Autologous gene-modified CAR T-cell therapy for relapsed/refractory multiple myeloma; patient T cells are engineered to express a CAR that recognizes myeloma-associated antigens and, upon binding, activates T-cell cytotoxicity.
Autologous patient T cells are gene-modified to express a chimeric antigen receptor that recognizes myeloma-associated surface antigens; upon antigen binding, CAR signaling activates and expands the T cells, inducing cytokine release and targeted cytotoxic killing of malignant plasma cells.
CAR T cells recognize the myeloma-associated surface antigen via the CAR, activate, and directly kill antigen-expressing cells through perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).
HER2-targeted antibody–drug conjugate of trastuzumab linked to a topoisomerase I inhibitor (deruxtecan) via a cleavable linker; exhibits high drug-to-antibody ratio and a bystander killing effect.
HER2-targeted antibody–drug conjugate composed of trastuzumab linked via a cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. Binding to HER2 drives internalization and lysosomal cleavage to release DXd, causing DNA damage (single-strand breaks) and apoptosis. The trastuzumab component also inhibits HER2 signaling and can mediate ADCC. High drug-to-antibody ratio and diffusible payload enable a bystander killing effect of neighboring HER2-low tumor cells.
ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor after lysosomal cleavage, causing DNA damage and apoptosis; Fc can also trigger ADCC. Bystander killing may occur via diffusible payload.
Genetically engineered autologous T cells expressing chimeric antigen receptors targeting CD20 and/or CD30 on lymphoma cells to trigger MHC-independent T-cell activation and cytotoxic killing; given as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells engineered to express chimeric antigen receptors that bind CD20 and/or CD30 on lymphoma cells, enabling MHC-independent recognition and activation via CD3ζ/costimulatory signaling, leading to T-cell expansion, cytokine release, and cytotoxic killing of CD20+/CD30+ tumor cells after lymphodepleting chemotherapy.
Anti-CD20 CAR-T cells bind CD20 on target cells, activating T-cell cytotoxic programs (perforin/granzyme-mediated lysis and apoptosis, with possible Fas–FasL and cytokine-mediated killing).
Genetically engineered autologous T cells expressing chimeric antigen receptors targeting CD20 and/or CD30 on lymphoma cells to trigger MHC-independent T-cell activation and cytotoxic killing; given as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells engineered to express chimeric antigen receptors that bind CD20 and/or CD30 on lymphoma cells, enabling MHC-independent recognition and activation via CD3ζ/costimulatory signaling, leading to T-cell expansion, cytokine release, and cytotoxic killing of CD20+/CD30+ tumor cells after lymphodepleting chemotherapy.
CAR-T cells bind CD30 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis and apoptosis (Fas/FasL), independent of MHC.