Adoptive cellular gene therapy using a patient’s T cells engineered with a piggyBac transposon to express an anti-CD19 chimeric antigen receptor; upon infusion, the cells target CD19+ B-lineage cells to deplete autoreactive clones and reduce autoantibodies in SLE.
Autologous T cells are gene-modified with a piggyBac transposon to express an anti-CD19 chimeric antigen receptor; upon infusion they recognize CD19 on B-lineage cells and induce CAR-mediated activation and cytotoxicity, depleting CD19+ B cells (including autoreactive clones) and reducing autoantibodies in SLE.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 and directly lyse target cells via immune synapse–mediated perforin/granzyme release and Fas–FasL apoptosis.
Autologous T cells engineered with the non-viral Sleeping Beauty transposon system to express an anti-CD19 chimeric antigen receptor incorporating 4-1BB costimulatory and CD3ζ activation domains, plus huEGFRt as a safety/selection tag; designed to mediate targeted cytotoxicity against CD19+ B-cell malignancies.
Autologous T cells are gene-modified using the Sleeping Beauty transposon to express an anti-CD19 chimeric antigen receptor with 4-1BB costimulatory and CD3zeta activation domains. Binding to CD19 on malignant B cells triggers T-cell activation, expansion, and targeted cytotoxic killing of CD19-positive cells; the huEGFRt tag enables selection, tracking, and potential antibody-mediated depletion for safety.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells, become activated via CD3ζ/4-1BB signaling, and kill CD19+ cells through T-cell cytolysis (perforin/granzyme release and Fas–FasL-mediated apoptosis).
A conditionally replicative oncolytic adenovirus engineered with an RGD-modified fiber to retarget entry to αv integrins (e.g., αvβ3/αvβ5) on pancreatic tumor cells; COX-2–linked selectivity enables tumor-restricted replication, inducing oncolysis and immunogenic cell death after endoscopic ultrasound–guided intratumoral injection.
RGDCRAdCOX2F is a conditionally replicative adenovirus engineered with an RGD-modified fiber to enter tumor cells via alpha v integrins (e.g., alpha v beta 3/alpha v beta 5). E1 expression is driven by a COX-2 promoter to restrict replication to COX-2–overexpressing tumors, resulting in selective intratumoral viral amplification, direct oncolysis, and immunogenic cell death with release of tumor antigens that can elicit anti-tumor immune responses.
NO
INDIRECT
The virus uses αv integrins for entry via its RGD-modified fiber, but killing requires COX-2–driven viral replication; αv expression alone is not sufficient, so oncolysis is not directly targeted to αv-positive cells.
A conditionally replicative oncolytic adenovirus engineered with an RGD-modified fiber to retarget entry to αv integrins (e.g., αvβ3/αvβ5) on pancreatic tumor cells; COX-2–linked selectivity enables tumor-restricted replication, inducing oncolysis and immunogenic cell death after endoscopic ultrasound–guided intratumoral injection.
RGDCRAdCOX2F is a conditionally replicative adenovirus engineered with an RGD-modified fiber to enter tumor cells via alpha v integrins (e.g., alpha v beta 3/alpha v beta 5). E1 expression is driven by a COX-2 promoter to restrict replication to COX-2–overexpressing tumors, resulting in selective intratumoral viral amplification, direct oncolysis, and immunogenic cell death with release of tumor antigens that can elicit anti-tumor immune responses.
YES
DIRECT
The RGD-modified adenovirus uses αvβ3 (integrin β3-containing) for entry; in COX-2–overexpressing cells it replicates and causes lytic oncolysis, directly killing the infected cells.
A conditionally replicative oncolytic adenovirus engineered with an RGD-modified fiber to retarget entry to αv integrins (e.g., αvβ3/αvβ5) on pancreatic tumor cells; COX-2–linked selectivity enables tumor-restricted replication, inducing oncolysis and immunogenic cell death after endoscopic ultrasound–guided intratumoral injection.
RGDCRAdCOX2F is a conditionally replicative adenovirus engineered with an RGD-modified fiber to enter tumor cells via alpha v integrins (e.g., alpha v beta 3/alpha v beta 5). E1 expression is driven by a COX-2 promoter to restrict replication to COX-2–overexpressing tumors, resulting in selective intratumoral viral amplification, direct oncolysis, and immunogenic cell death with release of tumor antigens that can elicit anti-tumor immune responses.
YES
DIRECT
RGD-modified adenovirus binds alpha v beta 5 integrin for entry; in COX-2–overexpressing cells, COX-2–driven E1 expression enables viral replication and lytic oncolysis, directly killing the infected cell.