An anti–folate receptor alpha (FRα) antibody-drug conjugate administered IV every 3 weeks. The monoclonal antibody binds FRα on tumor cells, is internalized via FRα-mediated endocytosis, and releases a cytotoxic payload intracellularly (with potential bystander effect) to induce tumor-cell death, targeting FRα-overexpressing epithelial tumors in recurrent gynecologic cancers.
IMGN151 (opugotamig olatansine) is a biparatopic monoclonal antibody targeting folate receptor alpha (FRα) conjugated via a cleavable linker to the maytansinoid DM21 (a microtubule inhibitor). After binding FRα on tumor cells, the ADC is internalized and the payload is released intracellularly, binding tubulin to disrupt microtubule dynamics, leading to cell-cycle arrest and tumor-cell death, with potential bystander killing of adjacent cells.
YES
DIRECT
An FRα-targeted ADC binds FRα, is internalized, and releases the maytansinoid DM21, which binds tubulin to disrupt microtubules, causing mitotic arrest and apoptosis (with possible bystander effect).
An anti–folate receptor alpha (FRα) antibody-drug conjugate administered IV every 3 weeks. The monoclonal antibody binds FRα on tumor cells, is internalized via FRα-mediated endocytosis, and releases a cytotoxic payload intracellularly (with potential bystander effect) to induce tumor-cell death, targeting FRα-overexpressing epithelial tumors in recurrent gynecologic cancers.
IMGN151 (opugotamig olatansine) is a biparatopic monoclonal antibody targeting folate receptor alpha (FRα) conjugated via a cleavable linker to the maytansinoid DM21 (a microtubule inhibitor). After binding FRα on tumor cells, the ADC is internalized and the payload is released intracellularly, binding tubulin to disrupt microtubule dynamics, leading to cell-cycle arrest and tumor-cell death, with potential bystander killing of adjacent cells.
NO
INDIRECT
IMGN151 binds FRα on tumor cells, is internalized, and releases the DM21 payload, which binds tubulin to disrupt microtubules and induce cell death (with possible bystander effect). Tubulin-expressing cells are not targeted directly; killing depends on FRα-mediated delivery.
HER2-targeted antibody–drug conjugate linking trastuzumab to a cleavable topoisomerase I inhibitor (DXd) payload; blocks HER2 signaling, mediates ADCC, and delivers cytotoxic payload to HER2-expressing cells.
HER2-targeted trastuzumab linked via a cleavable linker to a topoisomerase I inhibitor payload (DXd). After binding HER2 and internalization, DXd is released to inhibit Top1, causing DNA damage and apoptosis; the antibody also blocks HER2 signaling, mediates ADCC, and enables bystander killing of neighboring tumor cells.
YES
DIRECT
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis; Fc-mediated ADCC and bystander killing can also contribute.
HER2-targeted antibody–drug conjugate linking trastuzumab to a cleavable topoisomerase I inhibitor (DXd) payload; blocks HER2 signaling, mediates ADCC, and delivers cytotoxic payload to HER2-expressing cells.
HER2-targeted trastuzumab linked via a cleavable linker to a topoisomerase I inhibitor payload (DXd). After binding HER2 and internalization, DXd is released to inhibit Top1, causing DNA damage and apoptosis; the antibody also blocks HER2 signaling, mediates ADCC, and enables bystander killing of neighboring tumor cells.
NO
INDIRECT
The ADC binds HER2 on tumor cells, is internalized, and releases the DXd payload, which inhibits topoisomerase I to cause DNA damage and apoptosis; topoisomerase I expression alone is not directly targeted by the drug.
Trastuzumab coats HER2+ cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells) to induce antibody‑dependent cellular cytotoxicity (ADCC), leading to lysis of the target cells; signaling blockade contributes but ADCC is the primary killing mechanism.