A bispecific antibody–drug conjugate targeting EGFR and HER3 that delivers a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific EGFR/HER3-targeted antibody–drug conjugate that binds EGFR- and HER3-expressing tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor (brengitecan) to induce DNA damage and tumor cell death, with potential bystander effect.
YES
DIRECT
The bispecific ADC binds HER3 on target cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and cell death (with potential bystander effect).
A bispecific antibody–drug conjugate targeting EGFR and HER3 that delivers a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific EGFR/HER3-targeted antibody–drug conjugate that binds EGFR- and HER3-expressing tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor (brengitecan) to induce DNA damage and tumor cell death, with potential bystander effect.
NO
INDIRECT
The ADC binds EGFR/HER3 on tumor cells, is internalized, and releases the topoisomerase I–inhibiting payload (brengitecan) to induce DNA damage and cell death; DNA topoisomerase I is the intracellular enzyme inhibited, not the antigen targeted by the antibody.
Autologous, genetically engineered anti-CD19 chimeric antigen receptor (CAR) T-cell therapy that co-expresses and secretes human interleukin-18 (armored CAR). Designed for relapsed/refractory CD19+ non-Hodgkin lymphomas to mediate antigen-specific cytotoxicity against B-cell malignancies, while IL-18 enhances CAR-T expansion/persistence and induces a Th1-skewed proinflammatory environment (enhancing IFN-γ and activating NK cells and macrophages). Administered as a single IV infusion with dose escalation.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor and to secrete IL-18. CAR engagement of CD19 on B-cell malignancies triggers antigen-specific T-cell activation and cytolysis, while IL-18 secretion enhances CAR-T expansion and persistence and creates a Th1-skewed proinflammatory milieu, increasing IFN-γ and activating NK cells and macrophages.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19, activate, and kill target cells via perforin/granzyme-mediated cytolysis (with IL-18 enhancing CAR-T expansion and activity).
Autologous, genetically engineered anti-CD19 chimeric antigen receptor (CAR) T-cell therapy that co-expresses and secretes human interleukin-18 (armored CAR). Designed for relapsed/refractory CD19+ non-Hodgkin lymphomas to mediate antigen-specific cytotoxicity against B-cell malignancies, while IL-18 enhances CAR-T expansion/persistence and induces a Th1-skewed proinflammatory environment (enhancing IFN-γ and activating NK cells and macrophages). Administered as a single IV infusion with dose escalation.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor and to secrete IL-18. CAR engagement of CD19 on B-cell malignancies triggers antigen-specific T-cell activation and cytolysis, while IL-18 secretion enhances CAR-T expansion and persistence and creates a Th1-skewed proinflammatory milieu, increasing IFN-γ and activating NK cells and macrophages.
NO
INDIRECT
The CAR-T cells kill CD19+ targets via CAR-mediated T-cell cytolysis. Secreted IL-18 binds IL-18Rα to activate immune cells and enhance responses, but IL-18Rα-expressing cells are not targeted or directly killed by the therapy.
Autologous, genetically engineered anti-CD19 chimeric antigen receptor (CAR) T-cell therapy that co-expresses and secretes human interleukin-18 (armored CAR). Designed for relapsed/refractory CD19+ non-Hodgkin lymphomas to mediate antigen-specific cytotoxicity against B-cell malignancies, while IL-18 enhances CAR-T expansion/persistence and induces a Th1-skewed proinflammatory environment (enhancing IFN-γ and activating NK cells and macrophages). Administered as a single IV infusion with dose escalation.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor and to secrete IL-18. CAR engagement of CD19 on B-cell malignancies triggers antigen-specific T-cell activation and cytolysis, while IL-18 secretion enhances CAR-T expansion and persistence and creates a Th1-skewed proinflammatory milieu, increasing IFN-γ and activating NK cells and macrophages.
NO
INDIRECT
TmCD19-IL18 CAR T cells kill CD19+ targets via CAR-mediated cytolysis. IL-18 secretion signals through IL-18 receptors (including IL-18Rβ) to activate immune cells and enhance responses, but does not render IL-18Rβ-expressing cells cytotoxic targets.