Autologous, gene-modified anti-CD19 chimeric antigen receptor T-cell (CAR T) therapy given as a single infusion; engineered patient T cells target CD19 to deplete B cells/plasmablasts and reduce autoantibody-mediated pathology in idiopathic inflammatory myopathies.
Autologous T cells are engineered to express an anti-CD19 chimeric antigen receptor; after infusion, these CAR T cells recognize and kill CD19-positive B cells and plasmablasts, depleting autoreactive B-cell populations, lowering autoantibody production, and attenuating B cell–driven inflammation.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target B-lineage cells, become activated, and kill them via T-cell effector functions (perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis).
Humanized IgG1 anti-EGFR monoclonal antibody that blocks EGFR ligand binding and dimerization, inhibiting RAS–MAPK and PI3K–AKT signaling, reducing proliferation and radioresistance, and enabling ADCC.
Humanized IgG1 anti-EGFR monoclonal antibody that blocks EGFR ligand binding and dimerization, inhibiting RAS–MAPK and PI3K–AKT signaling to reduce proliferation and survival; Fc-mediated ADCC may contribute and it can enhance radiosensitivity.
YES
DIRECT
Fc-mediated ADCC by immune effector cells (e.g., NK cells) against EGFR-expressing cells; signaling blockade is mainly cytostatic, with radiosensitization enhancing kill with radiation.
Humanized anti-HER2 antibody–drug conjugate that binds HER2 and delivers the microtubule-disrupting payload MMAE, causing cell-cycle arrest and apoptosis; may also mediate ADCC.
Humanized anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule-disrupting payload MMAE to induce G2/M cell-cycle arrest and apoptosis; may additionally mediate antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
The anti-HER2 ADC binds HER2 on target cells, is internalized, and releases the MMAE payload that disrupts microtubules, causing G2/M arrest and apoptosis; its Fc can also mediate ADCC against HER2+ cells.
Autologous, non–genetically engineered, ex vivo–expanded polyclonal multi–tumor-associated antigen (multiTAA)–specific T-cell therapy that recognizes multiple shared TAAs on pancreatic adenocarcinoma via native, MHC-restricted TCRs to mediate cytotoxic killing and cytokine-driven immune activation.
Autologous, ex vivo-expanded polyclonal CD4+/CD8+ T cells with native, MHC-restricted TCRs specific for multiple shared tumor-associated antigens on pancreatic adenocarcinoma. After infusion, these T cells recognize antigen-MHC complexes on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine-driven immune activation; multi-antigen targeting reduces antigen-loss escape and may improve durability.
YES
DIRECT
Infused autologous T cells use native, MHC-restricted TCRs to recognize NY-ESO-1–derived peptides on tumor MHC and kill target cells via perforin/granzyme-mediated cytolysis (with supporting cytokine-driven activation).
Humanized anti-HER2 antibody–drug conjugate that binds HER2 and delivers the microtubule-disrupting payload MMAE, causing cell-cycle arrest and apoptosis; may also mediate ADCC.
Humanized anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule-disrupting payload MMAE to induce G2/M cell-cycle arrest and apoptosis; may additionally mediate antibody-dependent cellular cytotoxicity (ADCC).
NO
INDIRECT
The ADC targets HER2, is internalized, and releases MMAE, which binds beta-tubulin to disrupt microtubules and induce G2/M arrest and apoptosis; beta-tubulin is not the antigen recognized by the drug.