A humanized monoclonal antibody–drug conjugate targeting DLK1; after binding DLK1 on tumor cells, it is internalized and releases a cytotoxic payload to induce targeted tumor cell death. Evaluated in DLK1-expressing neuroendocrine neoplasms and adrenocortical carcinoma.
Humanized IgG1 antibody targeting DLK1 linked via a cleavable linker to a pyrrolobenzodiazepine (PBD) dimer; after binding DLK1 on tumor cells, the ADC is internalized and cathepsin-mediated cleavage releases the PBD payload, which creates DNA interstrand cross-links, inhibiting cell division and killing DLK1-expressing cancer cells.
YES
DIRECT
After binding DLK1, the ADC is internalized and linker cleavage releases a PBD dimer that creates DNA interstrand cross-links, blocking replication and killing the DLK1-expressing cell.
A humanized monoclonal antibody–drug conjugate targeting DLK1; after binding DLK1 on tumor cells, it is internalized and releases a cytotoxic payload to induce targeted tumor cell death. Evaluated in DLK1-expressing neuroendocrine neoplasms and adrenocortical carcinoma.
Humanized IgG1 antibody targeting DLK1 linked via a cleavable linker to a pyrrolobenzodiazepine (PBD) dimer; after binding DLK1 on tumor cells, the ADC is internalized and cathepsin-mediated cleavage releases the PBD payload, which creates DNA interstrand cross-links, inhibiting cell division and killing DLK1-expressing cancer cells.
NO
INDIRECT
ADCT-701 targets DLK1 on the cell surface; after internalization, cathepsin cleavage releases a PBD payload that binds the DNA minor groove and forms interstrand cross-links, killing DLK1-positive cells. DNA is the intracellular payload target, not the directly targeted antigen.
Izalontamab brengitecan (BMS-986507), an EGFR/HER3-directed bispecific antibody–drug conjugate that internalizes upon binding and releases the topoisomerase I inhibitor brengitecan to induce DNA strand breaks and bystander killing.
Bispecific EGFR/HER3-targeting antibody-drug conjugate that binds EGFR and HER3 on tumor cells, internalizes, and releases the topoisomerase I inhibitor brengitecan to induce DNA strand breaks, leading to tumor cell death and bystander killing.
YES
DIRECT
The ADC binds EGFR (and HER3) on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA strand breaks and cell death, with bystander killing of nearby cells.
Anti-CD52 monoclonal antibody used for T-cell depletion to prevent rejection and GVHD.
Humanized anti-CD52 IgG1 monoclonal antibody that binds CD52 on lymphocytes and induces complement-dependent cytotoxicity and antibody-dependent cell-mediated cytotoxicity, leading to depletion of CD52+ T and B cells (and other leukocytes) to reduce rejection and GVHD.
YES
DIRECT
Alemtuzumab binds CD52 on leukocytes and induces complement-dependent cytotoxicity and Fc-mediated ADCC (and phagocytosis), leading to lysis/depletion of CD52+ cells.
Izalontamab brengitecan (BMS-986507), an EGFR/HER3-directed bispecific antibody–drug conjugate that internalizes upon binding and releases the topoisomerase I inhibitor brengitecan to induce DNA strand breaks and bystander killing.
Bispecific EGFR/HER3-targeting antibody-drug conjugate that binds EGFR and HER3 on tumor cells, internalizes, and releases the topoisomerase I inhibitor brengitecan to induce DNA strand breaks, leading to tumor cell death and bystander killing.
YES
DIRECT
An EGFR/HER3-targeting ADC binds HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA strand breaks and apoptosis; bystander killing may also occur.