An antibody–drug conjugate (Blenrep; belantamab mafodotin-blmf) consisting of a humanized anti-BCMA IgG1 linked to mafodotin (MMAF). It binds BCMA on malignant plasma cells, is internalized, and releases MMAF to disrupt microtubules and induce apoptosis; the afucosylated IgG1 can mediate ADCC/ADCP.
Afucosylated anti-BCMA IgG1 antibody–drug conjugate that binds BCMA (TNFRSF17) on malignant plasma cells, is internalized, and releases the microtubule inhibitor MMAF to disrupt tubulin, leading to G2/M arrest and apoptosis; the afucosylated Fc also enhances ADCC/ADCP.
YES
DIRECT
The ADC binds BCMA on target cells, is internalized, and releases the microtubule inhibitor MMAF, causing G2/M arrest and apoptosis; its afucosylated Fc also enhances ADCC/ADCP against BCMA-expressing cells.
An antibody–drug conjugate (Blenrep; belantamab mafodotin-blmf) consisting of a humanized anti-BCMA IgG1 linked to mafodotin (MMAF). It binds BCMA on malignant plasma cells, is internalized, and releases MMAF to disrupt microtubules and induce apoptosis; the afucosylated IgG1 can mediate ADCC/ADCP.
Afucosylated anti-BCMA IgG1 antibody–drug conjugate that binds BCMA (TNFRSF17) on malignant plasma cells, is internalized, and releases the microtubule inhibitor MMAF to disrupt tubulin, leading to G2/M arrest and apoptosis; the afucosylated Fc also enhances ADCC/ADCP.
NO
INDIRECT
Belantamab targets BCMA, not tubulin. After BCMA-mediated internalization, the MMAF payload binds beta-tubulin to disrupt microtubules and cause G2/M arrest and apoptosis; tubulin expression alone does not lead to killing.
Subcutaneous CD20xCD3 bispecific T-cell–engaging antibody that redirects patient T cells via CD3 to lyse CD20-positive B-cell lymphoma; administered with step-up dosing.
Humanized CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T-cell cytotoxicity to lyse CD20-positive malignant B cells.
YES
DIRECT
The bispecific antibody crosslinks CD3 on T cells with CD20 on B cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme-mediated lysis) to kill CD20-positive cells.
Subcutaneous CD20xCD3 bispecific T-cell–engaging antibody that redirects patient T cells via CD3 to lyse CD20-positive B-cell lymphoma; administered with step-up dosing.
Humanized CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T-cell cytotoxicity to lyse CD20-positive malignant B cells.
NO
INDIRECT
Mosunetuzumab binds CD3 on T cells to activate them to kill CD20+ B cells; CD3+ T cells themselves are not targeted for killing.
TROP2-targeting antibody–drug conjugate composed of a humanized monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor; binds TROP2 on tumor cells, internalizes, and releases the topo‑I payload to cause DNA damage and cell death (with potential bystander effect).
TROP2-targeting IgG1k antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and via a cleavable linker releases the topoisomerase I inhibitor tirumotecan, inhibiting topo I to cause DNA damage, replication arrest, and apoptosis, with a potential bystander effect.
YES
DIRECT
ADC binds TROP2, is internalized, and releases a topoisomerase I inhibitor (tirumotecan) that causes DNA damage, replication arrest, and apoptosis in TROP2-expressing cells (with possible bystander effect).