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).
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.
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).
Anti-CCR8 monoclonal antibody designed to deplete/suppress CCR8+ tumor-infiltrating regulatory T cells and relieve immunosuppression.
Anti-CCR8 monoclonal antibody that targets CCR8 on tumor-infiltrating regulatory T cells, blocking CCL1–CCR8 signaling and depleting/suppressing CCR8+ Tregs in the tumor microenvironment to relieve immunosuppression and restore antitumor immune responses.
Antibody binding to CCR8 flags CCR8+ Tregs for Fc-mediated clearance, inducing ADCC/ADCP (and possibly CDC) by effector cells, leading to depletion of CCR8-expressing cells.
A humanized, defucosylated IgG1 monoclonal antibody targeting CCR4 on malignant cutaneous T cells and regulatory T cells; enhances NK cell–mediated ADCC and depletes CCR4+ cells.
Humanized, defucosylated IgG1 monoclonal antibody that binds CCR4 on malignant T cells and regulatory T cells; blocks CCR4 signaling and enhances NK cell–mediated ADCC via Fc receptor engagement, leading to depletion of CCR4+ cells and antitumor/immunomodulatory effects.
Anti-CCR4 IgG1 binds CCR4 on target cells and engages Fcγ receptors on NK cells to trigger ADCC, depleting CCR4+ cells (with possible contribution from ADCP/CDC).
Izalontamab brengitecan (BMS-986507), a bispecific EGFR/HER3-targeted antibody–drug conjugate that is internalized upon binding and releases a topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific EGFR/HER3-targeted antibody–drug conjugate that binds EGFR- and HER3-expressing tumor cells, is internalized, and releases a topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
An EGFR/HER3-targeted ADC binds EGFR on tumor cells, is internalized, and releases a topoisomerase I inhibitor (brengitecan) that causes DNA damage and kills the cell.