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.
NKG2D CAR‑NK cells bind ULBP1 on target cells, triggering NK activation and degranulation with perforin/granzymes, leading to target cell lysis/apoptosis.
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.
NKG2D CAR-NK cells bind ULBP2 on target cells, activating NK degranulation and killing via perforin/granzyme-mediated apoptosis (and death receptor pathways).
An antibody–drug conjugate (ADC) comprising a humanized anti‑HER2 IgG1 (trastuzumab sequence) linked via a cleavable tetrapeptide to an exatecan‑derived topoisomerase I inhibitor (DXd). It binds HER2 (ERBB2), is internalized, and releases the payload to inhibit topoisomerase I, causing DNA damage and apoptosis; also provides HER2 signaling blockade, ADCC, and a membrane‑permeable bystander effect.
HER2-targeted antibody-drug conjugate: trastuzumab binds HER2 and is internalized; a cleavable tetrapeptide linker releases deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor that stabilizes Top1-DNA cleavage complexes, causing DNA damage, replication arrest, and apoptosis; also provides HER2 signaling blockade, mediates ADCC, and enables a bystander killing effect.
Trastuzumab deruxtecan binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage, replication arrest, and apoptosis in HER2-expressing cells; it can also induce ADCC and a membrane-permeable bystander killing effect.
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.
NKG2D CAR-NK cells recognize ULBP3 via the NKG2D-based CAR, activate, and directly lyse target cells through perforin/granzyme release (and death-receptor pathways).
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.
NKG2D CAR-NK cells recognize ULBP4 on target cells, activating NK cytotoxicity and inducing perforin/granzyme-mediated lysis (with accompanying cytokine release).