Anti-HER2 (ERBB2) monoclonal antibody that binds HER2 on tumor cells, inhibits HER2 signaling, and induces antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody targeting HER2/ERBB2; binds HER2 on tumor cells, inhibits HER2 signaling and receptor dimerization, and triggers antibody-dependent cellular cytotoxicity (ADCC), leading to tumor cell death.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and recruits FcγR-expressing effector cells to mediate ADCC; it also inhibits HER2 signaling, promoting apoptosis.
An intravenous bispecific T‑cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells to redirect T cells and induce cytotoxic killing in DLL3‑expressing neuroendocrine cancers.
Obrixtamig (BI 764532) is an intravenous bispecific antibody that binds DLL3 on tumor cells and CD3 on T cells, physically bridging them to activate CD3/TCR signaling and redirect T‑cell cytotoxicity (perforin/granzyme and cytokines) to kill DLL3‑expressing neuroendocrine cancer cells.
YES
DIRECT
DLL3×CD3 bispecific antibody redirects T cells to DLL3+ cells, activating CD3/TCR and inducing perforin/granzyme-mediated cytolysis (and cytokine effects) of target cells.
An intravenous bispecific T‑cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells to redirect T cells and induce cytotoxic killing in DLL3‑expressing neuroendocrine cancers.
Obrixtamig (BI 764532) is an intravenous bispecific antibody that binds DLL3 on tumor cells and CD3 on T cells, physically bridging them to activate CD3/TCR signaling and redirect T‑cell cytotoxicity (perforin/granzyme and cytokines) to kill DLL3‑expressing neuroendocrine cancer cells.
NO
INDIRECT
The bispecific antibody binds CD3 on T cells to activate and redirect them to DLL3+ tumor cells, which are killed via perforin/granzyme-mediated cytotoxicity; CD3+ T cells are not killed.
Etentamig (ABBV-383; TNB-383B) is an intravenous bispecific T-cell–redirecting antibody that binds BCMA on plasma cells and CD3 on T cells to activate cytotoxic T cells and eliminate BCMA+ plasma cells, reducing amyloidogenic light chains.
Bispecific IgG4 antibody that binds BCMA on plasma cells and CD3 on T cells, creating an immune synapse that activates and redirects cytotoxic T cells to kill BCMA-expressing cells, thereby reducing amyloidogenic light-chain production (with low CD3 activation to limit cytokine release).
YES
DIRECT
Bispecific antibody binds BCMA on target cells and CD3 on T cells, forming an immune synapse that activates cytotoxic T cells to kill BCMA+ cells via perforin/granzyme-mediated apoptosis.
Autologous peripheral blood T cells engineered with the Sleeping Beauty transposon/transposase to express patient-specific TCRs recognizing mutated neoantigens; adoptive cellular gene therapy mediating HLA-restricted tumor cell killing.
Autologous peripheral blood T cells are genetically modified using the Sleeping Beauty transposon/transposase system to express patient-specific TCRs that recognize mutated neoantigen peptides presented by HLA on tumor cells. Upon infusion, TCR–HLA engagement activates the T cells to mediate targeted, HLA-restricted tumor cell killing via cytotoxic effector mechanisms (perforin/granzyme) and cytokine release.
YES
DIRECT
Engineered TCR-T cells recognize the patient-specific mutated neoantigen peptide presented by HLA on target cells and induce HLA-restricted killing via perforin/granzyme–mediated apoptosis (and related cytotoxic pathways).