Autologous CD19-directed chimeric antigen receptor T-cell (CAR-T) therapy produced via the PrimeCAR platform (~3-day manufacturing) with a high T-naive cell fraction; administered as a single IV infusion after lymphodepletion to treat relapsed/refractory CD19+ B-cell non-Hodgkin lymphoma. Mechanism: engineered T cells expressing a CD19-binding CAR activate via CD3ζ, proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxicity against CD19+ B cells.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor; upon binding CD19 on B cells, the CAR signals via CD3ζ to activate and expand the T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of CD19+ malignant and normal B cells.
CD19 CAR-T cells bind CD19 on B cells, signal via CD3ζ, and directly lyse CD19+ cells through perforin/granzyme (and death receptor) pathways.
An antibody–drug conjugate composed of a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (irinotecan’s active metabolite), delivering a topoisomerase I inhibitor to Trop-2–expressing tumor cells to induce DNA single-strand breaks and apoptosis.
Humanized anti–Trop-2 monoclonal antibody linked to SN-38 (irinotecan’s active metabolite). The antibody binds Trop-2 on tumor cells, is internalized, and the linker is cleaved to release SN-38, which inhibits topoisomerase I by stabilizing Topo I–DNA complexes, causing DNA single-strand breaks, replication arrest, and apoptosis; may also exert a bystander cytotoxic effect.
ADC binds TROP2 on tumor cells, is internalized, and releases SN-38 intracellularly to inhibit topoisomerase I, causing DNA damage, replication arrest, and apoptosis (with possible bystander killing).
Recombinant humanized bispecific anti-HER2 IgG monoclonal antibody that binds two distinct HER2 epitopes to block HER2 homo/heterodimerization and signaling; mediates Fcγ-dependent ADCC.
Recombinant humanized bispecific anti‑HER2 IgG that binds two non‑overlapping HER2 epitopes to block HER2 homo/heterodimerization and downstream signaling (PI3K/AKT/MAPK) and mediates Fcγ receptor–dependent ADCC against HER2‑overexpressing tumor cells.
Anti-HER2 bispecific IgG binds HER2 on target cells and engages Fcγ receptors on NK cells/macrophages to trigger antibody-dependent cellular cytotoxicity (ADCC), leading to lysis/apoptosis of HER2+ cells; also blocks HER2 signaling.
Anti-HER2 IgG monoclonal antibody (binds domain II) that prevents HER2 dimerization and induces ADCC.
Humanized anti‑HER2 IgG1 monoclonal antibody that binds HER2 extracellular domain II, blocking HER2 homo/heterodimerization and downstream PI3K/AKT/MAPK signaling, and engaging Fcγ receptors to mediate antibody‑dependent cellular cytotoxicity (ADCC), leading to tumor cell growth inhibition and apoptosis.
Anti‑HER2 IgG1 binds HER2 and engages Fcγ receptors on NK cells/other effectors to trigger ADCC, killing HER2+ cells; HER2 signaling blockade can also promote apoptosis.
Anti-HER2 IgG monoclonal antibody (binds domain IV) that inhibits HER2 signaling and induces ADCC.
Humanized IgG1 monoclonal antibody against HER2 (binds domain IV) that blocks HER2 signaling/dimerization and downstream PI3K/AKT/MAPK pathways, inhibits HER2 ectodomain shedding, and triggers Fcγ-mediated ADCC against HER2-overexpressing tumor cells.
Binds HER2 on target cells and engages Fcγ receptors on effector cells (e.g., NK cells) to trigger antibody‑dependent cellular cytotoxicity, killing HER2+ cells (with some complement activation possible).