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.
YES
DIRECT
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).
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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).
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.
NO
INDIRECT
Mirvetuximab soravtansine targets FRα on the cell surface, is internalized, and releases DM4, which binds β‑tubulin to disrupt microtubules and induce mitotic arrest/apoptosis. β‑tubulin itself is not the targeted antigen; expression alone does not lead to selective killing.