An autologous anti-GPRC5D chimeric antigen receptor (CAR) T-cell therapy in which a patient’s T cells are engineered to express a CAR targeting GPRC5D, leading to antigen-dependent T-cell activation and cytolytic killing of GPRC5D-positive myeloma cells.
Autologous T cells are gene-modified to express a chimeric antigen receptor targeting GPRC5D. Antigen engagement activates CAR signaling (CD3z with costimulatory domains), leading to T-cell activation, proliferation, cytokine release, and antigen-dependent cytolytic killing of GPRC5D-positive myeloma cells.
Anti-GPRC5D CAR T cells bind GPRC5D on target cells and, upon CAR activation, kill them via T-cell cytolysis (perforin/granzyme and Fas–FasL–mediated apoptosis).
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.
Autologous TILs recognize MAGE-A3 peptide epitopes presented on HLA by tumor cells via native TCRs, triggering cytolysis through perforin/granzyme release (and Fas–FasL) with supportive cytokine effects.
An anti-CD33 antibody–drug conjugate that binds CD33 on AML blasts and, after internalization, releases the cytotoxic payload calicheamicin to induce DNA double-strand breaks and apoptosis; immune effector functions are minor relative to payload delivery.
Humanized anti-CD33 antibody–drug conjugate that binds CD33 on AML blasts, is internalized, and intracellularly releases the cytotoxic payload calicheamicin, causing DNA double-strand breaks and apoptotic cell death; immune effector functions are minimal relative to payload-mediated cytotoxicity.
Anti-CD33 ADC binds CD33, is internalized, and releases calicheamicin inside target cells, causing DNA double-strand breaks and apoptotic death; immune effector functions are minimal.
Investigational CD30-directed antibody-drug conjugate (SGN-35T) administered intravenously as monotherapy; a monoclonal antibody binds CD30 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death in relapsed/refractory CD30-positive lymphomas.
CD30-targeted monoclonal antibody–drug conjugate that binds CD30 on tumor cells, is internalized, and releases a cytotoxic payload intracellularly to induce death of CD30-positive malignant cells.
CD30-targeted antibody–drug conjugate binds CD30, is internalized, and releases an intracellular cytotoxic payload that kills CD30-positive cells (e.g., via microtubule disruption/apoptosis).
Human IgG1 monoclonal antibody against PD-L1 that blocks PD-1/PD-L1 interaction, preventing PD-1 signaling and restoring cytotoxic T-cell activation and antitumor function; can also mediate ADCC against PD-L1–expressing tumor cells.
Avelumab binds PD-L1 on target cells and, via its IgG1 Fc, engages FcγR-bearing effectors (e.g., NK cells) to mediate ADCC (and potentially ADCP), killing PD-L1–expressing cells; it also blocks PD-1/PD-L1 to restore CTL activity.