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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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).
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.
NO
INDIRECT
Heparan sulfate serves mainly as an attachment factor for HSV-1; cells are killed only if they are permissive to viral replication, which causes direct oncolysis and secondary immune-mediated killing, not due to heparan sulfate expression per se.