Autologous CAR-T cells incorporating an NKG2D-based receptor to bind stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, triggering T-cell activation and cytotoxicity across diverse tumors.
Autologous T cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, initiating CD3ζ/costimulatory signaling to activate T cells, drive cytokine release and proliferation, and mediate MHC-independent cytotoxic tumor killing.
NKG2D-based CAR-T cells bind ULBP6 on target cells, activate via CD3ζ/costimulatory signaling, form an immune synapse, and kill the bound cells through perforin/granzyme (and death-receptor) pathways.
Anti-HER2 antibody–drug conjugate (trastuzumab deruxtecan/Enhertu) that targets HER2, internalizes, and releases a deruxtecan topoisomerase I inhibitor payload to induce DNA damage in tumor cells.
HER2-targeted antibody–drug conjugate composed of trastuzumab linked to deruxtecan (a topoisomerase I inhibitor). After HER2 binding and internalization, the payload is released to inhibit Top1, causing DNA damage, cell cycle arrest, and apoptosis; also elicits ADCC and a bystander killing effect.
Binds HER2, is internalized, and releases a deruxtecan Top1 inhibitor payload causing DNA damage and apoptosis; also induces ADCC and bystander killing.
Autologous dual-target CAR-T cell therapy directed against BCMA (TNFRSF17) and CD19 for relapsed/refractory multiple myeloma; engineered T cells recognize BCMA/CD19 to activate cytotoxic killing of malignant plasma/B-lineage cells.
Autologous T cells are genetically engineered to express dual chimeric antigen receptors targeting BCMA (TNFRSF17) and CD19. Upon binding to BCMA- or CD19-expressing malignant plasma/B-lineage cells, the CAR-T cells activate, release cytokines, and mediate perforin/granzyme-dependent cytotoxic killing; dual targeting aims to reduce antigen escape and deepen anti-myeloma responses.
BCMA-targeted CAR-T cells bind BCMA on target cells, activate, and kill via perforin/granzyme-mediated cytolysis (and related T-cell effector mechanisms).
Autologous dual-target CAR-T cell therapy directed against BCMA (TNFRSF17) and CD19 for relapsed/refractory multiple myeloma; engineered T cells recognize BCMA/CD19 to activate cytotoxic killing of malignant plasma/B-lineage cells.
Autologous T cells are genetically engineered to express dual chimeric antigen receptors targeting BCMA (TNFRSF17) and CD19. Upon binding to BCMA- or CD19-expressing malignant plasma/B-lineage cells, the CAR-T cells activate, release cytokines, and mediate perforin/granzyme-dependent cytotoxic killing; dual targeting aims to reduce antigen escape and deepen anti-myeloma responses.
CD19-specific CAR-T cells bind CD19 on target cells and kill them via perforin/granzyme-mediated cytotoxicity (and related apoptosis pathways).
An allogeneic cytokine-induced killer (CIK) cell therapy genetically engineered via transposon to express a CD19-directed chimeric antigen receptor (anti-CD19 scFv with CD3ζ signaling and CD28/OX40 costimulation) for treatment of relapsed/refractory CD19+ B-cell malignancies (NHL, CLL).
Allogeneic cytokine-induced killer (CIK) T cells engineered via transposon to express a CD19-targeted CAR with CD3ζ signaling and CD28/OX40 costimulation. CAR engagement of CD19 on B cells triggers T/CIK activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate CD19+ malignant B cells.
CARCIK-CD19 cells recognize CD19 on target cells via the CAR, become activated, and kill the CD19+ cells through perforin/granzyme-mediated cytotoxicity (and related T-cell effector mechanisms).