An antibody–drug conjugate (Blenrep) targeting BCMA on malignant plasma cells; internalization releases MMAF to disrupt microtubules and induce apoptosis, and can mediate ADCC/ADCP.
Afucosylated anti-BCMA monoclonal antibody conjugated to MMAF; binds BCMA on malignant plasma cells and is internalized, releasing MMAF that inhibits tubulin polymerization leading to G2/M arrest and apoptosis; also engages Fc-mediated effector functions (ADCC/ADCP).
YES
DIRECT
The ADC binds BCMA on target cells, is internalized, and releases MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC/ADCP also kills BCMA+ cells.
An antibody–drug conjugate (Blenrep) targeting BCMA on malignant plasma cells; internalization releases MMAF to disrupt microtubules and induce apoptosis, and can mediate ADCC/ADCP.
Afucosylated anti-BCMA monoclonal antibody conjugated to MMAF; binds BCMA on malignant plasma cells and is internalized, releasing MMAF that inhibits tubulin polymerization leading to G2/M arrest and apoptosis; also engages Fc-mediated effector functions (ADCC/ADCP).
NO
INDIRECT
Belantamab mafodotin binds BCMA on target cells; after internalization, the MMAF payload binds the vinca site on β-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC can also contribute.
Subcutaneous GPRC5D×CD3 bispecific T‑cell–redirecting monoclonal antibody that binds CD3 on T cells and GPRC5D on malignant plasma cells, activating T‑cell cytotoxicity; off‑tumor GPRC5D expression in oral/keratinized tissues is linked to dysgeusia.
Bispecific monoclonal antibody that binds CD3 on T cells and GPRC5D on malignant plasma cells, cross-linking T cells to tumor cells to drive T-cell activation, cytokine release, and cytotoxic lysis of GPRC5D-expressing cells; off-tumor GPRC5D in oral/keratinized tissues is linked to dysgeusia.
YES
DIRECT
Talquetamab links CD3 on T cells to GPRC5D on target cells, triggering T‑cell activation and perforin/granzyme‑mediated lysis of GPRC5D‑expressing cells.
Subcutaneous GPRC5D×CD3 bispecific T‑cell–redirecting monoclonal antibody that binds CD3 on T cells and GPRC5D on malignant plasma cells, activating T‑cell cytotoxicity; off‑tumor GPRC5D expression in oral/keratinized tissues is linked to dysgeusia.
Bispecific monoclonal antibody that binds CD3 on T cells and GPRC5D on malignant plasma cells, cross-linking T cells to tumor cells to drive T-cell activation, cytokine release, and cytotoxic lysis of GPRC5D-expressing cells; off-tumor GPRC5D in oral/keratinized tissues is linked to dysgeusia.
NO
INDIRECT
Talquetamab binds CD3ε on T cells to activate and redirect them; the activated T cells kill GPRC5D-positive tumor cells via perforin/granzyme cytolysis, not the CD3ε-expressing T cells.
Autologous, gene-modified T cells engineered to express an anti-CD7 chimeric antigen receptor; administered as a single infusion of 2×10^8 CAR+ T cells to target CD7-expressing malignant cells in r/r T-ALL/LBL and CD7-positive AML. Mechanism involves CAR-mediated CD3ζ/costimulatory signaling leading to MHC-independent activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxicity; expected on-target depletion of normal CD7+ T/NK cells (T-cell aplasia).
Autologous T cells engineered to express an anti‑CD7 chimeric antigen receptor. CAR binding to CD7 triggers CD3ζ and costimulatory signaling, driving MHC‑independent T‑cell activation, expansion, cytokine release, and perforin/granzyme‑mediated killing of CD7‑positive malignant cells (r/r T‑ALL/LBL and CD7+ AML), with expected on‑target depletion of normal CD7+ T/NK cells (T‑cell aplasia).
YES
DIRECT
Anti-CD7 CAR-T cells bind CD7 and, upon CAR activation, directly kill CD7-positive cells via MHC-independent perforin/granzyme-mediated cytotoxicity (and associated death-receptor pathways).