Anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity, ADCC, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B cells, leading to B‑cell depletion primarily via complement‑dependent cytotoxicity (CDC), antibody‑dependent cellular cytotoxicity (ADCC) and phagocytosis, and induction of apoptosis of CD20‑positive cells.
Anti‑CD20 antibody binding triggers complement-mediated lysis (CDC) and Fc receptor–mediated ADCC/phagocytosis by immune effector cells; can also induce apoptosis of CD20+ cells.
Autologous T cells engineered via lentiviral vector to express a second-generation CD7-targeted CAR with 4-1BB costimulation and CD3 signaling; manufactured from CD7− T cells to prevent fratricide; mediates recognition and killing of CD7+ tumor cells with enhanced persistence/expansion.
Autologous T cells engineered via lentiviral vector to express a second-generation CD7-targeted CAR with CD3z signaling and 4-1BB costimulation, manufactured from CD7− T cells to prevent fratricide. Upon binding CD7 on tumor cells, the CAR activates the T cells to proliferate and mediate cytotoxic killing of CD7+ malignant cells, with 4-1BB enhancing persistence and expansion.
CD7-targeted CAR-T cells bind CD7 on target cells, triggering CD3z/4-1BB signaling and killing via perforin/granzyme-mediated lysis and apoptosis (and death-receptor pathways).
Donor PBMC-derived, partially HLA-matched cytotoxic T lymphocytes expanded to recognize AML1-ETO (RUNX1-RUNX1T1) fusion peptides; HLA-A*11:01 or HLA-A*02:01 restricted; TCR-mediated perforin/granzyme cytotoxicity against t(8;21) AML blasts.
Adoptive transfer of donor PBMC-derived cytotoxic T lymphocytes that have been selected and expanded for TCR specificity to AML1‑ETO (RUNX1‑RUNX1T1) fusion neoantigen peptides presented by HLA-A*11:01 or HLA-A*02:01. Upon antigen recognition on t(8;21) AML blasts, TCR engagement triggers perforin/granzyme-mediated cytolysis and cytokine-driven killing. Cells are not genetically engineered and require partial HLA matching for activity.
Adoptively transferred TCR-specific CTLs recognize the AML1-ETO junctional peptide on HLA class I and directly lyse target cells via perforin/granzyme-mediated apoptosis (with possible Fas/FasL contribution).
Donor PBMC-derived, partially HLA-matched cytotoxic T lymphocytes expanded to recognize AML1-ETO (RUNX1-RUNX1T1) fusion peptides; HLA-A*11:01 or HLA-A*02:01 restricted; TCR-mediated perforin/granzyme cytotoxicity against t(8;21) AML blasts.
Adoptive transfer of donor PBMC-derived cytotoxic T lymphocytes that have been selected and expanded for TCR specificity to AML1‑ETO (RUNX1‑RUNX1T1) fusion neoantigen peptides presented by HLA-A*11:01 or HLA-A*02:01. Upon antigen recognition on t(8;21) AML blasts, TCR engagement triggers perforin/granzyme-mediated cytolysis and cytokine-driven killing. Cells are not genetically engineered and require partial HLA matching for activity.
Adoptively transferred CTLs recognize the AML1-ETO junctional peptide presented on HLA-A*11:01 or HLA-A*02:01 via their TCR and induce perforin/granzyme-mediated apoptosis of the target cells.
Universal (allogeneic) anti-GCC CAR-T cell therapy made from healthy-donor T cells; engineered with a CAR whose scFv binds guanylyl cyclase C (GCC) to induce T-cell cytotoxicity and cytokine release against GCC-positive metastatic colorectal cancer cells.
Allogeneic T cells engineered to express a CAR with an scFv specific for guanylyl cyclase C (GCC). Upon binding GCC on tumor cells, CAR signaling activates the T cells to release cytotoxic granules (perforin/granzymes) and cytokines, leading to targeted lysis of GCC-positive metastatic colorectal cancer cells.
Anti-GCC CAR-T cells bind GCC on target cells, form an immune synapse, and kill via perforin/granzyme-mediated lysis (and ancillary cytokine/Fas–FasL signaling).