Since normal T cells also express the CD7 molecule, to address the self-destruction phenomenon observed during CD7-CAR-T preparation, researchers pioneered the use of CD7 nanobodies to recombine and express them with an endoplasmic reticulum retention sequence. This strategy confines T cell CD7 antigens within the endoplasmic reticulum and Golgi apparatus, creating a CD7-negative state on T cell surfaces. This approach effectively prevents "self-destruction" among CAR-T cells, ultimately enabling successful production of CD7-CAR-T cells. 

The mechanism of CD7-CAR-T cells involves transducing T cells with both CD7-CAR lentivirus and CD7 membrane-blocking lentivirus. This dual-transduction approach creates CD7-CAR-T cells that lack CD7 surface expression, preventing immune cell-mediated "self-destruction" while enabling the cells to specifically recognize and eliminate CD7-positive T-cell tumors through their unique CD7-CAR molecules. 

Brightened： 

• The worlds leading CAR-T product for T-cell malignancies

• Ex vivo CAR-T products that cannot be disrupted by in vivo CAR-T

The GUIDED® platform genetically modifies the patients own T cells to express chimeric antigen receptors that recognize and attack cancer cells, without the need for complex cell preparation processes in vitro.

The platform achieves this through targeted modification and engineering of lentivirus envelope glycoproteins (including "de-targeting" and "T-cell re-targeting" of the viral membrane), enabling specific transfection of quiescent human T cells and NK cell subsets. This enables in vivo delivery of CAR molecules, directly generating CAR-T and CAR-NK cells within the body. Additionally, the lentivirus has undergone stability-enhancing optimizations to reduce immune rejection risks and improve CAR-T transfection efficiency. Leveraging BioGenomics mature CAR technology platform and prior technical expertise, the CAR structure of the In-vivo-CAR product has also been significantly optimized. 

Brightened：

• Overcoming conventional lentiviral transduction； 

• High efficiency in resting T and NK cells；

• Superior clinical safety profile

This platform is dedicated to developing bispecific antibodies targeting CD16A×PD- 1×TAA (B cells). By integrating NK cell-mediated targeted elimination and superimposing PD-1 agonist therapy to deplete autoreactive T cells, we have established a multi-tiered, multi-mechanism paradigm for treating autoimmune diseases. The drug design combines high efficacy, safety, and clinical feasibility, achieving deep therapeutic effects on autoimmune disorders through synergistic targeting of autoreactive T cells and B cells. 

Brightened: 

•  NKCE is designed for autoimmune diseases 

• Unique molecular design of targeted self-reactive T cells 

• The worlds first triple-specific NKCE 

• Clinical safety has been significantly improved

The platform product isolates the Vδ1T cell subtype from peripheral blood of healthy donors, serving as the foundational platform for cellular therapies. As the predominant tissue-resident lymphocytes in humans, Vδ1T cells demonstrate the strongest chemotactic ability among all immune cell types – a critical attribute that distinguishes them from αβ T cells, NK cells, and Vδ2T cells. Therefore, selecting Vδ1T cells for developing cellular therapy drugs can effectively address key challenges in drug homing. 

Vδ1T cells were obtained in sufficient quantities through in vitro transfection, amplification, and preparation processes. After being aliquoted, the cells were cryopreserved. During patient treatment, the cryopreserved cell preparations could be directly thawed and reinfused, truly realizing the characteristics of "ready-to-use" spot-on cell drugs. 

Brightened： 

• A universal “off the shelif”UCAR-T cell product based on V1T cells 

• Strong homing ability and overcome tumor antigen heterogeneity 

• An ideal cell drug choice for solid tumor treatment 

• The worlds leading CMC

This platform specializes in developing PD-1 nanobody-based agonist drugs for autoimmune diseases. These therapeutics specifically bind to and activate the PD-1 receptor on T cell surfaces, enhancing their inhibitory signaling pathways. This mechanism effectively suppresses the activation and function of CD4+ T cells (including Tfh), reduces their ability to assist B cells, and ultimately decreases the production of auto-reactive antibodies. Leveraging nanobodies advantages of small molecular weight, strong tissue penetration, high stability, and low immunogenicity, the PD-1 agonists developed by our platform not only enhance therapeutic efficacy but also improve drug development efficiency and drug-likeness. This innovative approach provides a novel and viable pathway for autoimmune disease treatment.

Brightened： 

• Precise immune regulation mechanism: By specifically activating T cell PD-1 receptor, effectively inhibiting the activity of PD-1 high expressing T cells such as CD4⁺ /Tfh, reducing the production of auto-reactive antibodies, providing a source intervention strategy for autoimmune diseases, this platform is an ideal therapeutic choice for autoimmune pathogenic T cells. 

• Antibody-enhanced drug performance: relying on the nanobody technology, the tissue penetration, stability and drug formation of drugs are significantly improved, the immunogenicity is reduced, and the development and transformation of high-efficiency biological drugs are accelerated. 

• Scarce assets that belong to the Blue Ocean and are relatively difficult to develop.