A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-ALL cells and CD3 on T cells to redirect T-cell cytotoxicity against CD19-positive leukemic blasts.
A BiTE antibody construct that simultaneously binds CD19 on B-lineage cells and CD3 on T cells, physically bridging T cells to CD19+ targets to trigger T-cell activation and cytolytic killing (perforin/granzyme–mediated) of CD19-expressing leukemic blasts independent of native TCR specificity.
Blinatumomab bridges CD3+ T cells to CD19+ cells, activating T-cell cytotoxicity and perforin/granzyme-mediated killing of CD19-expressing targets.
A humanized, full-length bispecific IgG2 kappa antibody (Elrexfio) that redirects T cells by binding BCMA on multiple myeloma cells and CD3 on T cells, forming an immune synapse to activate TCR/CD3 signaling and induce T cell–mediated cytotoxicity and cytokine release against BCMA-positive cells.
Elranatamab is a humanized bispecific antibody that binds BCMA on multiple myeloma cells and CD3 on T cells, crosslinking them to form an immune synapse, activate TCR/CD3 signaling, and induce T cell–mediated cytotoxicity and cytokine release against BCMA-positive cells.
Elranatamab bridges CD3+ T cells to BCMA-expressing cells, forming an immune synapse that activates T cells to kill the target via perforin/granzyme-mediated cytolysis and apoptosis.
An autologous NKG2D-based CAR T-cell therapy in which patient T cells are gene-engineered to express a chimeric antigen receptor using the NKG2D receptor ectodomain fused to intracellular activation/costimulatory domains (e.g., CD3ζ). The cells target stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumor cells to mediate cytotoxicity and cytokine release.
Autologous T cells are engineered to express an NKG2D-based CAR (NKG2D ectodomain fused to 4-1BB and CD3ζ signaling domains) that recognizes stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumors, activating T cells to release cytokines and mediate perforin/granzyme-dependent cytotoxicity against NKG2DL-positive cancer cells.
NKG2D-CAR T cells bind ULBP4 on target cells, become activated, and kill the engaged cells via perforin/granzyme-mediated cytotoxicity (with associated cytokine release).
An engineered bispecific IgM T-cell–engaging antibody administered intravenously that binds CD38 on myeloma cells and CD3 on T cells, redirecting T cells to mediate T-cell–dependent cellular cytotoxicity and triggering complement-dependent cytotoxicity.
Engineered bispecific IgM antibody that binds CD38 on tumor cells and CD3 on T cells, crosslinking to redirect T cells for T-cell-dependent cellular cytotoxicity; the IgM format also activates complement to mediate complement-dependent cytotoxicity against CD38-positive cells.
Bispecific IgM binds CD38 on target cells and CD3 on T cells to redirect T-cell cytotoxicity, and its IgM format activates complement to mediate complement-dependent lysis of CD38+ cells.
IV investigational immunotherapy; the specific cellular target and mechanism are not disclosed in the trial record.
Anti-5T4 monoclonal antibody linked to the microtubule-disrupting payload monomethyl auristatin E (MMAE). After binding to 5T4-expressing tumor cells and internalization, MMAE inhibits tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis; 5T4 is overexpressed on many tumors with limited normal tissue expression.
An anti-5T4 antibody-drug conjugate binds 5T4 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis of 5T4-expressing cells.