Anti-GD2 IgG1 monoclonal antibody that targets GD2 on neuroblastoma cells to mediate ADCC and complement-dependent cytotoxicity.
Chimeric IgG1 monoclonal antibody targeting GD2 on tumor cells; flags GD2-positive cells for immune elimination by engaging Fcγ receptor–bearing effectors to mediate antibody-dependent cell-mediated cytotoxicity (and phagocytosis) and activates complement to drive complement-dependent cytotoxicity.
Anti-GD2 IgG1 binds GD2 on target cells and recruits Fcγ receptor–bearing effectors to mediate ADCC/ADCP, and activates complement to induce CDC, killing GD2-positive cells.
Autologous, genetically engineered chimeric antigen receptor T-cell therapy in which patient T cells are modified to express CARs targeting CLL1 (CLEC12A) and CD33; antigen engagement activates T cells to induce cytotoxic killing of AML cells. Administered as a single IV infusion (approximately 1.0–2.5×10^6 CAR+ T cells/kg).
Autologous T cells are genetically engineered to express chimeric antigen receptors that recognize CLL1 (CLEC12A) and CD33 on AML cells; antigen engagement activates CAR signaling independent of the native TCR, driving T‑cell activation, proliferation, cytokine release, and cytotoxic killing of AML blasts and leukemic stem/progenitor cells expressing either antigen.
CLL1-targeted CAR-T cells bind CLL1 on target cells, activating CAR signaling and inducing cytolysis via perforin/granzyme release and apoptosis (e.g., Fas/FasL).
Antibody–drug conjugate targeting TROP2 that is internalized and releases a topoisomerase I inhibitor payload to induce DNA damage and tumor cell death.
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload, causing DNA damage and tumor cell death (with potential bystander effect).
The anti-TROP2 ADC binds TROP2, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage (Top1 inhibition) leading to tumor cell death; bystander killing may also occur.
Autologous, genetically engineered chimeric antigen receptor T-cell therapy in which patient T cells are modified to express CARs targeting CLL1 (CLEC12A) and CD33; antigen engagement activates T cells to induce cytotoxic killing of AML cells. Administered as a single IV infusion (approximately 1.0–2.5×10^6 CAR+ T cells/kg).
Autologous T cells are genetically engineered to express chimeric antigen receptors that recognize CLL1 (CLEC12A) and CD33 on AML cells; antigen engagement activates CAR signaling independent of the native TCR, driving T‑cell activation, proliferation, cytokine release, and cytotoxic killing of AML blasts and leukemic stem/progenitor cells expressing either antigen.
CAR-T cells bind CD33 on target cells, triggering T-cell activation and cytolysis via perforin/granzyme release and Fas/FasL-mediated apoptosis.
An antibody–drug conjugate targeting folate receptor alpha; a humanized anti-FRα IgG1 linked to the maytansinoid payload DM4 that, after receptor-mediated internalization, releases DM4 to inhibit tubulin polymerization, causing mitotic arrest and apoptosis.
A humanized anti–folate receptor alpha (FRα) IgG1 monoclonal antibody conjugated to the maytansinoid payload DM4; after FRα binding and receptor-mediated internalization, linker cleavage releases DM4 to inhibit tubulin polymerization, disrupting microtubules and inducing mitotic arrest and apoptosis, with potential local bystander effect.
The anti‑FRα antibody–drug conjugate binds FRα, is internalized, and releases the DM4 payload that inhibits tubulin polymerization, leading to mitotic arrest and apoptosis (with possible local bystander effect).