Humanized IgG1 monoclonal antibody against EGFR that blocks EGF/TGF-α binding, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling and potentially mediating ADCC.
Humanized IgG1 monoclonal antibody targeting EGFR (HER1); blocks EGF/TGF-α binding to EGFR, preventing receptor activation and downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling, inhibiting tumor cell proliferation and survival; Fc may mediate ADCC against EGFR-expressing cells.
Fc-mediated ADCC by immune effector cells (e.g., NK cells) against EGFR-expressing cells; may also engage complement (CDC). Signaling blockade is mainly antiproliferative.
Autologous CAR T-cell therapy: patient T cells are genetically modified to express a chimeric antigen receptor targeting a B-cell surface antigen; given as a single IV infusion after lymphodepletion to activate cytotoxic T-cell responses and eliminate malignant B cells (with expected on-target B-cell aplasia).
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting CD19 on B cells. Upon binding CD19, CAR signaling (CD3ζ with co-stimulation) activates and expands the T cells, inducing cytotoxic killing of malignant B cells; administered after lymphodepletion, with expected on-target B-cell aplasia.
Anti-CD19 CAR T cells bind CD19, triggering CAR (CD3ζ + costimulation) activation and killing target B cells via perforin/granzyme-mediated cytolysis and apoptosis.
Anti-CLDN18.2 antibody–drug conjugate that binds claudin 18.2 on tumor cells, is internalized, and releases a cytotoxic payload to selectively kill CLDN18.2-positive cells.
An anti-CLDN18.2 IgG1 antibody linked via a cleavable linker to a topoisomerase I inhibitor; after binding CLDN18.2 on tumor cells, the ADC is internalized and the payload is released to inhibit topoisomerase I, blocking DNA replication and inducing cell-cycle arrest and apoptosis in CLDN18.2-positive cells.
The ADC binds CLDN18.2 on target cells, is internalized, and releases a topoisomerase I inhibitor that blocks DNA replication, leading to cell-cycle arrest and apoptosis.
Autologous BCMA-directed CAR T-cell therapy; engineered T cells target and kill BCMA-positive malignant plasma cells.
Autologous T cells engineered with a BCMA-directed chimeric antigen receptor recognize BCMA on malignant plasma cells and, upon antigen engagement, activate T‑cell cytotoxicity (perforin/granzyme release and cytokine signaling) to kill BCMA‑positive cells and mediate tumor clearance.
BCMA-directed CAR T cells bind BCMA on target cells and induce T‑cell cytotoxicity (perforin/granzyme-mediated lysis and related apoptotic signaling) to kill BCMA-positive cells.