Autologous cellular immunotherapy consisting of patient-derived, tumor-specific T cells (TIL-like) expanded ex vivo via antigen presentation and infused intravenously to recognize leukemia neoantigens/associated antigens via TCR and mediate cytotoxic killing of malignant blasts.
Autologous tumor‑reactive T cells are enriched and expanded ex vivo via antigen presentation and then infused intravenously; they use their endogenous TCRs to recognize leukemia neoantigens/leukemia‑associated antigens in an HLA‑restricted manner and mediate cytotoxic killing of malignant blasts via perforin/granzyme pathways.
YES
DIRECT
Adoptively transferred T cells recognize HLA-presented leukemia-associated peptides via their endogenous TCRs and directly kill target cells through perforin/granzyme-mediated cytotoxicity.
Off-the-shelf allogeneic CAR T-cell therapy engineered to express a CAR targeting CD38 to promote T-cell mediated cytotoxicity against AML cells expressing CD38.
Allogeneic off-the-shelf T cells engineered with a CD38-specific chimeric antigen receptor bind CD38 on AML cells, triggering CAR signaling and T-cell activation to mediate cytotoxic killing (perforin/granzyme) of CD38-expressing leukemic cells.
YES
DIRECT
CD38-targeted CAR T cells bind CD38 on target cells; CAR signaling activates T-cell cytotoxicity, killing CD38+ cells via perforin/granzyme-mediated apoptosis (and related death pathways).
Off-the-shelf allogeneic CAR T-cell therapy engineered to express a CAR targeting CD123 (IL-3Rα) to drive antigen-specific T-cell killing of AML blasts and leukemic stem cells.
Allogeneic (off-the-shelf) T cells engineered to express a chimeric antigen receptor targeting CD123 (IL-3Rα). CAR engagement of CD123 on AML blasts and leukemic stem cells triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells.
YES
DIRECT
CAR T cells recognize CD123 on target cells, form an immunologic synapse, and induce apoptosis via perforin/granzyme release (and possibly Fas/FasL).
A recombinant humanized anti-CD52 monoclonal antibody (biologic immunosuppressant) administered subcutaneously as part of conditioning for allogeneic hematopoietic cell transplantation. It binds CD52 on mature lymphocytes and other immune cells, depleting them via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity to reduce donor–recipient alloreactivity and graft-versus-host disease risk.
Humanized anti-CD52 monoclonal antibody that binds CD52 on mature lymphocytes and other CD52+ immune cells, depleting them via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity to suppress alloimmune activation and reduce graft-versus-host disease risk during allogeneic transplantation conditioning.
YES
DIRECT
Alemtuzumab binds CD52 on target cells and recruits immune effectors, causing complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP, leading to depletion of CD52+ cells.
IgG1 monoclonal antibody targeting CD38 on myeloma plasma cells; induces ADCC, CDC, and ADCP, can trigger direct apoptosis, and depletes CD38+ immunosuppressive cells to enhance T/NK-cell activity.
Human IgG1k monoclonal antibody targeting CD38; binds CD38 on myeloma/plasma cells to induce antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP), can trigger direct apoptosis, and depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs) to enhance T/NK-cell activity.
YES
DIRECT
Anti-CD38 IgG1 binds CD38 on target cells and triggers Fc-mediated ADCC by NK cells, complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and can induce direct apoptosis.