Anti-CD30 antibody–drug conjugate (ADC) linked to MMAE; binds CD30 on malignant T cells, internalizes, and releases MMAE to disrupt microtubules, causing G2/M arrest and apoptosis (possible bystander effect).
Anti-CD30 monoclonal antibody linked via a cleavable valine-citrulline linker to MMAE; upon binding CD30 and internalization, MMAE is released to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis (with potential bystander effect).
NO
INDIRECT
Brentuximab vedotin targets CD30, is internalized, and releases MMAE, which inhibits beta-tubulin polymerization to cause mitotic arrest and apoptosis; beta-tubulin is affected only after CD30-mediated delivery (possible bystander effect).
An intravenous anti-BAFF receptor (BAFF-R) monoclonal antibody that blocks BAFF signaling, depletes B cells, and reduces autoantibody production.
Monoclonal antibody against BAFF receptor (BAFF-R) that blocks BAFF signaling and depletes B cells (via Fc-mediated cytotoxicity), reducing autoreactive B-cell survival and autoantibody production.
YES
DIRECT
Ianalumab binds BAFF-R on B cells and, via its Fc, engages immune effectors to trigger ADCC/ADCP (and CDC), leading to depletion of BAFF-R–expressing cells.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy; patient T cells are engineered to express an anti-CD19 scFv with CD28/CD3ζ signaling domains, triggering activation, expansion, and cytotoxic killing of CD19-positive B-cell lymphoma.
Autologous T cells are transduced to express a CD19-specific CAR with an anti-CD19 scFv, CD28 costimulatory, and CD3ζ signaling domains. After infusion, the CAR T cells recognize CD19 on B cells independent of MHC, become activated, proliferate, release cytotoxic mediators and cytokines, and selectively kill CD19-positive malignant B cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells and kill them via T-cell cytolysis (immune synapse formation, perforin/granzyme release, apoptosis).
Autologous, gene-modified CD19-directed chimeric antigen receptor (CAR) T-cell therapy derived from the patient's T cells and given as a single infusion to deplete CD19+ B cells and reduce autoantibody production in SLE.
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor; upon binding CD19 on B-lineage cells, the CAR T cells activate, proliferate, and kill CD19+ cells via cytotoxic mechanisms, depleting B cells and reducing autoantibody production to reset humoral autoimmunity.
YES
DIRECT
CD19 CAR T cells bind CD19 on target cells, become activated, and kill CD19+ cells via perforin/granzyme-mediated cytolysis and apoptosis (e.g., Fas–FasL), depleting B cells.
An anti-HER2 antibody-drug conjugate comprising the humanized IgG1 monoclonal antibody trastuzumab linked via a cleavable linker to the membrane-permeable topoisomerase I inhibitor deruxtecan (DXd). It binds HER2 on tumor cells, is internalized, and releases DXd intracellularly to inhibit Topo-I, causing DNA damage and apoptosis; the payload’s bystander effect can kill adjacent low-HER2 cells, and the IgG1 Fc may engage ADCC.
Humanized anti-HER2 IgG1 (trastuzumab) linked via a cleavable linker to the membrane-permeable topoisomerase I inhibitor deruxtecan (DXd). After binding HER2 and internalization, the linker is cleaved to release DXd, which inhibits Topo-I, causing DNA damage, cell-cycle arrest, and apoptosis; the payload exerts a bystander killing effect on adjacent low-HER2 cells and the IgG1 Fc can engage ADCC.
YES
DIRECT
The ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan, causing DNA damage, cell-cycle arrest, and apoptosis in HER2+ cells; the IgG1 Fc can also engage ADCC, with a bystander effect from the membrane-permeable payload.