Autologous gene-modified chimeric antigen receptor T-cell therapy; patient T cells engineered ex vivo to express a CAR targeting Nectin-4 (PVRL4) on tumor cells, enabling MHC-independent recognition, T-cell activation, cytokine release, and cytotoxic killing.
Autologous T cells are genetically engineered ex vivo to express a chimeric antigen receptor that recognizes Nectin-4 (PVRL4) on tumor cells. CAR engagement triggers CD3ζ/co-stimulatory signaling, leading to MHC-independent T-cell activation, cytokine release, expansion, and direct cytotoxic killing of Nectin-4–positive cancer cells.
CAR-T cells bind Nectin-4 on target cells and, via CD3ζ/co-stimulatory signaling, activate cytotoxic effector functions (perforin/granzyme release and death-receptor pathways) to lyse Nectin-4–positive cells.
A TROP2-targeting antibody-drug conjugate with a topoisomerase I inhibitor payload; binds TROP2 on tumor cells, is internalized, and releases the payload to induce DNA damage (with potential bystander effect).
TROP2-directed monoclonal antibody linked to a topoisomerase I inhibitor payload; upon binding TROP2 on tumor cells the ADC is internalized and releases the payload, inhibiting topoisomerase I to induce DNA damage and tumor cell death, with potential bystander effect.
The anti-TROP2 ADC binds TROP2, is internalized, and releases a topoisomerase I inhibitor payload that induces DNA damage and tumor cell death (with potential bystander effect).
Autologous, gene-modified CD22-directed CAR T-cell therapy; engineered T cells activate upon CD22 engagement to proliferate and kill CD22+ B-cell lymphoma cells; may cause B-cell aplasia.
Autologous T cells engineered to express a CD22-directed chimeric antigen receptor. Upon binding CD22 on B-cell lymphoma cells, CAR signaling (CD3zeta plus costimulatory domains) activates the T cells, driving proliferation, cytokine release, and perforin/granzyme-mediated killing of CD22+ cells, often causing on-target B-cell aplasia.
CD22-directed CAR T cells bind CD22 on target cells and, upon activation, kill them via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Allogeneic, off-the-shelf induced pluripotent stem cell–derived natural killer cells engineered with a chimeric antigen receptor targeting CLL1 (CLEC12A) on AML blasts to redirect NK recognition and trigger cytotoxic killing via perforin/granzyme and death-receptor pathways while sparing normal hematopoietic stem cells.
Allogeneic iPSC-derived natural killer cells engineered with a chimeric antigen receptor targeting CLL1 (CLEC12A) on AML blasts, redirecting NK recognition to CLL1-positive leukemic cells and inducing cytotoxic killing via perforin/granzyme release and death receptor pathways (e.g., FasL/TRAIL), with intent to spare normal hematopoietic stem cells due to low/absent CLL1 expression.
CAR-engineered NK cells recognize CLL1 on target cells and kill them via NK effector functions, including perforin/granzyme-mediated lysis and death-receptor pathways (FasL/TRAIL).
Allogeneic, off-the-shelf induced pluripotent stem cell–derived natural killer cells engineered with a chimeric antigen receptor targeting CD33 (Siglec-3) on AML blasts to redirect NK recognition and trigger cytotoxic killing via perforin/granzyme and death-receptor pathways while sparing normal hematopoietic stem cells.
Allogeneic iPSC-derived natural killer cells engineered with an anti-CD33 chimeric antigen receptor bind CD33 on AML blasts, redirecting NK activation to induce cytotoxic killing via degranulation (perforin/granzyme) and death-receptor pathways (e.g., FasL/TRAIL), with intent to spare normal hematopoietic stem cells with low/absent CD33 expression.
CAR-engineered NK cells bind CD33 on target cells, triggering NK activation and killing via degranulation (perforin/granzyme) and death-receptor pathways (FasL/TRAIL).