An antibody–drug conjugate targeting Trop-2 that delivers the topoisomerase I inhibitor SN-38 to tumor cells, causing DNA damage and tumor cell death with a bystander effect.
Humanized anti-Trop-2 antibody (hRS7) delivers the topoisomerase I inhibitor SN-38 to Trop-2–expressing tumor cells. After binding and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I-DNA covalent complexes, causing DNA breaks, replication arrest, and apoptosis; released payload can also produce a bystander cytotoxic effect.
Anti-TROP2 ADC binds and is internalized; linker cleavage releases SN-38 (topoisomerase I inhibitor) in TROP2+ cells, causing DNA damage, replication arrest, and apoptosis; released payload can also cause bystander killing.
Autologous T cells genetically engineered to express patient-specific T-cell receptors that recognize 1–5 tumor-specific neoantigen peptides presented by HLA, enabling antigen-specific T-cell activation and tumor cell killing.
Autologous T cells are genetically engineered to express patient-specific T-cell receptors that recognize tumor neoantigen peptides presented by the patient's HLA. Binding of the neoantigen-HLA complex activates TCR signaling, driving T-cell activation, clonal expansion, cytokine release, and perforin/granzyme-mediated cytotoxicity, resulting in antigen-specific tumor cell killing.
Engineered TCR T cells recognize the neoantigen–HLA (peptide–MHC) complex on target cells, form an immunologic synapse, and induce apoptosis via perforin/granzyme release and Fas–FasL signaling.
Autologous, gene-engineered TCR-T cell therapy expressing an HLA-A*11:01–restricted T-cell receptor targeting mutant KRAS G12V on tumor cells.
Autologous T cells are genetically engineered to express an HLA-A*11:01–restricted T-cell receptor that recognizes mutant KRAS G12V peptides presented on tumor cells. Antigen engagement activates the T cells to mediate targeted cytotoxicity (perforin/granzyme release and cytokine secretion), leading to selective killing of KRAS G12V–positive tumor cells.
Engineered TCR-T cells recognize the HLA-A*11:01–presented KRAS G12V peptide and kill target cells via perforin/granzyme-mediated cytotoxicity (apoptosis).
Autologous, gene-engineered TCR-T cell therapy expressing an HLA-A*11:01–restricted T-cell receptor targeting mutant KRAS G12D on tumor cells.
Autologous T cells are genetically engineered to express an HLA-A*11:01–restricted T-cell receptor that recognizes the KRAS G12D neoantigen on tumor cells, enabling antigen-specific activation and cytotoxic killing via TCR signaling and release of perforin/granzymes.
Engineered TCR-T cells recognize the KRAS G12D peptide presented by HLA-A*11:01 and, upon TCR engagement, kill the target cell via cytolytic granule release (perforin/granzymes) leading to apoptosis.
Allogeneic natural killer (NK) cells derived from cord blood and engineered with a chimeric antigen receptor targeting CD19 to mediate NK cytotoxicity (perforin/granzyme) against CD19-positive B-cell malignancies, with low risk of GVHD/CRS.
Allogeneic cord blood–derived natural killer cells genetically engineered with a CD19-directed chimeric antigen receptor. CAR engagement of CD19 on malignant B cells triggers NK activation and perforin/granzyme-mediated cytotoxicity, with low risk of graft-versus-host disease and typically reduced cytokine release compared with CAR-T cells.
CAR engagement of CD19 on target cells activates the NK cell, causing degranulation with perforin and granzymes that induce lysis/apoptosis of CD19+ cells.