HER2-targeted antibody-drug conjugate that binds HER2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload causing DNA damage and tumor cell death (potential bystander effect).
Anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor, stabilizing topo I–DNA complexes and causing DNA breaks, replication arrest, and apoptosis; potential bystander killing of adjacent cells.
The anti-HER2 ADC binds HER2, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that traps topo I–DNA complexes, causing DNA breaks, replication arrest, and apoptosis (with possible bystander killing).
An autologous, gene-modified CAR T-cell therapy that co-targets CD19 and CD20. Patient T cells are engineered to express a chimeric antigen receptor recognizing CD19 and CD20 on B cells; antigen binding triggers T-cell activation, cytotoxic killing, cytokine release, and in vivo expansion, resulting in deep B-cell depletion and aiming to reduce antigen escape versus single-antigen approaches.
Autologous T cells are gene-modified to express a chimeric antigen receptor that recognizes both CD19 and CD20 on B cells. CAR engagement activates the T cells, driving cytotoxic killing, cytokine release, and in vivo expansion, resulting in profound depletion of CD19+/CD20+ B cells and reducing antigen-escape compared with single-antigen CARs.
CAR T cells recognize CD19 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis and apoptosis.
An autologous, gene-modified CAR T-cell therapy that co-targets CD19 and CD20. Patient T cells are engineered to express a chimeric antigen receptor recognizing CD19 and CD20 on B cells; antigen binding triggers T-cell activation, cytotoxic killing, cytokine release, and in vivo expansion, resulting in deep B-cell depletion and aiming to reduce antigen escape versus single-antigen approaches.
Autologous T cells are gene-modified to express a chimeric antigen receptor that recognizes both CD19 and CD20 on B cells. CAR engagement activates the T cells, driving cytotoxic killing, cytokine release, and in vivo expansion, resulting in profound depletion of CD19+/CD20+ B cells and reducing antigen-escape compared with single-antigen CARs.
CAR T cells bind CD20 via the CAR, become activated, and lyse target cells through perforin/granzyme-mediated cytotoxicity and apoptosis (e.g., death receptor pathways).
Intratumoral, genetically engineered oncolytic herpes simplex virus (HSV-1) designed for direct oncolysis, immune activation, and transgene delivery; includes virulence gene deletions and expresses a recombinant bispecific antibody. Evaluated primarily in head and neck squamous cell carcinoma.
Intratumoral, genetically engineered HSV-1 that selectively replicates in tumor cells due to virulence gene deletions, causing direct oncolysis and local spread; releases tumor antigens to activate dendritic cells and cytotoxic T cells; delivers a transgene encoding a recombinant bispecific antibody to further enhance antitumor immunity and counter local immunosuppression. Evaluated primarily in head and neck squamous cell carcinoma.
HSV-1 uses Nectin-1 (CD111) as an entry receptor (gD binding); after entry the engineered virus selectively replicates in tumor cells, causing lytic oncolysis.
Intratumoral, genetically engineered oncolytic herpes simplex virus (HSV-1) designed for direct oncolysis, immune activation, and transgene delivery; includes virulence gene deletions and expresses a recombinant bispecific antibody. Evaluated primarily in head and neck squamous cell carcinoma.
Intratumoral, genetically engineered HSV-1 that selectively replicates in tumor cells due to virulence gene deletions, causing direct oncolysis and local spread; releases tumor antigens to activate dendritic cells and cytotoxic T cells; delivers a transgene encoding a recombinant bispecific antibody to further enhance antitumor immunity and counter local immunosuppression. Evaluated primarily in head and neck squamous cell carcinoma.
Oncolytic HSV-1 uses HVEM as an entry receptor to infect cells; the engineered virus then selectively replicates in tumor cells and causes direct lysis (with additional secondary immune-mediated killing from released antigens).