Engineered natural killer cells expressing a chimeric antigen receptor specific for CD123 (IL-3 receptor α), administered intravenously as cellular immunotherapy to eliminate CD123-positive AML/BPDCN cells.
Engineered natural killer cells expressing a chimeric antigen receptor that binds CD123 (IL‑3 receptor α) on AML/BPDCN cells. CAR engagement activates NK signaling and triggers cytotoxicity (perforin/granzyme release and cytokine secretion), leading to targeted lysis of CD123-positive malignant blasts and stem-like leukemic cells.
CAR-engineered NK cells bind CD123 on target cells, triggering NK activation and degranulation (perforin/granzyme) and death-receptor signaling, causing lysis/apoptosis of CD123-positive cells.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting CD70; binding to CD70 on tumor cells triggers T-cell activation, cytokine release, and cytotoxic killing.
Autologous T cells engineered to express a chimeric antigen receptor recognizing CD70. CAR engagement of CD70 on tumor cells triggers CD3ζ/co-stimulatory signaling, leading to T‑cell activation, expansion, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of CD70‑expressing cancer cells.
CAR engagement of CD70 activates CAR‑T cells to release perforin and granzymes (and other cytotoxic pathways), inducing apoptosis/lysis of CD70‑expressing cells.
An antibody-drug conjugate carrying a topoisomerase I inhibitor payload; binds a tumor cell-surface antigen, is internalized, and releases the payload to induce DNA damage and tumor cell death.
An anti-nectin-4 IgG1 antibody-drug conjugate that binds nectin-4 on tumor cells, is internalized, and via a cleavable linker releases a topoisomerase I inhibitor payload. The payload inhibits topoisomerase I, disrupting DNA replication and causing DNA damage, cell-cycle arrest, and apoptosis in nectin-4–expressing cancer cells.
ADC binds Nectin-4 on tumor cells, is internalized, and a cleavable linker releases a topoisomerase I inhibitor intracellularly, causing DNA damage, cell-cycle arrest, and apoptosis of Nectin-4–expressing cells.
Allogeneic cord blood–derived natural killer cells engineered with a TROP2-specific CAR and an IL-15 transgene to provide targeted NK cytotoxicity against TROP2-positive tumor cells and enhance NK survival and persistence.
Allogeneic cord blood–derived NK cells engineered with a TROP2-specific chimeric antigen receptor to direct antigen-specific NK cytotoxicity against TROP2-positive tumor cells; co-expression of IL-15 supports NK activation, survival, proliferation, and persistence in vivo.
TROP2-specific CAR on NK cells binds TROP2 on target cells, activating NK cytotoxicity with degranulation (perforin/granzyme-mediated apoptosis) and death-receptor pathways; IL-15 supports NK activity and persistence.
An oncolytic adenovirus with replication driven by the survivin (BIRC5) promoter active in high-grade glioma cells; pk7 polylysine fiber modification enables CAR-independent entry via heparan sulfate proteoglycans, producing tumor-selective oncolysis and potential anti-tumor immune activation.
Engineered adenovirus that replicates selectively in survivin (BIRC5)-expressing glioma cells; pk7 polylysine fiber modification enables CAR-independent entry via heparan sulfate proteoglycans, leading to tumor-restricted viral replication, oncolysis, and secondary activation of anti-tumor immune responses.
The adenovirus replicates only in cells with active survivin (BIRC5) promoter, leading to selective viral replication and lytic oncolysis of those cells.