Anti-HER2 IgG1 monoclonal antibody that blocks HER2 signaling, promotes receptor downregulation, and triggers antibody‑dependent cellular cytotoxicity (engaging NK cells).
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2); blocks HER2 signaling and dimerization, promotes receptor downregulation, and triggers antibody-dependent cellular cytotoxicity via Fc engagement of NK cells, leading to killing of HER2-overexpressing tumor cells.
NO
INDIRECT
Trastuzumab binds HER2 on tumor cells; its Fc engages FCGR3A (CD16A) on NK cells to trigger ADCC that kills HER2+ cells, not the CD16A-expressing cells.
Humanized IgG1 bispecific antibody targeting GPRC5D on myeloma/plasma cells and CD3 on T cells; administered subcutaneously to engage T cells and redirect cytotoxicity against GPRC5D-expressing malignant plasma cells in relapsed/refractory multiple myeloma.
Humanized IgG1 bispecific antibody that simultaneously binds GPRC5D on myeloma/plasma cells and CD3 on T cells, bringing T cells into proximity with tumor cells to form an immune synapse and activate T-cell mediated cytotoxicity against GPRC5D-expressing malignant plasma cells.
YES
DIRECT
Bispecific antibody binds GPRC5D on tumor cells and CD3 on T cells, forming an immune synapse that activates T-cell cytotoxicity (perforin/granzyme-mediated killing) of GPRC5D-expressing cells.
Humanized IgG1 bispecific antibody targeting GPRC5D on myeloma/plasma cells and CD3 on T cells; administered subcutaneously to engage T cells and redirect cytotoxicity against GPRC5D-expressing malignant plasma cells in relapsed/refractory multiple myeloma.
Humanized IgG1 bispecific antibody that simultaneously binds GPRC5D on myeloma/plasma cells and CD3 on T cells, bringing T cells into proximity with tumor cells to form an immune synapse and activate T-cell mediated cytotoxicity against GPRC5D-expressing malignant plasma cells.
NO
INDIRECT
CD3 on T cells is engaged to activate and redirect T cells, which then kill GPRC5D+ myeloma cells via immune synapse formation and perforin/granzyme-mediated lysis; CD3+ cells themselves are not targeted for killing.
CRISPR-edited, allogeneic anti-BCMA CAR T-cell therapy engineered from donor T cells to target BCMA on malignant plasma cells and induce T-cell–mediated cytotoxicity.
CRISPR-edited, allogeneic T cells engineered with an anti-BCMA chimeric antigen receptor bind BCMA on malignant plasma cells, triggering T‑cell activation and cytotoxic killing. TRAC knockout removes endogenous TCR to reduce graft‑versus‑host disease, while B2M knockout and insertion of a B2M–HLA‑E fusion minimize host T- and NK‑cell rejection, enhancing persistence and antitumor activity.
YES
DIRECT
Anti-BCMA CAR T cells recognize BCMA on target cells and induce T-cell–mediated killing via perforin/granzyme release and death-receptor pathways.
Allogeneic, genetically modified natural killer cells engineered to express an anti-BCMA chimeric antigen receptor that recognizes BCMA (TNFRSF17) on malignant plasma cells and triggers NK-mediated cytotoxicity and cytokine release to kill tumor cells.
Allogeneic NK cells engineered to express an anti-BCMA chimeric antigen receptor bind BCMA (TNFRSF17) on malignant plasma cells, activating NK and CAR signaling to induce perforin/granzyme-mediated cytotoxicity and cytokine release, resulting in tumor cell apoptosis.
YES
DIRECT
Anti-BCMA CAR-engineered NK cells bind BCMA on target cells, activate NK/CAR signaling, and kill through immune-synapse formation with perforin/granzyme-mediated cytolysis (and death-receptor pathways), inducing apoptosis.