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.
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.
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.
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.
HER2-directed antibody-drug conjugate linking trastuzumab to the maytansinoid microtubule inhibitor DM1, delivering the cytotoxic payload to HER2-expressing cancer cells to disrupt microtubules and inhibit proliferation.
HER2-directed antibody-drug conjugate linking trastuzumab to the maytansinoid DM1. Binds HER2 on tumor cells, is internalized, and releases DM1 intracellularly to inhibit microtubule function, causing mitotic arrest and apoptosis; also retains trastuzumab-mediated HER2 signaling blockade and ADCC.
Binds HER2, is internalized, and releases the DM1 payload that disrupts microtubules, causing mitotic arrest and apoptosis (with additional Fc-mediated ADCC).
Anti-CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and induction of apoptosis.
Binds CD20 on B cells and induces killing via Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity, and direct apoptosis upon CD20 cross-linking.
Gene-modified autologous T cells expressing a chimeric antigen receptor targeting CD19 on malignant B cells; mediates cytotoxicity and cytokine release.
Autologous T cells genetically engineered to express a CD19-specific chimeric antigen receptor; upon binding CD19 on malignant B cells, the CAR provides activation and co-stimulatory signaling (e.g., CD3zeta with CD28/4-1BB), driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated lysis of CD19+ cells.
CD19-specific CAR-T cells bind CD19 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.