Gene-modified natural killer (NK) cells engineered to express a chimeric antigen receptor based on NKG2D, enabling recognition of stress-induced ligands (MICA, MICB, ULBP family) on tumor cells and triggering NK cytotoxicity and cytokine release; infused after lymphodepleting chemotherapy to promote expansion and persistence.
Gene‑modified natural killer cells expressing an NKG2D‑based chimeric antigen receptor recognize stress‑induced ligands (MICA, MICB, ULBP family) on tumor cells, triggering NK activation, perforin/granzyme‑mediated cytotoxicity, and cytokine release; lymphodepleting chemotherapy is used to enhance CAR‑NK expansion and persistence.
YES
DIRECT
NKG2D CAR-NK cells recognize ULBP4 on target cells, activating NK cytotoxicity and inducing perforin/granzyme-mediated lysis (with accompanying cytokine release).
Gene-modified natural killer (NK) cells engineered to express a chimeric antigen receptor based on NKG2D, enabling recognition of stress-induced ligands (MICA, MICB, ULBP family) on tumor cells and triggering NK cytotoxicity and cytokine release; infused after lymphodepleting chemotherapy to promote expansion and persistence.
Gene‑modified natural killer cells expressing an NKG2D‑based chimeric antigen receptor recognize stress‑induced ligands (MICA, MICB, ULBP family) on tumor cells, triggering NK activation, perforin/granzyme‑mediated cytotoxicity, and cytokine release; lymphodepleting chemotherapy is used to enhance CAR‑NK expansion and persistence.
YES
DIRECT
NKG2D-based CAR on NK cells recognizes ULBP5 on target cells, triggering NK activation and degranulation, leading to perforin/granzyme-mediated killing (with possible death-receptor signaling).
Gene-modified natural killer (NK) cells engineered to express a chimeric antigen receptor based on NKG2D, enabling recognition of stress-induced ligands (MICA, MICB, ULBP family) on tumor cells and triggering NK cytotoxicity and cytokine release; infused after lymphodepleting chemotherapy to promote expansion and persistence.
Gene‑modified natural killer cells expressing an NKG2D‑based chimeric antigen receptor recognize stress‑induced ligands (MICA, MICB, ULBP family) on tumor cells, triggering NK activation, perforin/granzyme‑mediated cytotoxicity, and cytokine release; lymphodepleting chemotherapy is used to enhance CAR‑NK expansion and persistence.
YES
DIRECT
NKG2D-based CAR on NK cells binds ULBP6 on target cells, triggering NK activation and degranulation with perforin/granzyme-mediated cytolysis (with possible death receptor signaling).
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting carcinoembryonic antigen (CEA/CEACAM5), providing CD3ζ and costimulatory signaling to activate T cells and induce cytotoxicity against CEA-positive tumor cells.
Autologous T lymphocytes engineered to express a chimeric antigen receptor targeting CEA/CEACAM5. CAR engagement on CEA-positive tumor cells delivers CD3ζ and costimulatory signaling, activating and expanding the T cells to release cytokines and kill targets via perforin/granzyme-mediated cytotoxicity.
YES
DIRECT
CEA-specific CAR T cells bind CEA on target cells, become activated via CD3ζ/costimulatory signaling, and kill targets through perforin/granzyme-mediated cytolysis (and Fas/FasL).
Chimeric IgG1 anti-EGFR monoclonal antibody that blocks EGFR signaling and mediates ADCC.
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the receptor’s extracellular domain to block ligand binding, activation, and dimerization, thereby inhibiting downstream RAS/MAPK and PI3K/AKT signaling and tumor cell proliferation. Its Fc region also engages Fcγ receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) against EGFR-expressing cells.
YES
DIRECT
IgG1 antibody binds EGFR on target cells; its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate ADCC (and can activate complement), resulting in lysis of EGFR-expressing cells.