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 PRAME-derived peptide epitopes presented on HLA via native TCRs, triggering cytolytic degranulation (perforin/granzymes) and death receptor/cytokine-mediated killing of the target cell.
Polyclonal rabbit antithymocyte globulin; IV antibody biologic that depletes T cells via complement-mediated lysis, opsonization, and apoptosis, and can modulate/deplete other leukocyte subsets.
Polyclonal rabbit antithymocyte immunoglobulin that binds multiple T‑cell surface antigens, causing complement-mediated lysis, opsonization/ADCC, and apoptosis to deplete T lymphocytes; can also modulate or deplete other leukocyte subsets, resulting in immunosuppression.
Polyclonal antibodies in RATG bind CD2 on T cells and trigger complement-dependent lysis and Fc-mediated ADCC/opsonization, and can induce apoptosis, depleting CD2+ cells.
Polyclonal rabbit antithymocyte globulin; IV antibody biologic that depletes T cells via complement-mediated lysis, opsonization, and apoptosis, and can modulate/deplete other leukocyte subsets.
Polyclonal rabbit antithymocyte immunoglobulin that binds multiple T‑cell surface antigens, causing complement-mediated lysis, opsonization/ADCC, and apoptosis to deplete T lymphocytes; can also modulate or deplete other leukocyte subsets, resulting in immunosuppression.
Polyclonal rabbit ATG binds CD3 on T cells and triggers complement-dependent lysis, Fc-mediated ADCC/opsonization, and apoptosis, depleting CD3+ cells.
Polyclonal rabbit antithymocyte globulin; IV antibody biologic that depletes T cells via complement-mediated lysis, opsonization, and apoptosis, and can modulate/deplete other leukocyte subsets.
Polyclonal rabbit antithymocyte immunoglobulin that binds multiple T‑cell surface antigens, causing complement-mediated lysis, opsonization/ADCC, and apoptosis to deplete T lymphocytes; can also modulate or deplete other leukocyte subsets, resulting in immunosuppression.
Antithymocyte polyclonal IgG binds CD25 on T cells and triggers complement-dependent lysis and Fc-mediated ADCC/opsonophagocytosis, leading to lysis/apoptosis of CD25+ cells.
A HER2-targeted antibody-drug conjugate consisting of a humanized anti-HER2 IgG1 (trastuzumab) linked to a topoisomerase I inhibitor payload (deruxtecan); binds HER2 (including low expressers), is internalized, releases the payload to inhibit Topo I causing DNA damage and apoptosis, with a membrane-permeable bystander effect; the antibody can also mediate ADCC.
HER2-targeted ADC: trastuzumab binds HER2 on tumor cells (including low expressers), is internalized, and releases the topoisomerase I inhibitor deruxtecan (DXd), causing DNA damage, replication arrest, and apoptosis; the membrane-permeable payload enables bystander killing, and the IgG1 Fc can mediate ADCC.
The ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan, causing DNA damage and apoptosis; the IgG1 Fc can also mediate ADCC, with a membrane-permeable payload enabling bystander killing.