Autologous TCR-T cells engineered via mRNA to transiently express HBV antigen–specific T-cell receptors that recognize HBV peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, driving TCR/MHC class I–dependent activation and cytotoxicity against HBV-related hepatocellular carcinoma; administered by weekly IV infusion at 5–10×10^6 cells/kg.
Autologous T cells are transiently mRNA-engineered to express HBV-specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, triggering TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma cells.
Engineered TCR-T cells recognize the HLA-A*02:01–HBV peptide complex on tumor cells and induce TCR/MHC I–dependent killing via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous TCR-T cells engineered via mRNA to transiently express HBV antigen–specific T-cell receptors that recognize HBV peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, driving TCR/MHC class I–dependent activation and cytotoxicity against HBV-related hepatocellular carcinoma; administered by weekly IV infusion at 5–10×10^6 cells/kg.
Autologous T cells are transiently mRNA-engineered to express HBV-specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, triggering TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma cells.
Engineered TCR-T cells recognize the HBV peptide–HLA-A*24:02 complex via their TCR, leading to MHC I–dependent activation and killing of target cells through perforin/granzyme (and Fas–FasL) cytotoxic pathways.
A bispecific monoclonal antibody administered intravenously (QW, Q2W, or Q3W) as monotherapy that dual-targets PD-1 on T cells and HER2 on tumor cells to restore/augment T-cell activation and direct activity toward HER2-expressing tumors, for advanced solid malignancies.
Bispecific monoclonal antibody that binds PD-1 on T cells and HER2 on tumor cells, simultaneously blocking PD-1 checkpoint signaling to restore/augment T‑cell activation and tethering T cells to HER2‑expressing tumors to focus T‑cell–mediated killing; may also inhibit HER2-driven signaling in tumor cells.
The bispecific antibody bridges PD-1+ T cells to HER2+ tumor cells and blocks PD-1, enabling focused T‑cell–mediated killing (immune synapse formation and perforin/granzyme cytotoxicity).
Trop-2–directed antibody–drug conjugate that delivers SN-38 (a topoisomerase I inhibitor) to tumor cells to induce DNA damage.
TROP2-directed antibody-drug conjugate that binds TROP2 on tumor cells, is internalized, and releases SN-38 to inhibit topoisomerase I, causing DNA breaks and apoptotic cell death.
The ADC binds TROP-2, is internalized, and releases SN-38 (a topoisomerase I inhibitor) that induces DNA damage and apoptosis in the target cell.
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD5; antigen binding triggers CAR signaling (CD3ζ/co-stimulatory domains) leading to expansion and cytotoxic killing of CD5-positive malignant T cells.
Autologous T cells are engineered to express a chimeric antigen receptor targeting CD5; antigen binding triggers CD3ζ and co‑stimulatory signaling, driving T‑cell activation, expansion, and perforin/granzyme‑mediated cytotoxic killing of CD5‑positive malignant T cells.
CD5-targeted CAR T cells bind CD5, activate via CD3zeta/co-stimulatory signaling, and kill CD5+ cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.