Off-the-shelf allogeneic CAR NK cell therapy with a logic-gated NOT design targeting CD33 and/or FLT3 and an inhibitory CAR to spare healthy cells; includes IL-15 support to enhance NK persistence/function for AML/MDS.
Off-the-shelf allogeneic NK cells engineered with an OR-gated activating CAR targeting CD33 and/or FLT3 and a NOT-gated inhibitory CAR recognizing EMCN to spare healthy hematopoietic stem cells; includes calibrated-release IL-15 to enhance NK persistence and function. Antigen engagement triggers NK activation and cytolytic killing of CD33/FLT3-positive AML/MDS cells while minimizing on-target/off-tumor toxicity.
NO
INDIRECT
SENTI-202 CAR-NK cells kill CD33 or FLT3 positive cells via CAR-triggered NK cytolysis (perforin/granzymes). IL-2Rβ (CD122) is not a targeted antigen; released IL-15 signals through CD122 to support immune cells rather than killing CD122+ cells.
Off-the-shelf allogeneic CAR NK cell therapy with a logic-gated NOT design targeting CD33 and/or FLT3 and an inhibitory CAR to spare healthy cells; includes IL-15 support to enhance NK persistence/function for AML/MDS.
Off-the-shelf allogeneic NK cells engineered with an OR-gated activating CAR targeting CD33 and/or FLT3 and a NOT-gated inhibitory CAR recognizing EMCN to spare healthy hematopoietic stem cells; includes calibrated-release IL-15 to enhance NK persistence and function. Antigen engagement triggers NK activation and cytolytic killing of CD33/FLT3-positive AML/MDS cells while minimizing on-target/off-tumor toxicity.
NO
INDIRECT
CD132 (common gamma chain) is part of the IL-15 receptor on NK cells; SENTI-202’s IL-15 stimulates NK cells via CD132 to enhance their killing of CD33/FLT3-positive tumor cells. Cells expressing CD132 are not targeted or directly killed.
Therapeutic monoclonal antibody–drug conjugates that bind cell-surface Trop2, internalize, and release a cytotoxic payload to kill Trop2-positive tumor cells.
Monoclonal antibody binds cell-surface Trop2 on tumor cells, undergoes receptor-mediated internalization, and linker cleavage releases an intracellular cytotoxic payload (e.g., topoisomerase I inhibitor), causing DNA damage and tumor cell death with potential bystander effect in Trop2-positive cancers.
YES
DIRECT
ADC binds Trop-2 on the cell surface, is internalized, and releases a cytotoxic payload (e.g., topoisomerase I inhibitor) that causes DNA damage and tumor cell death, with potential bystander killing.
Therapeutic monoclonal antibody–drug conjugates that bind cell-surface Trop2, internalize, and release a cytotoxic payload to kill Trop2-positive tumor cells.
Monoclonal antibody binds cell-surface Trop2 on tumor cells, undergoes receptor-mediated internalization, and linker cleavage releases an intracellular cytotoxic payload (e.g., topoisomerase I inhibitor), causing DNA damage and tumor cell death with potential bystander effect in Trop2-positive cancers.
NO
INDIRECT
The ADC binds Trop2 on the cell surface, is internalized, and releases a topoisomerase I–inhibiting payload that causes DNA damage and cell death. DNA topoisomerase I is the enzymatic target of the payload, but cells are selected for killing by Trop2 expression (with possible bystander effect), not by topoisomerase I expression.
Autologous CD19-directed CAR T-cell therapy (Relma-cel) in which patient T cells are gene-modified to express an anti-CD19 chimeric antigen receptor, leading to activation and lysis of CD19+ B-lineage cells to deplete B cells and modulate autoimmunity.
Autologous T cells are genetically engineered to express an anti-CD19 chimeric antigen receptor with costimulatory domains. After infusion, the CAR T cells recognize CD19 on B-lineage cells, activate, proliferate, secrete cytotoxic molecules and cytokines, and lyse CD19+ cells, leading to profound B-cell depletion (for malignant or autoreactive B-cell elimination).
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target B cells, activate, and kill them via perforin/granzyme-mediated cytolysis (and related effector mechanisms).