A humanized anti-HER2 monoclonal antibody that binds HER2 domain IV, inhibits signaling, and mediates ADCC.
Humanized monoclonal antibody targeting HER2 that binds domain IV on the HER2 receptor, inhibiting HER2-driven signaling (e.g., PI3K/AKT/MAPK) and preventing receptor activation/shed extracellular domain; its Fc engages immune effector cells via Fcγ receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on target cells and its Fc engages FcγR-bearing immune cells (e.g., NK cells) to mediate antibody‑dependent cellular cytotoxicity (ADCC), killing HER2+ cells; it may also trigger complement and inhibit survival signaling.
Claudin18.2-targeting antibody–drug conjugate; binds CLDN18.2 on tumor cells, is internalized, and releases a microtubule-disrupting cytotoxic payload causing tumor cell death.
Anti-CLDN18.2 monoclonal antibody linked via a cleavable linker to the microtubule-disrupting payload MMAE. After binding CLDN18.2 on tumor cells and internalization, MMAE is released to inhibit tubulin polymerization, inducing G2/M arrest and apoptosis in CLDN18.2-expressing cells; the antibody may also engage immune effector functions.
ADC binds CLDN18.2, is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in CLDN18.2-positive cells; Fc-mediated ADCC may also contribute.
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD19 for treatment of relapsed or refractory non-Hodgkin lymphoma.
Autologous T cells engineered to express a chimeric antigen receptor targeting CD19 on B cells. Antigen binding activates CAR signaling (CD3ζ plus costimulatory domains such as CD28 or 4-1BB), driving T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytolysis of CD19-positive malignant B cells.
CAR engagement of CD19 activates the engineered T cells to kill CD19+ cells via perforin/granzyme-mediated cytolysis (and related apoptotic pathways).
Autologous gene-modified T cells engineered to express a bivalent CAR targeting CD79b and CD19, administered as a single IV infusion to mediate cytotoxic killing of malignant B cells and reduce antigen escape.
Autologous gene-modified T cells expressing a bivalent CAR that binds CD19 and CD79b on malignant B cells; CAR engagement activates T-cell signaling, cytokine release, and cytotoxic killing, with dual targeting designed to limit antigen escape.
CAR T cells recognize CD19 on target cells, become activated, and kill them via perforin/granzyme release and death receptor pathways (e.g., Fas–FasL).
Autologous gene-modified T cells engineered to express a bivalent CAR targeting CD79b and CD19, administered as a single IV infusion to mediate cytotoxic killing of malignant B cells and reduce antigen escape.
Autologous gene-modified T cells expressing a bivalent CAR that binds CD19 and CD79b on malignant B cells; CAR engagement activates T-cell signaling, cytokine release, and cytotoxic killing, with dual targeting designed to limit antigen escape.
CAR T cells bind CD79b on malignant B cells via the CAR and directly lyse them through T-cell effector mechanisms (perforin/granzyme and death-receptor pathways) upon engagement.