Autologous CAR T-cell therapy engineered to express a STEAP2-specific chimeric antigen receptor; upon binding STEAP2 on prostate cancer cells, it activates T cells to proliferate, release cytokines, and lyse STEAP2-positive tumor cells. Administered intravenously after lymphodepleting chemotherapy.
Autologous T cells engineered to express a STEAP2-specific CAR and a dominant-negative TGF-β receptor II. Upon binding STEAP2 on prostate cancer cells, CAR signaling activates T cells to proliferate, secrete cytokines, and kill target cells via cytotoxic mechanisms, while the dnTGFBRII blocks immunosuppressive TGF-β signaling to enhance activity in the tumor microenvironment.
NO
INDIRECT
Cells expressing TGF-β1 are not directly targeted. AZD0754 CAR T cells kill STEAP2-positive tumor cells via perforin/granzyme-mediated cytolysis; the dnTGFβRII arm only blocks TGF-β signaling in the CAR T cells.
Autologous CAR T-cell therapy engineered to express a STEAP2-specific chimeric antigen receptor; upon binding STEAP2 on prostate cancer cells, it activates T cells to proliferate, release cytokines, and lyse STEAP2-positive tumor cells. Administered intravenously after lymphodepleting chemotherapy.
Autologous T cells engineered to express a STEAP2-specific CAR and a dominant-negative TGF-β receptor II. Upon binding STEAP2 on prostate cancer cells, CAR signaling activates T cells to proliferate, secrete cytokines, and kill target cells via cytotoxic mechanisms, while the dnTGFBRII blocks immunosuppressive TGF-β signaling to enhance activity in the tumor microenvironment.
NO
INDIRECT
TGF-β2 is not targeted for killing; the dnTGFBRII only blocks TGF-β signaling in the CAR T cells. Cytotoxicity is directed against STEAP2-positive cells via CAR-activated T-cell perforin/granzyme pathways, not against TGF-β2–expressing cells.
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.
NO
INDIRECT
This CAR T therapy targets CD19, killing CD19+ cells via T‑cell cytotoxicity (perforin/granzyme). EGFR is only a truncated tag (huEGFRt) on the CAR T cells for selection/depletion and is not a cytotoxic target; EGFR+ cells are not targeted.
Autologous CAR T-cell therapy engineered to express a STEAP2-specific chimeric antigen receptor; upon binding STEAP2 on prostate cancer cells, it activates T cells to proliferate, release cytokines, and lyse STEAP2-positive tumor cells. Administered intravenously after lymphodepleting chemotherapy.
Autologous T cells engineered to express a STEAP2-specific CAR and a dominant-negative TGF-β receptor II. Upon binding STEAP2 on prostate cancer cells, CAR signaling activates T cells to proliferate, secrete cytokines, and kill target cells via cytotoxic mechanisms, while the dnTGFBRII blocks immunosuppressive TGF-β signaling to enhance activity in the tumor microenvironment.
NO
INDIRECT
TGF-β3 is not the CAR target. The dnTGFβRII only blocks TGF-β signaling in the CAR T cells. Killing is directed to STEAP2-positive cells via CAR T cell cytotoxicity (perforin/granzyme-mediated lysis).
An intravenous antibody-drug conjugate targeting Nectin-4; the monoclonal antibody binds Nectin-4 on tumor cells, is internalized, and releases a cytotoxic payload intracellularly to kill the cancer cell. Intended for Nectin-4-expressing epithelial tumors (e.g., urothelial carcinoma, TNBC, NSCLC, esophageal, pancreatic, ovarian, cervical, HNSCC, prostate).
A monoclonal antibody targets Nectin-4 on tumor cells, is internalized, and via a cleavable linker releases the camptothecin analog/topoisomerase I inhibitor LSN3889710, inhibiting DNA replication and inducing cell cycle arrest and apoptosis in Nectin-4–expressing tumors.
YES
DIRECT
ADC binds Nectin-4 on tumor cells, is internalized, and a cleavable linker releases the topoisomerase I inhibitor LSN3889710, causing DNA replication inhibition/DNA damage leading to cell cycle arrest and apoptosis.