A TROP-2–targeting antibody-drug conjugate (humanized anti–TROP-2 IgG1) linked to SN-38, the active metabolite of irinotecan. After binding TROP-2 on tumor cells, the ADC is internalized and releases SN-38 to inhibit topoisomerase I, causing DNA damage and apoptosis; the membrane-permeable payload may produce a bystander effect. Also known by the brand name Trodelvy.
Humanized anti-TROP-2 IgG1 antibody linked to SN-38; binds TROP-2 on tumor cells, is internalized and cleaved to release SN-38, which inhibits topoisomerase I by stabilizing topo I-DNA complexes, causing DNA damage and apoptosis; the membrane-permeable payload can produce a bystander effect.
YES
INDIRECT
After the ADC binds TROP-2 and is internalized, it releases SN-38, which inhibits DNA topoisomerase I, stabilizing topo I–DNA complexes and causing DNA damage and apoptosis (with possible bystander killing).
Gene-modified gamma-delta T cells engineered to express an anti-CD19 chimeric antigen receptor. Binding to CD19 on B-lineage cells triggers T-cell activation and perforin/granzyme-mediated cytotoxicity, leading to depletion of CD19+ B cells and plasmablasts, reduced autoantibody production, and modulation of antigen presentation and inflammatory cytokine signaling.
Gene-modified gamma-delta T cells expressing an anti-CD19 chimeric antigen receptor bind CD19 on B-lineage cells, triggering CAR-mediated activation and perforin/granzyme cytotoxicity. This depletes CD19+ B cells and plasmablasts, reducing autoantibody production and modulating antigen presentation and inflammatory cytokine signaling.
YES
DIRECT
Anti-CD19 CAR gamma-delta T cells bind CD19 on B cells, activate via the CAR, and kill targets through perforin/granzyme-mediated cytolysis (apoptosis).
An antibody–drug conjugate consisting of a humanized monoclonal antibody targeting folate receptor alpha (FOLRα) that, upon internalization into FOLRα-positive tumor cells, releases a cleavable cytotoxic payload that inhibits microtubules/tubulin, leading to mitotic arrest and apoptosis.
Humanized anti-FOLRα monoclonal antibody binds FOLRα on tumor cells, is internalized, and releases a cleavable microtubule/tubulin-inhibiting cytotoxic payload, causing mitotic arrest and apoptosis in FOLRα-positive cancer cells.
YES
DIRECT
ADC binds FOLR1 on tumor cells, is internalized, and releases a cleavable tubulin/microtubule‑inhibiting payload, causing mitotic arrest and apoptosis of FOLR1-positive cells.
An antibody–drug conjugate consisting of a humanized monoclonal antibody targeting folate receptor alpha (FOLRα) that, upon internalization into FOLRα-positive tumor cells, releases a cleavable cytotoxic payload that inhibits microtubules/tubulin, leading to mitotic arrest and apoptosis.
Humanized anti-FOLRα monoclonal antibody binds FOLRα on tumor cells, is internalized, and releases a cleavable microtubule/tubulin-inhibiting cytotoxic payload, causing mitotic arrest and apoptosis in FOLRα-positive cancer cells.
NO
INDIRECT
The ADC binds FOLRα on tumor cells, is internalized, and releases a tubulin-inhibiting payload that causes mitotic arrest and apoptosis. Tubulin is the intracellular payload target, not the antigen engaged by the drug, so killing is determined by FOLRα expression rather than tubulin expression.
A bispecific antibody–drug conjugate targeting EGFR and HER3 that delivers a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific EGFR/HER3-targeted antibody–drug conjugate that binds EGFR- and HER3-expressing tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor (brengitecan) to induce DNA damage and tumor cell death, with potential bystander effect.
YES
DIRECT
The bispecific ADC binds EGFR on tumor cells, is internalized, and releases the camptothecin-class topoisomerase I inhibitor brengitecan, causing DNA damage and apoptosis (with potential bystander effect).