Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting B-cell antigens (CD19 and/or CD22 for B-ALL/B-NHL or BCMA for multiple myeloma) and to co-express interleukin-15 (IL-15) to enhance T-cell activation, proliferation, survival, and persistence for antitumor cytotoxicity.
Autologous T lymphocytes are engineered to express a chimeric antigen receptor targeting B‑cell antigens (CD19 and/or CD22, or BCMA). Antigen engagement triggers CAR/CD3ζ signaling, leading to T‑cell activation and cytotoxic killing of tumor cells via perforin/granzymes and cytokine release. Co‑expressed IL‑15 delivers autocrine IL‑15R–JAK/STAT signaling that enhances T‑cell activation, proliferation, survival, and persistence, improving antitumor efficacy.
NO
INDIRECT
IL-15 produced by the engineered T cells signals through IL-2Rβ (CD122) on the CAR T cells to boost their activation, proliferation, and persistence; the CAR T cells then kill CD19/CD22/BCMA-positive tumor cells via CAR/CD3ζ activation and perforin/granzyme-mediated lysis. IL-2Rβ-expressing cells are not the cytotoxic targets.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting B-cell antigens (CD19 and/or CD22 for B-ALL/B-NHL or BCMA for multiple myeloma) and to co-express interleukin-15 (IL-15) to enhance T-cell activation, proliferation, survival, and persistence for antitumor cytotoxicity.
Autologous T lymphocytes are engineered to express a chimeric antigen receptor targeting B‑cell antigens (CD19 and/or CD22, or BCMA). Antigen engagement triggers CAR/CD3ζ signaling, leading to T‑cell activation and cytotoxic killing of tumor cells via perforin/granzymes and cytokine release. Co‑expressed IL‑15 delivers autocrine IL‑15R–JAK/STAT signaling that enhances T‑cell activation, proliferation, survival, and persistence, improving antitumor efficacy.
NO
INDIRECT
CAR T cells kill CD19/CD22/BCMA-expressing tumor cells via perforin/granzyme cytotoxicity. CD132 is part of the IL-15 receptor used for autocrine support of the CAR T cells; cells expressing CD132 are not targeted or killed.
Autologous dual-target CAR-T cell therapy engineered to express CARs recognizing BCMA and CD19; administered as a single IV infusion after lymphodepleting chemotherapy to drive antigen-specific T-cell activation and cytotoxicity against malignant plasma cells and B-cell lineage progenitors.
Autologous T cells engineered to express dual chimeric antigen receptors recognizing BCMA and CD19; upon binding BCMA/CD19 on malignant plasma cells and B-lineage cells, CAR signaling (CD3ζ with co-stimulatory costimulation) activates T-cell proliferation, cytokine release, and cytotoxic killing, eliminating BCMA+ myeloma cells and CD19+ progenitors to reduce antigen escape.
YES
DIRECT
Dual CAR-T cells recognize BCMA on target cells and, upon CAR signaling, directly kill them via T-cell effector mechanisms (perforin/granzyme release and death-receptor pathways).
Autologous dual-target CAR-T cell therapy engineered to express CARs recognizing BCMA and CD19; administered as a single IV infusion after lymphodepleting chemotherapy to drive antigen-specific T-cell activation and cytotoxicity against malignant plasma cells and B-cell lineage progenitors.
Autologous T cells engineered to express dual chimeric antigen receptors recognizing BCMA and CD19; upon binding BCMA/CD19 on malignant plasma cells and B-lineage cells, CAR signaling (CD3ζ with co-stimulatory costimulation) activates T-cell proliferation, cytokine release, and cytotoxic killing, eliminating BCMA+ myeloma cells and CD19+ progenitors to reduce antigen escape.
YES
DIRECT
CAR-T cells bind CD19 on target cells, triggering CD3ζ/co-stimulatory signaling and T-cell effector functions that kill via perforin/granzyme-mediated cytolysis and Fas/FasL-induced apoptosis.
Fully human IgG1-like bispecific monoclonal antibody targeting EGFR and MET for dual receptor blockade with potential Fc-mediated effector functions.
Fully human IgG1-like bispecific monoclonal antibody that binds EGFR and MET to block ligand binding and receptor activation, suppressing downstream signaling (e.g., MAPK and PI3K/AKT) with potential Fc-mediated effector functions such as ADCC/ADCP against target-expressing tumor cells.
YES
DIRECT
IgG1-like Fc engages Fcγ receptors on NK cells/macrophages to mediate ADCC/ADCP against EGFR-expressing cells; signaling blockade may add apoptotic pressure.