A TROP2-targeted antibody–drug conjugate (SKB264/MK-2870) composed of a humanized anti-TROP2 monoclonal antibody linked to a camptothecin-class topoisomerase I inhibitor payload. After binding TROP2 on urothelial carcinoma cells and internalization, it releases the payload to inhibit topoisomerase I, causing DNA single-strand breaks, replication stress, S-phase arrest, and apoptosis; a bystander effect may occur. Administered intravesically in this trial.
Humanized anti‑TROP2 IgG1 ADC that binds TROP2 on tumor cells, is internalized, and releases the camptothecin‑class topoisomerase I inhibitor tirumotecan via cleavable linker, causing topoisomerase I inhibition, DNA single‑strand breaks, S‑phase arrest, and apoptosis, with a potential bystander effect.
ADC binds TROP2 on tumor cells, is internalized, and releases the topoisomerase I inhibitor tirumotecan via a cleavable linker, causing DNA single-strand breaks, S-phase arrest, and apoptosis (with possible bystander effect).
Intravenous bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-lineage leukemia cells and CD3 on T cells, redirecting endogenous T cells to eliminate CD19+ blasts via immune-synapse formation and perforin/granzyme-mediated cytotoxicity.
A bispecific single-chain antibody construct (BiTE) that binds CD19 on B-lineage cells and CD3 on T cells, bringing them together to form an immune synapse and activate T cells, leading to perforin/granzyme-mediated cytotoxic killing of CD19-positive leukemia cells.
Blinatumomab bridges CD19+ cells to CD3+ T cells, activating T cells to kill the CD19-expressing cells via perforin/granzyme-mediated cytotoxicity.
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting GD2; infused intravenously to kill GD2-positive diffuse midline glioma cells.
Autologous T cells engineered to express a chimeric antigen receptor specific for GD2 bind GD2 on tumor cells and, upon CAR signaling, activate T-cell effector functions (granzyme/perforin-mediated cytotoxicity and cytokine release) to kill GD2-positive diffuse midline glioma cells.
GD2 CAR T cells bind GD2 on target cells and, upon CAR signaling, kill them via perforin/granzyme-mediated cytotoxicity (with contributory cytokine/Fas–FasL pathways).
Autologous T cells engineered to express a CD19-directed chimeric antigen receptor; administered intraventricularly as an adjunct/rescue dose to deplete CD19-positive B cells.
Autologous T cells are gene‑modified to express a chimeric antigen receptor specific for CD19. Upon binding CD19 on B cells, the CAR provides activation and costimulatory signals that trigger T‑cell cytotoxicity (perforin/granzyme) and cytokine release, leading to targeted depletion of CD19‑positive B cells; in this study, administered intraventricularly as an adjunct/rescue dose.
CAR engagement of CD19 activates the infused T cells, which kill CD19+ cells via perforin/granzyme-mediated cytotoxicity (and Fas/FasL apoptosis).
TROP2-targeted antibody-drug conjugate delivering a topoisomerase I inhibitor payload; binds TROP2 on tumor cells, internalizes, and releases cytotoxin to induce DNA damage and apoptosis (with potential bystander effect).
TROP2-targeted antibody–drug conjugate; binds TROP2 on tumor cells, is internalized, and releases a cleavable topoisomerase I inhibitor payload (tirumotecan) that inhibits Topo I, inducing DNA damage, replication arrest, and apoptosis, with potential bystander killing.
ADC binds TROP2 on target cells, is internalized, and releases a topoisomerase I inhibitor payload that induces DNA damage/replication arrest, leading to apoptosis (with possible bystander killing).