Gene-modified cellular therapy consisting of 0.5–3×10^9 CAR-positive natural killer (NK) cells designed to redirect NK cytotoxicity and immune modulation toward pathogenic immune cells; administered after lymphodepletion.
Gene‑modified natural killer cells engineered with a chimeric antigen receptor (CAR) to redirect NK recognition and cytotoxicity toward disease-driving immune cells. Upon CAR engagement of the target antigen (not disclosed), the NK cells mediate killing via perforin/granzyme pathways and cytokine-driven immune modulation, aiming to deplete pathogenic autoreactive lymphocytes. Lymphodepletion is used to enhance CAR‑NK engraftment and persistence.
CAR-engineered NK cells bind the antigen and kill target cells via NK degranulation with perforin/granzyme–mediated apoptosis (and ancillary cytokine-mediated cytotoxicity).
Autologous CD19-directed CAR T-cell therapy; genetically modified T cells expressing a CAR with CD3ζ and a costimulatory domain to target and kill CD19+ malignant B cells.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor with CD3ζ signaling and a costimulatory domain. Upon binding CD19 on B cells, the CAR activates T-cell cytotoxicity, cytokine release, and proliferation, resulting in targeted killing and depletion of CD19+ malignant (and normal) B cells.
CAR T cells bind CD19 and directly kill CD19+ cells via perforin/granzyme-mediated cytolysis and death-receptor (e.g., Fas) apoptosis, with cytokine release enhancing cytotoxicity.
Also known as DuoBody CD3xCD30; a subcutaneous bispecific IgG T-cell–redirecting antibody that co-binds CD3 on T cells and CD30 on tumor cells to form an immune synapse, activate TCR/CD3 signaling, and induce cytotoxicity and cytokine release in CD30+ malignancies.
Fc-silenced bispecific IgG1 that co-binds CD3 on T cells and CD30 on tumor cells, forming an immune synapse to activate TCR/CD3 signaling and redirect cytotoxic T lymphocytes to kill CD30+ tumor cells with associated cytokine release.
Bispecific T-cell engager binds CD30 on target cells and CD3 on T cells, forming an immune synapse that activates TCR/CD3 signaling; redirected CTLs kill CD30+ cells via perforin/granzyme-mediated cytolysis.
HER2-directed antibody-drug conjugate composed of trastuzumab linked to a topoisomerase I inhibitor (deruxtecan); binds HER2, inhibits HER2 signaling and mediates ADCC, then internalizes to release a topo-I payload that induces DNA damage with a potential bystander effect.
HER2-directed antibody-drug conjugate composed of trastuzumab linked to a topoisomerase I inhibitor (deruxtecan). Trastuzumab binds HER2 to inhibit signaling and mediate ADCC, then the complex is internalized and the payload is released to inhibit topoisomerase I, causing DNA damage and cell death, with potential bystander effect.
The HER2-binding ADC is internalized and releases deruxtecan (topoisomerase I inhibitor), causing DNA damage and apoptosis in HER2+ cells; Fc can also mediate ADCC, with potential bystander killing from the membrane-permeable payload.
Humanized IgG1 anti-HER2 monoclonal antibody that blocks ERBB2/HER2 signaling and mediates ADCC against HER2-amplified tumor cells.
Humanized IgG1 anti-HER2 monoclonal antibody that binds ERBB2/HER2 on tumor cells, inhibits HER2 receptor activation and downstream PI3K/AKT/MAPK signaling, and engages Fc receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing cells.
Trastuzumab binds HER2 and recruits Fc receptor-bearing immune cells to kill HER2+ cells via ADCC (with possible CDC); HER2 signaling blockade can also promote apoptosis.