Autologous, genetically engineered T-cell therapy expressing a single CAR with tandem scFv domains targeting CD19 or CD22 and a 4-1BB co-stimulatory domain; infused IV at 1–2×10^6 CAR-T/kg to induce T-cell cytotoxicity against malignant B cells and enhance activation, proliferation, and persistence.
Autologous T cells are genetically engineered to express a single tandem scFv CAR that recognizes CD19 or CD22 and signals via CD3zeta with a 4-1BB co-stimulatory domain. Engagement of CD19 or CD22 on malignant B cells triggers T-cell cytotoxicity and cytokine release and enhances T-cell activation, proliferation, and persistence; dual targeting helps prevent antigen-loss escape.
CAR T cells bind CD19 via the tandem scFv, become activated through CD3ζ/4-1BB signaling, and kill target cells via perforin/granzyme-mediated lysis and death-receptor pathways.
Autologous, genetically engineered T-cell therapy expressing a single CAR with tandem scFv domains targeting CD19 or CD22 and a 4-1BB co-stimulatory domain; infused IV at 1–2×10^6 CAR-T/kg to induce T-cell cytotoxicity against malignant B cells and enhance activation, proliferation, and persistence.
Autologous T cells are genetically engineered to express a single tandem scFv CAR that recognizes CD19 or CD22 and signals via CD3zeta with a 4-1BB co-stimulatory domain. Engagement of CD19 or CD22 on malignant B cells triggers T-cell cytotoxicity and cytokine release and enhances T-cell activation, proliferation, and persistence; dual targeting helps prevent antigen-loss escape.
CAR T cells bind CD22 via the tandem scFv, activating CD3ζ/4-1BB signaling and killing CD22+ cells via perforin/granzyme–mediated apoptosis (and Fas–FasL), with cytokine release.
Autologous double-negative (CD4−/CD8−) T cells transduced via lentiviral vector to express an anti-CD19 chimeric antigen receptor; depletes CD19+ B-lineage cells and plasmablasts to reduce autoantibody production and B cell–mediated inflammation.
Autologous double-negative (CD4-/CD8-) T cells are lentivirally engineered to express an anti-CD19 chimeric antigen receptor; CAR engagement of CD19 triggers targeted cytotoxicity against CD19+ B-lineage cells and plasmablasts, reducing autoantibody production and B cell–mediated inflammation.
Anti-CD19 CAR-engineered double-negative T cells bind CD19 on target cells and induce cytotoxicity via immune synapse formation with perforin/granzyme-mediated apoptosis (and Fas–FasL pathways).
First-in-human antibody-drug conjugate targeting folate receptor alpha (FRα); binds FRα, is internalized, and releases a cytotoxic payload to kill FRα-expressing tumor cells.
Humanized IgG1 ADC targeting folate receptor alpha (FRα). After FRα binding and internalization, a cleavable linker releases the topoisomerase I inhibitor exatecan, causing DNA damage (single- and double-strand breaks), cell cycle arrest, and apoptosis, with potential bystander killing of neighboring tumor cells.
ADC binds FRα on tumor cells, is internalized, cleavable linker releases exatecan (topoisomerase I inhibitor) causing DNA strand breaks, cell-cycle arrest, and apoptosis; with potential bystander killing.
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting GPRC5D and CD19, redirecting T-cell cytotoxicity against malignant plasma cells and B-lineage/myeloma subclones.
Autologous T cells engineered to express a chimeric antigen receptor recognizing GPRC5D and CD19 on malignant plasma cells and B-lineage/myeloma subclones; antigen engagement activates CAR signaling, triggering T‑cell activation, cytokine release, and perforin/granzyme-mediated cytotoxicity to eradicate tumor cells and reduce antigen escape.
CAR T cells bind CD19 via the CAR; antigen engagement activates the T cell to form an immunologic synapse and kill CD19+ cells via perforin/granzyme release (and death receptor pathways).