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.
Anti-CD22 CAR T cells bind CD22 on target cells, triggering CAR/CD3zeta signaling and T-cell cytolysis via perforin/granzyme (and Fas-FasL) pathways; IL-15 enhances T-cell activation and persistence.
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.
CAR T cells recognize BCMA via the CAR, triggering CD3ζ signaling and T-cell effector functions that kill BCMA+ cells via perforin/granzyme-mediated cytolysis (with supportive cytokine-mediated apoptosis).
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.
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.
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.
IgG1-like Fc engages Fcγ receptors on NK cells/macrophages to mediate ADCC/ADCP against EGFR-expressing cells; signaling blockade may add apoptotic pressure.