Anti-Claudin18.2 antibody–drug conjugate that targets CLDN18.2-expressing tumor cells and delivers a cytotoxic payload; intravenous administration.
Monoclonal antibody targeting Claudin18.2 delivers the microtubule inhibitor MMAE via a cleavable linker; after binding to CLDN18.2 on tumor cells and internalization, MMAE is released intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in CLDN18.2-expressing cells.
NO
INDIRECT
The ADC binds CLDN18.2 on tumor cells, is internalized, and releases MMAE, which binds beta-tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis; beta-tubulin expression alone does not make cells targets for killing.
Chimeric anti-CD20 monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and induces depletion via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
YES
DIRECT
CD20+ cells are eliminated via antibody-dependent cellular cytotoxicity (FcγR-mediated NK/macrophage killing), complement-dependent cytotoxicity (C1q-mediated lysis), and apoptosis triggered by CD20 crosslinking.
HER2-directed antibody-drug conjugate (ADC) that binds HER2 on tumor cells, is internalized, and releases a microtubule-inhibiting cytotoxic payload to induce mitotic arrest and apoptosis.
HER2-directed trastuzumab-based ADC that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases an auristatin (duostatin-5) microtubule inhibitor, blocking tubulin polymerization to induce mitotic arrest and apoptosis.
YES
DIRECT
The ADC binds HER2, is internalized, and releases an auristatin (duostatin-5) payload that inhibits tubulin polymerization, causing mitotic arrest and apoptosis of HER2-expressing cells.
HER2-directed antibody-drug conjugate (ADC) that binds HER2 on tumor cells, is internalized, and releases a microtubule-inhibiting cytotoxic payload to induce mitotic arrest and apoptosis.
HER2-directed trastuzumab-based ADC that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases an auristatin (duostatin-5) microtubule inhibitor, blocking tubulin polymerization to induce mitotic arrest and apoptosis.
NO
INDIRECT
A166 targets HER2, is internalized, and releases an auristatin payload that binds beta‑tubulin to disrupt microtubules and induce mitotic arrest/apoptosis. Beta‑tubulin is not the targeted antigen; cytotoxicity requires HER2-mediated delivery.
Autologous chimeric antigen receptor T-cell therapy engineered to express an IL13Rα2-specific CAR. Upon binding IL13Rα2 on glioma cells, CAR signaling (CD3ζ with costimulatory domains) activates cytotoxic T-cell responses and cytokine secretion to kill tumor cells; delivered via intraventricular infusions.
Autologous T cells engineered to express an IL13Rα2-specific CAR (CD3ζ with costimulatory domains). Binding IL13Rα2 on glioma cells triggers CAR signaling, activating T-cell cytotoxicity and cytokine release to lyse IL13Rα2-positive tumor cells; administered via intraventricular infusions.
YES
DIRECT
CAR-T cells recognize IL13RA2 on target cells, triggering T-cell activation and killing via perforin/granzyme-mediated cytolysis (and Fas–FasL), with supportive cytokine release.