Investigational monoclonal antibody immunotherapy targeting CCR8 on intratumoral regulatory T cells; designed to mediate Fc-dependent depletion of CCR8+ Tregs and/or block CCR8–CCL1 signaling to reduce immunosuppression.
Monoclonal antibody targeting CCR8 on intratumoral regulatory T cells; mediates Fc-dependent depletion (e.g., ADCC/ADCP) of CCR8+ Tregs and blocks CCL1–CCR8 signaling, reducing immunosuppression and enhancing antitumor T-cell responses.
The antibody binds CCR8 on Tregs and engages Fcγ receptors on effector cells, inducing ADCC/ADCP to deplete CCR8+ cells.
Personalized cellular immunotherapy using patient-derived tumor-resident T cells (primarily CD8+ and CD4+) expanded ex vivo and reinfused as a single IV infusion (e.g., 2.0×10^7 cells/kg) to recognize tumor/neoantigens via TCR–MHC interactions and mediate cytotoxicity through perforin/granzyme and cytokine release.
Autologous tumor-resident T cells (CD8+/CD4+) expanded ex vivo and reinfused; they recognize patient-specific tumor/neoantigens via native TCR–MHC I/II interactions and mediate cytotoxicity through perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF-α), enhancing antitumor immunity within the tumor microenvironment.
TILs recognize NY-ESO-1 peptide epitopes presented on MHC via native TCRs and directly kill target cells through perforin/granzyme-mediated apoptosis (with additional Fas–FasL and cytokine effects).
Donor-derived T lymphocytes genetically engineered to express a chimeric antigen receptor targeting CD70, administered intrathecally to eliminate CD70-positive glioma cells via CAR-mediated T-cell activation and cytotoxicity.
Donor-derived T cells engineered with a CD70-specific chimeric antigen receptor recognize CD70 on glioma cells independently of MHC, triggering CAR-mediated T-cell activation (CD3ζ with costimulation) and effector functions, including perforin/granzyme cytotoxicity and cytokine release, to eliminate CD70-positive tumor cells; administered intrathecally for CNS delivery.
CD70-specific CAR T cells bind CD70 on target cells and, upon CAR activation (CD3ζ + costimulation), kill them via perforin/granzyme-mediated cytolysis (and death receptor pathways).
Antibody–drug conjugate targeting Nectin‑4; after binding and internalization it releases the MMAE microtubule inhibitor to disrupt tubulin polymerization and induce apoptosis (with possible bystander and ADCC effects).
Humanized anti–Nectin-4 monoclonal antibody conjugated to the microtubule inhibitor MMAE. After binding Nectin-4 on tumor cells and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis; potential bystander killing and ADCC may contribute.
ADC binds Nectin-4 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; Fc-mediated ADCC and bystander effects may also contribute.