Allogeneic cord blood–derived NK cells engineered to express a CD5-directed chimeric antigen receptor and constitutive IL-15 with an inducible caspase 9 (iC9) safety switch; redirects NK cytotoxicity to CD5+ malignant lymphocytes and supports NK survival and persistence.
Allogeneic cord blood–derived NK cells engineered with a CD5-specific chimeric antigen receptor to redirect NK cytotoxicity against CD5+ malignant lymphocytes. A constitutive IL-15 transgene enhances NK survival, proliferation, and persistence, while an inducible caspase-9 (iC9) safety switch enables rapid elimination of the cells if severe toxicity occurs.
CD5-specific CAR on engineered NK cells binds CD5 on target cells, triggering NK degranulation (perforin/granzyme-mediated cytolysis and apoptosis) leading to direct killing of CD5+ cells.
A chimeric anti-CD20 IgG1 monoclonal antibody that targets CD20-positive B cells and induces complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and kills them via complement-dependent cytotoxicity and Fc-mediated ADCC (and phagocytosis), and can also induce apoptosis.
Anti-CD47 monoclonal antibody that blocks the CD47–SIRPalpha 'don't eat me' signal to enhance macrophage phagocytosis and antigen presentation.
AK117 is an anti-CD47 monoclonal antibody that blocks the CD47–SIRPα immune checkpoint (“don’t eat me” signal), thereby enhancing macrophage-mediated tumor cell phagocytosis and improving antigen presentation to stimulate antitumor immune responses.
Blocking CD47–SIRPα removes the 'don’t eat me' signal and opsonizes CD47+ cells, enabling macrophage antibody-dependent cellular phagocytosis (ADCP) and killing.
Humanized IgG1 monoclonal antibody targeting EGFR; blocks ligand binding and downstream EGFR signaling (RAS/RAF/MEK/ERK, PI3K/AKT) and may trigger ADCC.
Humanized IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor activation, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to suppress tumor cell proliferation and survival; Fc region may engage ADCC and can enhance radiosensitivity.
IgG1 anti-EGFR antibody blocks EGFR signaling and engages FcγR-bearing effector cells (e.g., NK cells, macrophages) to mediate ADCC, killing EGFR+ cells; may also trigger some CDC.
Autologous, genetically modified CAR T-cell therapy engineered to dual-target NKG2D ligands (e.g., MICA/MICB/ULBP family) and CLDN18.2 on tumor cells, activating T-cell cytotoxicity to treat advanced NKG2DL+/CLDN18.2+ solid tumors.
Autologous T cells engineered with a tandem/bispecific CAR that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP family) and CLDN18.2 on tumor cells. Target engagement activates CAR signaling, leading to T-cell cytotoxic killing via perforin/granzyme release and cytokine production, selectively lysing NKG2DL+/CLDN18.2+ cancer cells.
Bispecific CAR-T cells co-recognize CLDN18.2 and NKG2D ligands on tumor cells, activating CAR signaling and inducing contact-dependent killing via perforin/granzyme release and cytokine-mediated cytotoxicity.