A HER2-directed antibody–drug conjugate composed of a humanized anti-HER2 IgG1 (disitamab) linked to the microtubule inhibitor monomethyl auristatin E (MMAE, vedotin). After binding HER2 on tumor cells and internalization, MMAE is released to disrupt microtubules, inducing G2/M arrest and apoptosis, with potential bystander effect and Fc-mediated ADCC.
Humanized anti-HER2 IgG1 (disitamab) linked to the microtubule inhibitor MMAE (vedotin). After binding HER2 on tumor cells and internalization, the linker is cleaved to release MMAE, which disrupts microtubules, causing G2/M arrest and apoptosis; membrane-permeable MMAE can exert a bystander effect, and the IgG1 Fc may mediate ADCC.
YES
DIRECT
The ADC binds HER2, is internalized, and releases MMAE intracellularly to disrupt microtubules, causing G2/M arrest and apoptosis; additional bystander killing and Fc-mediated ADCC may contribute.
A HER2-directed antibody–drug conjugate composed of a humanized anti-HER2 IgG1 (disitamab) linked to the microtubule inhibitor monomethyl auristatin E (MMAE, vedotin). After binding HER2 on tumor cells and internalization, MMAE is released to disrupt microtubules, inducing G2/M arrest and apoptosis, with potential bystander effect and Fc-mediated ADCC.
Humanized anti-HER2 IgG1 (disitamab) linked to the microtubule inhibitor MMAE (vedotin). After binding HER2 on tumor cells and internalization, the linker is cleaved to release MMAE, which disrupts microtubules, causing G2/M arrest and apoptosis; membrane-permeable MMAE can exert a bystander effect, and the IgG1 Fc may mediate ADCC.
NO
INDIRECT
The ADC targets HER2, is internalized, and releases MMAE that binds beta-tubulin to disrupt microtubules and kill HER2-targeted cells (with possible bystander effect). Tubulin expression alone is not the targeting determinant.
Bispecific T‑cell–engaging antibody (BCMA×CD3) that redirects cytotoxic T cells to kill BCMA-positive malignant plasma cells.
Humanized bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to activate cytotoxic T lymphocytes and mediate targeted lysis of BCMA-positive cells via immune synapse formation and perforin/granzyme release.
YES
DIRECT
Bispecific T-cell engager binds BCMA on target cells and CD3 on T cells, forming an immune synapse that triggers T-cell degranulation (perforin/granzyme) and kills BCMA-positive cells.
Bispecific T‑cell–engaging antibody (BCMA×CD3) that redirects cytotoxic T cells to kill BCMA-positive malignant plasma cells.
Humanized bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to activate cytotoxic T lymphocytes and mediate targeted lysis of BCMA-positive cells via immune synapse formation and perforin/granzyme release.
NO
INDIRECT
CD3 is on T cells and is used to engage and activate them; the activated T cells kill BCMA-positive tumor cells via immune synapse formation and perforin/granzyme release. CD3+ cells themselves are not targeted for lysis.
Bispecific T‑cell–engaging antibody (GPRC5D×CD3) that redirects T cells to GPRC5D-positive myeloma cells.
Humanized bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, cross-linking T cells to GPRC5D+ targets to form an immune synapse and trigger T-cell activation and cytotoxic killing (perforin/granzyme) of tumor cells while sparing most normal tissues.
YES
DIRECT
Talquetamab bridges CD3 on T cells to GPRC5D on target cells, forming an immune synapse that activates T cells to kill GPRC5D+ cells via perforin/granzyme-mediated cytolysis.