CD47-blocking SIRPa–Fc fusion protein (myeloid checkpoint inhibitor) that disrupts CD47–SIRPa signaling to enhance macrophage phagocytosis and dendritic cell antigen presentation.
CD47-blocking SIRPa–Fc fusion protein (myeloid checkpoint inhibitor) that binds CD47 on tumor cells, blocks CD47–SIRPa signaling to remove the anti-phagocytic "don’t-eat-me" signal, enhances macrophage phagocytosis and dendritic cell antigen presentation, and promotes downstream anti-tumor T-cell responses.
YES
INDIRECT
CD47 blockade removes SIRPa-mediated 'don't eat me' signaling, enabling macrophage phagocytosis of CD47+ cells and promoting downstream T-cell–mediated killing.
CD3/CD19 bispecific T-cell engager (BiTE) that redirects CD3+ T cells to kill CD19+ B-precursor leukemia cells.
A CD3/CD19 bispecific T‑cell engager (BiTE) that binds CD3 on T cells and CD19 on B‑lineage leukemia/lymphoma cells, forming an immunologic synapse that activates T cells to kill CD19+ targets via perforin/granzyme release and cytokine-mediated cytotoxicity, independent of MHC.
YES
DIRECT
Blinatumomab bridges CD3+ T cells to CD19+ cells, forming an immunologic synapse that triggers T‑cell perforin/granzyme release and cytokine-mediated killing (MHC-independent).
Oral, selective BCL-2 inhibitor (BH3 mimetic) that induces apoptosis.
Selective BCL-2 inhibitor (BH3 mimetic) that binds and neutralizes anti-apoptotic BCL-2, displacing pro-apoptotic proteins to restore mitochondrial apoptosis and induce cancer cell death.
YES
DIRECT
Selective BH3-mimetic inhibition of BCL-2 in target cells releases pro-apoptotic proteins, activates BAX/BAK, induces mitochondrial outer membrane permeabilization, caspase activation, and apoptotic cell death.
CD3/CD19 bispecific T-cell engager (BiTE) that redirects CD3+ T cells to kill CD19+ B-precursor leukemia cells.
A CD3/CD19 bispecific T‑cell engager (BiTE) that binds CD3 on T cells and CD19 on B‑lineage leukemia/lymphoma cells, forming an immunologic synapse that activates T cells to kill CD19+ targets via perforin/granzyme release and cytokine-mediated cytotoxicity, independent of MHC.
NO
INDIRECT
Blinatumomab binds CD3ε on T cells to activate/redirect them to CD19+ cells; T cells then kill CD19+ targets via perforin/granzyme. CD3+ cells are not directly killed.
Autologous T cells genetically modified to express a chimeric antigen receptor targeting B-cell maturation antigen (BCMA/TNFRSF17) on multiple myeloma cells, enabling antigen-specific T-cell activation and cytotoxicity.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds BCMA (TNFRSF17) on multiple myeloma cells, leading to antigen-specific T‑cell activation, proliferation, cytokine release, and cytotoxic killing of BCMA‑expressing tumor cells.
YES
DIRECT
BCMA-specific CAR-T cells bind BCMA on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis and apoptosis (including death-receptor pathways).