Natural killer cells genetically engineered to express a chimeric antigen receptor using the NKG2D ectodomain, enabling recognition of stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells and triggering NK activation, degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis. Administered as two IV infusions on days 2–3 after each chemotherapy cycle with dose escalation.
Genetically engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells, triggering NK activation with degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis (e.g., TRAIL/Fas) to kill tumor cells.
YES
DIRECT
NKG2D CAR–NK cells recognize ULBP4 via the NKG2D ectodomain and directly kill target cells through NK degranulation (perforin/granzyme) and death receptor–mediated apoptosis (e.g., TRAIL/Fas).
Natural killer cells genetically engineered to express a chimeric antigen receptor using the NKG2D ectodomain, enabling recognition of stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells and triggering NK activation, degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis. Administered as two IV infusions on days 2–3 after each chemotherapy cycle with dose escalation.
Genetically engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells, triggering NK activation with degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis (e.g., TRAIL/Fas) to kill tumor cells.
YES
DIRECT
NKG2D CAR on NK cells binds ULBP5 on target cells, triggering NK activation and cytotoxicity via perforin/granzyme degranulation and death receptor–mediated apoptosis (e.g., TRAIL/Fas).
Third-generation, irreversible EGFR tyrosine kinase inhibitor (also known as alflutinib) designed to target activating and T790M EGFR mutations.
Furmonertinib (alflutinib) is a third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor that covalently binds the ATP site (e.g., Cys797) of EGFR, potently inhibiting activating and T790M resistance mutations. This blocks EGFR phosphorylation and downstream MAPK and PI3K–AKT signaling, suppressing proliferation and inducing death of EGFR-mutant tumor cells, including those with T790M-mediated resistance.
YES
DIRECT
Furmonertinib irreversibly inhibits mutant EGFR kinase (e.g., covalent binding at Cys797), blocking EGFR phosphorylation and downstream MAPK/PI3K–AKT signaling, leading to growth arrest and apoptosis of EGFR-mutant tumor cells (including T790M).
Natural killer cells genetically engineered to express a chimeric antigen receptor using the NKG2D ectodomain, enabling recognition of stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells and triggering NK activation, degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis. Administered as two IV infusions on days 2–3 after each chemotherapy cycle with dose escalation.
Genetically engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells, triggering NK activation with degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis (e.g., TRAIL/Fas) to kill tumor cells.
YES
DIRECT
NKG2D CAR-NK cells recognize ULBP6 on target cells and directly kill them via NK degranulation (perforin/granzyme) and death receptor–mediated apoptosis (TRAIL/Fas).
Anti-CD20 monoclonal antibody that depletes CD20-positive B cells via ADCC, complement-dependent cytotoxicity, and apoptosis, reducing antiplatelet autoantibody production.
Anti-CD20 monoclonal antibody that binds CD20 on pre‑B and mature B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby reducing pathogenic autoantibody production.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity (CDC), and apoptosis triggered by CD20 ligation.