Autologous, genetically engineered CAR T-cell therapy that dual-targets CD19 and CD22 to deplete malignant B cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors that recognize CD19 and CD22 on B cells. Upon antigen engagement, the CAR T cells activate, proliferate, release cytokines, and kill malignant B cells via cytotoxic mechanisms (perforin/granzyme), leading to depletion of CD19+/CD22+ tumor cells and on-target B-cell aplasia.
CAR T cells recognize CD22 on target cells and induce cytolysis via perforin/granzyme and apoptosis pathways after CAR engagement.
Allogeneic, cord blood–derived, gene-modified NK cell therapy expressing an affinity-enhanced TCR specific for NY-ESO-1 peptide presented by HLA-A*02 and engineered to secrete IL-15 to enhance survival and persistence; intended to recognize and kill NY-ESO-1–positive tumor cells.
Allogeneic cord blood–derived NK cells are gene-modified to express an affinity‑enhanced TCR specific for the NY‑ESO‑1 peptide presented by HLA‑A*02, enabling antigen-specific recognition of NY‑ESO‑1–positive tumor cells. Upon engagement, the cells mediate cytotoxic killing via TCR-driven activation and NK effector mechanisms. Engineered autocrine IL‑15 secretion supports NK cell survival, proliferation, and persistence in vivo.
Engineered NK cells expressing an NY-ESO-1–specific, HLA-A*02–restricted TCR recognize peptide–HLA on target cells and directly kill them via cytotoxic degranulation (perforin/granzymes) and death-receptor pathways.
TROP2-targeted antibody–drug conjugate delivering a topoisomerase I inhibitor payload to TROP2-expressing tumor cells, leading to DNA damage and tumor cell death after internalization.
Anti-TROP2 monoclonal antibody linked to a topoisomerase I inhibitor; binds TROP2 on tumor cells, is internalized, and releases the cytotoxic payload to inhibit topoisomerase I, causing DNA damage and tumor cell death.
The ADC binds TROP2 on target cells, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage (leading to apoptosis), directly killing TROP2-expressing cells.
Genetically engineered natural killer cells expressing a CD19-specific chimeric antigen receptor; designed to bind CD19 on B-ALL cells and trigger NK-mediated cytotoxicity.
Genetically engineered natural killer cells expressing a CD19-specific chimeric antigen receptor bind CD19 on malignant B cells, redirecting and activating NK effector functions (perforin/granzyme-mediated cytotoxicity and cytokine release) to selectively lyse CD19-positive B-ALL cells, independent of MHC.
CD19-specific CAR-NK cells bind CD19 on target cells, triggering NK activation and direct lysis via perforin/granzyme-mediated cytotoxicity.
Donor-derived memory T cells genetically engineered to express an NKG2D-based chimeric antigen receptor targeting stress-induced NKG2D ligands (MICA/MICB/ULBPs) on tumor cells, intended to trigger T-cell cytotoxicity and overcome immune evasion; administered intravenously with optional intratumoral injection after lymphodepleting conditioning.
Donor-derived memory T cells are genetically engineered to express an NKG2D-based chimeric antigen receptor that recognizes stress-induced NKG2D ligands (MICA/MICB/ULBPs) on tumor cells, leading to CAR-mediated T-cell activation, cytokine release, and targeted cytotoxic killing, with the memory phenotype supporting persistence and the approach aiming to overcome tumor immune evasion.
NKG2D-CAR T cells recognize MICA on target cells, form an immune synapse, and mediate T-cell cytotoxicity via perforin/granzyme release (and Fas–FasL), leading to apoptosis of the MICA+ cell.