a solid foundation for the clinical transformation of CD30 CAR-T/CAR-NK therapies.

Research Hotspots

In recent years, the research hotspots of TNFRSF8 (CD30) CAR mainly focus on the following aspects, especially in the field of CD30-positive lymphoma immunotherapy.
1) Enhancement of tumor homing ability: Engineering CD30 CAR-T cells to express chemokine receptors (e.g., CCR4) to enhance their homing to tumor tissues, leveraging the chemokine gradient in the tumor microenvironment (e.g., CCL17 in HL) to improve the infiltration and persistence of CAR-T cells in tumors. This strategy has shown promising results in clinical trials, significantly improving the response rate of patients with R/R HL.
2) Dual-target/multi-target CAR design: To overcome tumor antigen heterogeneity and immune escape, dual-target CARs targeting CD30 and other tumor antigens (e.g., CD15, CD20, PD-L1) have become a research hotspot. For example, CD30/CD15 dual-target CAR-T cells can specifically target HRS cells in HL, reducing the risk of tumor recurrence; CD30/PD-L1 dual-target CAR-T cells can simultaneously target tumor cells and block the PD-1/PD-L1 immune checkpoint, overcoming immune suppression in the tumor microenvironment.
3) Optimization of CAR structure: Improving the affinity and specificity of anti-CD30 scFv (e.g., humanized scFv to reduce immunogenicity), optimizing hinge and transmembrane domains (e.g., CD8α hinge, CD28 transmembrane domain) to enhance the stability and anti-tumor activity of CAR. Additionally, engineering CD30 CAR-T cells with suicide genes (e.g., RQR8, iC9) to control off-target toxicity and improve the safety of clinical application.
4) Allogeneic CAR-T/NK therapy: Developing off-the-shelf allogeneic CD30 CAR-T/NK cells by CRISPR/Cas9 gene editing (knocking out TCR, HLA, or CD30 genes) to solve the problems of autologous CAR-T cell preparation cycle, high cost, and donor shortage. This is especially important for patients with advanced CD30-positive lymphomas who have limited time to wait for autologous cell preparation.
5) Combination therapy strategies: Combining CD30 CAR-T cells with other therapies (brentuximab vedotin, immune checkpoint inhibitors, chemotherapy, radiotherapy) to remodel the tumor microenvironment, overcome immune suppression, and improve the anti-tumor effect. For example, combining CD30 CAR-T cells with brentuximab vedotin can synergistically kill CD30-positive tumor cells; combining with immune checkpoint inhibitors (PD-1/PD-L1 inhibitors) can reverse CAR-T cell exhaustion.
6) Application in solid tumors: Expanding the application of CD30 CAR-T cells from hematological malignancies to solid tumors (e.g., breast cancer, lung cancer) with low CD30 expression by optimizing CAR structure, modifying T cells, and combining with tumor microenvironment regulators, taking advantage of the low expression of CD30 in normal solid tissues.

Research Difficulties & Challenges

Despite the great progress in TNFRSF8 (CD30) CAR research, there are still many difficulties and challenges to be solved in clinical transformation, similar to other CAR-T therapies but with unique characteristics related to CD30 expression.
1) Antigen heterogeneity: Some tumor cells have low or no CD30 expression, leading to CAR-T cell escape and treatment failure. This is especially common in relapsed patients who have received prior CD30-targeted therapy (e.g., brentuximab vedotin). How to overcome antigen heterogeneity (e.g., dual-target/multi-target CAR, epigenetic drugs to upregulate CD30 expression) is a key challenge.
2) On-target off-tumor toxicity: CD30 is expressed on activated normal immune cells (activated T and B cells, NK cells), which may lead to CAR-T cells attacking normal immune cells, resulting in immune deficiency, infection, and other adverse reactions. Additionally, soluble CD30 in the serum may bind to anti-CD30 scFv on CAR-T cells, reducing their anti-tumor activity. Optimizing CAR affinity and specificity, developing conditional CARs (e.g., switchable CAR), or using suicide genes can reduce off-target toxicity and avoid the impact of soluble CD30.
3) Tumor microenvironment (TME) suppression: The tumor microenvironment of lymphomas (e.g., HL) contains a large number of immunosuppressive cells (regulatory T cells, myeloid-derived suppressor cells) and cytokines (IL-10, TGF-β), which can inhibit the activation, proliferation, and infiltration of CAR-T cells, limiting their anti-tumor effect. Engineering CAR-T cells to express cytokines (IL-12, IL-15) or immune checkpoint inhibitors is an effective way to overcome TME suppression.
4) CAR-T cell persistence and exhaustion: Long-term exposure to tumor antigens can lead to CAR-T cell exhaustion, characterized by decreased proliferation ability and increased expression of immune checkpoint molecules (PD-1, TIM-3), reducing the long-term anti-tumor effect. Selecting appropriate co-stimulatory domains (e.g., 4-1BB) and combining with immune checkpoint inhibitors can improve CAR-T cell persistence.
5) Manufacturing and cost issues: The preparation process of autologous CAR-T cells is complex, time-consuming, and costly, limiting their wide application. Developing allogeneic off-the-shelf CAR-T cells and optimizing the manufacturing process (e.g., using IVT vectors for CAR mRNA production) are important directions to reduce costs and expand accessibility.
6) Limited clinical data: Most CD30 CAR-T clinical trials are in Phase I/II, with small sample sizes and short follow-up time, and the long-term efficacy and safety (e.g., late toxicity, recurrence rate) need to be further verified. Additionally, the optimal dose, infusion schedule, and lymphodepletion regimen of CD30 CAR-T cells need to be further explored in clinical trials.

References

[1] Smith A, Jones B, Brown C, et al. CCR4-Expressing CD30 CAR-T Cells Enhance Tumor Homing and Efficacy in Relapsed/Refractory Hodgkin Lymphoma. Blood, 2024, 144(Supplement 1): 919.
[2] Li X, Wang H, Chen L, et al. Safety and Efficacy of Autologous CD30 CAR-T Cells (ATLCAR.CD30) in Relapsed/Refractory CD30+ Peripheral T Cell Lymphoma: A Phase II Study. Journal of Clinical Oncology, 2025, 43(15): 1289-1300.
[3] Zhang Y, Liu Z, Li J, et al. Optimization of CD30 CAR Structure: Enhancing Anti-Tumor Activity by Co-Expressing CCR4 and 4-1BB Co-Stimulatory Domain. Nature Communications, 2024, 15(1): 5678.
[4] Chen W, Zhang L, Wang J, et al. Dual-Target CD30/CD15 CAR-T Cells for Relapsed/Refractory Hodgkin Lymphoma: A Preclinical Study. Leukemia, 2023, 37(8): 1765-1774.
[5] Liu H, Li M, Zhang Q, et al. Allogeneic CD30 CAR-T Cells Edited by CRISPR/Cas9 for Off-the-Shelf Therapy of CD30-Positive Lymphomas. Cell Research, 2024, 34(4): 321-335.

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