Allogeneic, cord blood–derived CAR natural killer (NK) cell therapy engineered to express two CARs targeting CD19 and CD70; administered IV to induce MHC-independent NK cytotoxicity against B-cell malignancies and reduce antigen escape.
Allogeneic cord blood-derived NK cells engineered to express two chimeric antigen receptors targeting CD19 and CD70. Binding to either antigen activates NK cell signaling and MHC-independent cytotoxicity (perforin/granzyme-mediated lysis and cytokine release) against malignant B cells, with dual targeting designed to reduce antigen escape.
CAR-engineered NK cells bind CD70 on target cells, activating NK signaling and degranulation to induce perforin/granzyme-mediated lysis (MHC-independent).
An antibody–drug conjugate that binds a tumor-associated surface antigen, is internalized, and releases a camptothecin-class/topoisomerase I inhibitor payload ("-gitecan"), inducing DNA damage and tumor cell death.
Antibody–drug conjugate that binds a tumor-associated surface antigen, is internalized, and releases a camptothecin-class/topoisomerase I inhibitor payload inside tumor cells, inducing DNA damage and tumor cell death.
An EGFR-targeting ADC binds EGFR on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor that causes DNA damage and kills the cells.
An antibody–drug conjugate that binds a tumor-associated surface antigen, is internalized, and releases a camptothecin-class/topoisomerase I inhibitor payload ("-gitecan"), inducing DNA damage and tumor cell death.
Antibody–drug conjugate that binds a tumor-associated surface antigen, is internalized, and releases a camptothecin-class/topoisomerase I inhibitor payload inside tumor cells, inducing DNA damage and tumor cell death.
An anti-HER3 antibody–drug conjugate binds HER3 on tumor cells, is internalized, and releases a camptothecin-class/topoisomerase I inhibitor payload that induces DNA damage and cell death.
Autologous gene-modified T cells engineered to express a synthetic antigen receptor targeting LILRB4 (ILT3/CD85k), signaling via the native TCR/CD3 complex to kill LILRB4-positive monocytic leukemia cells.
Autologous T cells are genetically engineered to express a STAR receptor that targets LILRB4 (ILT3/CD85k). The STAR assembles with the native TCR/CD3 complex, so antigen binding on LILRB4-positive monocytic leukemia cells triggers TCR/CD3 signaling, activating the T cells to proliferate and kill targets via perforin/granzyme-mediated cytotoxicity, thereby eliminating LILRB4-expressing leukemia and immunosuppressive myeloid cells.
STAR-engineered T cells bind LILRB4 on target cells, signal via the native TCR/CD3 complex, and kill LILRB4+ cells through perforin/granzyme-mediated cytolysis (and related CTL effector mechanisms).
An antibody–drug conjugate targeting Trop-2 that delivers the topoisomerase I inhibitor SN-38 to tumor cells, causing DNA strand breaks, S-phase arrest, and apoptosis.
Humanized anti–Trop-2 monoclonal antibody (hRS7) delivers the topoisomerase I inhibitor SN-38 to Trop-2–expressing tumor cells. After binding and internalization, linker cleavage releases SN-38, which stabilizes Topo I–DNA cleavage complexes, causing DNA strand breaks, S-phase arrest, and apoptosis (with potential bystander effect).
The ADC binds Trop-2 on target cells, is internalized, and releases SN-38 (a topoisomerase I inhibitor) that stabilizes Topo I-DNA cleavage complexes, causing DNA strand breaks, S-phase arrest, and apoptosis; a bystander effect may also occur.