Patient-derived T cells engineered to express a CAR targeting BCMA (TNFRSF17) on plasma cells; CAR signaling activates T cells to proliferate and kill BCMA-expressing multiple myeloma cells via cytotoxic mechanisms.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on plasma cells. BCMA engagement triggers CAR CD3zeta and co-stimulatory signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA-expressing multiple myeloma cells via HLA-independent recognition.
YES
DIRECT
CAR engagement of BCMA activates T cells to kill BCMA+ cells via perforin/granzyme-mediated cytotoxicity (and related apoptotic/lytic pathways).
A subcutaneous bispecific T-cell–engaging antibody that binds BCMA on malignant plasma cells and CD3 on T cells to redirect T-cell cytotoxicity.
Bispecific T‑cell–engaging antibody that binds BCMA on myeloma cells and CD3 on T cells, forming an immunologic synapse to activate T cells and induce targeted cytotoxic killing of BCMA‑expressing plasma cells.
YES
DIRECT
Elranatamab links CD3 on T cells to BCMA on target cells, activating T cells to form an immunologic synapse and kill BCMA-expressing cells via perforin/granzyme-mediated apoptosis (and Fas–FasL signaling).
A subcutaneous bispecific T-cell–engaging antibody that binds BCMA on malignant plasma cells and CD3 on T cells to redirect T-cell cytotoxicity.
Bispecific T‑cell–engaging antibody that binds BCMA on myeloma cells and CD3 on T cells, forming an immunologic synapse to activate T cells and induce targeted cytotoxic killing of BCMA‑expressing plasma cells.
NO
INDIRECT
Elranatamab binds CD3ε on T cells to activate and redirect them to BCMA+ myeloma cells, which are killed via T‑cell–mediated perforin/granzyme cytotoxicity; CD3+ T cells themselves are not targeted for killing.
Autologous dendritic cell vaccine pulsed with folate receptor alpha peptides, administered intradermally to prime and expand FRα-specific CD8+ and CD4+ T cells, enhance Th1/Th17 responses and anti-FRα IgG, promoting killing of FRα-positive ovarian tumor cells.
Autologous dendritic cells pulsed with folate receptor alpha peptides present FRα epitopes on MHC I/II to prime and expand FRα-specific CD8+ cytotoxic T cells and CD4+ Th1/Th17 responses, also inducing anti-FRα IgG, leading to immune-mediated killing of FRα-positive ovarian tumor cells.
YES
INDIRECT
The DC vaccine primes FRα-specific CD8+ T cells (with Th1 help). These CTLs recognize FRα-derived peptides on MHC I of tumor cells and kill them via perforin/granzyme (±Fas–FasL); induced anti-FRα IgG may also mediate ADCC.
An IV IgG-based bispecific immunotherapy antibody that conditionally agonizes CD28 on T cells when co-engaged with EGFR on tumor cells, localizing CD28 costimulation to EGFR-positive tumors to boost T-cell activation, proliferation, cytokine release, and cytotoxicity while limiting systemic immune activation.
IgG-based bispecific antibody that binds EGFR on tumor cells and CD28 on T cells to provide conditional CD28 costimulation only when both targets are engaged at the tumor site, enhancing T-cell activation, proliferation, cytokine release, and cytotoxicity against EGFR-positive tumors while limiting systemic immune activation.
YES
INDIRECT
The bispecific bridges EGFR on tumor cells and CD28 on T cells to provide localized CD28 costimulation, enhancing TCR-dependent T‑cell killing (e.g., perforin/granzyme, Fas/FasL) of EGFR-positive cells; the drug itself is not directly cytotoxic and does not redirect via CD3.