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.
NO
INDIRECT
LM-302 binds CLDN18.2 on tumor cells, is internalized, and releases MMAE, which inhibits tubulin polymerization to cause G2/M arrest and apoptosis. Tubulin itself is not the antibody target; only CLDN18.2+ cells are directly targeted and killed.
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
Autologous T cells genetically engineered with a murine-derived anti-CD19 chimeric antigen receptor to target CD19 on B-ALL blasts, triggering CD3ζ-mediated activation, cytokine release, and cytotoxic killing; induces B-cell aplasia.
Autologous T cells genetically engineered to express a murine-derived anti-CD19 chimeric antigen receptor bind CD19 on B-cell leukemia cells. CAR engagement triggers CD3zeta-mediated signaling (with costimulation), activating T cells to proliferate, release cytokines, and exert cytotoxic killing, leading to depletion of CD19+ B cells (B-cell aplasia).
YES
DIRECT
CD19 CAR T cells bind CD19 on target cells; CAR activation triggers T‑cell cytotoxicity via perforin/granzyme degranulation and death‑receptor (e.g., Fas/FasL) pathways, killing CD19+ cells.