An anti-BCMA antibody–drug conjugate linking belantamab to the cytotoxic payload MMAF; after BCMA-mediated internalization, MMAF disrupts microtubules causing cell death, and the antibody retains Fc-mediated ADCC/ADCP.
Belantamab mafodotin is an anti-BCMA antibody–drug conjugate that binds BCMA on malignant plasma cells, is internalized, and releases the MMAF payload to inhibit microtubules and induce cell death; the afucosylated IgG1 antibody also engages Fc receptors to promote ADCC and ADCP.
NO
INDIRECT
The ADC binds BCMA on target cells, is internalized, and releases MMAF, which binds beta‑tubulin to disrupt microtubules and kill BCMA+ cells; beta‑tubulin itself is not the antigen targeted by the drug.
Subcutaneous bispecific T‑cell–engaging antibody that binds CD3 on T cells and CD20 on B cells to form an immune synapse, activate TCR/CD3 signaling, and induce T‑cell–mediated cytotoxicity; used here with step‑up dosing around CAR‑T.
Subcutaneous bispecific antibody that binds CD3 on T cells and CD20 on B cells, bringing them into proximity to form an immune synapse, activate TCR/CD3 signaling, and trigger T‑cell–mediated cytotoxicity (perforin/granzyme) against CD20+ B‑cell malignancies.
YES
DIRECT
Epcoritamab bridges CD3+ T cells to CD20+ cells, forming an immune synapse that activates TCR/CD3 signaling and induces perforin/granzyme-mediated T‑cell cytotoxicity against CD20-expressing cells.
An anti-BCMA antibody–drug conjugate linking belantamab to the cytotoxic payload MMAF; after BCMA-mediated internalization, MMAF disrupts microtubules causing cell death, and the antibody retains Fc-mediated ADCC/ADCP.
Belantamab mafodotin is an anti-BCMA antibody–drug conjugate that binds BCMA on malignant plasma cells, is internalized, and releases the MMAF payload to inhibit microtubules and induce cell death; the afucosylated IgG1 antibody also engages Fc receptors to promote ADCC and ADCP.
NO
INDIRECT
Belantamab targets BCMA on tumor cells; its afucosylated Fc binds CD16a on NK cells to trigger ADCC against BCMA+ cells. CD16a-expressing cells are not targeted or killed by the drug.
An anti-BCMA antibody–drug conjugate linking belantamab to the cytotoxic payload MMAF; after BCMA-mediated internalization, MMAF disrupts microtubules causing cell death, and the antibody retains Fc-mediated ADCC/ADCP.
Belantamab mafodotin is an anti-BCMA antibody–drug conjugate that binds BCMA on malignant plasma cells, is internalized, and releases the MMAF payload to inhibit microtubules and induce cell death; the afucosylated IgG1 antibody also engages Fc receptors to promote ADCC and ADCP.
NO
INDIRECT
Belantamab mafodotin targets BCMA, not Fc gamma receptor IIa (CD32a). Its afucosylated IgG1 Fc engages CD32a on immune effector cells to drive ADCC/ADCP against BCMA+ cells, and the MMAF payload kills BCMA-expressing cells after internalization; CD32a+ cells are not targeted for killing.
Autologous, gene-modified chimeric antigen receptor T-cell (CAR-T) therapy engineered to express a dual-target CAR recognizing CD19 and CD22 on B-lineage cells; CAR signaling (CD3ζ with costimulation) activates T-cell cytotoxicity and cytokine release to eliminate malignant B lymphoblasts, with dual targeting intended to reduce antigen-escape relapse in relapsed/refractory B-ALL.
Autologous T cells are gene-modified to express a dual-target chimeric antigen receptor recognizing CD19 and CD22 on B-lineage cells. Antigen engagement triggers CAR signaling (CD3ζ with costimulation), inducing T-cell cytotoxicity and cytokine release to eliminate malignant B lymphoblasts; dual targeting is intended to reduce antigen-escape relapse and leads to on-target B-cell depletion.
YES
DIRECT
CD19-expressing cells are recognized by the CD19-directed CAR on the infused T cells, which then kill targets via cytotoxic granule release (perforin/granzyme) and death-receptor pathways, leading to lysis/apoptosis of CD19+ cells.