A patient-specific neoantigen peptide vaccine designed to elicit anti-tumor immunity by promoting dendritic cell/MHC presentation of tumor-derived neoantigens, priming and expanding tumor-specific CD8+ cytotoxic and CD4+ helper T cells and generating immune memory.
Patient-specific tumor neoantigen peptides are taken up by dendritic cells and presented on MHC class I and II, priming and expanding neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells to mediate tumor cell killing and establish durable immune memory.
NO
INDIRECT
Neoantigen peptides presented by dendritic cells activate TCRs on CD8+ T cells, which then kill tumor cells presenting the neoantigens via perforin/granzyme; TCR-expressing T cells are activated, not targeted for killing.
Intravenous anti‑SLAMF7 monoclonal antibody that enhances NK‑cell–mediated ADCC and immune activation in multiple myeloma.
Humanized monoclonal antibody against SLAMF7 (CS1) that binds SLAMF7 on myeloma cells and NK cells, promoting NK cell–mediated antibody-dependent cellular cytotoxicity via FcγR engagement and directly activating NK cells through SLAMF7 signaling to enhance immune-mediated tumor cell killing.
YES
INDIRECT
Elotuzumab binds SLAMF7 on tumor cells; its Fc engages FcγRIIIa on NK cells to trigger NK cell–mediated ADCC, with additional NK activation via SLAMF7 signaling, leading to lysis of SLAMF7+ cells.
Autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are genetically engineered to express a CAR (with CD3ζ and costimulatory domains) that binds CD19; engagement triggers T-cell activation, proliferation, and perforin/granzyme-mediated cytotoxicity, eliminating CD19+ malignant B cells and causing expected B-cell aplasia. Administered by intravenous autotransfusion for relapsed/refractory CD19+ B-ALL/B-lymphoblastic lymphoma.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor containing CD3ζ and costimulatory domains. Upon binding CD19 on malignant B cells, the CAR triggers T-cell activation, expansion, and perforin/granzyme-mediated cytotoxicity, eliminating CD19+ cells and causing on‑target B‑cell aplasia.
YES
DIRECT
CAR T cells bind CD19 and kill target cells via T-cell activation with perforin/granzyme-mediated cytolysis (and Fas/FasL), causing elimination of CD19+ cells.
Autologous CD19-directed CAR T-cell therapy. Patient T cells are modified to express a CAR with CD3ζ and costimulatory domains; upon binding CD19 on malignant B cells, they activate, expand, and kill targets via perforin/granzyme pathways, leading to depletion of CD19+ cells and B-cell aplasia. Given by intravenous autotransfusion for relapsed/refractory CD19+ B-ALL/B-lymphoblastic lymphoma.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor (CAR) containing CD3ζ and costimulatory domains. Upon binding CD19 on malignant B cells, CAR signaling activates and expands the T cells, which mediate cytotoxicity via perforin/granzyme, leading to targeted elimination of CD19+ cells and on‑target B‑cell aplasia.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target cells, become activated, form an immune synapse, and kill via perforin/granzyme–mediated cytolysis (and Fas/FasL apoptosis).
Autologous CD19-directed CAR T-cell therapy. Engineered patient T cells express a CAR (CD3ζ with costimulatory domains) that recognizes CD19; receptor engagement triggers CAR/TCR signaling, T-cell proliferation, and targeted cytotoxicity, eradicating CD19+ malignant B cells and producing on-target B-cell aplasia. Administered via intravenous autotransfusion for relapsed/refractory CD19+ B-ALL/B-lymphoblastic lymphoma.
Autologous T cells engineered to express a CD19-directed chimeric antigen receptor (CD3ζ with costimulatory domains). Binding to CD19 activates the CAR, driving T-cell activation, expansion, and perforin/granzyme-mediated cytotoxicity to eliminate CD19-positive malignant B cells, with expected on-target B-cell aplasia.
YES
DIRECT
CAR engagement of CD19 on target cells activates infused T cells, causing contact-dependent killing via perforin/granzyme (and Fas–FasL) pathways, lysing CD19+ cells.