Autologous peripheral blood lymphocytes genetically engineered to express T-cell receptors specific for KRAS G12D or G12V neoantigens (HLA class I/II–restricted) to recognize mutant KRAS peptides and kill tumor cells.
Autologous T cells are genetically engineered to express HLA class I/II-restricted T-cell receptors specific for KRAS G12D or G12V neoantigen peptides; binding of these mutant KRAS peptides on tumor cells triggers T-cell activation and cytotoxic killing (perforin/granzyme-mediated lysis) of the target cells.
Engineered TCR T cells recognize the HLA-presented KRAS G12D peptide and directly kill target cells via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Autologous peripheral blood lymphocytes genetically engineered to express T-cell receptors specific for KRAS G12D or G12V neoantigens (HLA class I/II–restricted) to recognize mutant KRAS peptides and kill tumor cells.
Autologous T cells are genetically engineered to express HLA class I/II-restricted T-cell receptors specific for KRAS G12D or G12V neoantigen peptides; binding of these mutant KRAS peptides on tumor cells triggers T-cell activation and cytotoxic killing (perforin/granzyme-mediated lysis) of the target cells.
Engineered TCR-transduced T cells recognize the HLA-presented KRAS G12V peptide on tumor cells and kill them via perforin/granzyme-mediated cytotoxicity (apoptosis/lysis).
Fully humanized IgG1 antibody-drug conjugate targeting B7-H3 (CD276); binding triggers internalization and delivery of a cytotoxic payload with potential Fc-mediated effector activity.
Fully humanized IgG1 antibody-drug conjugate targeting B7-H3 (CD276). Upon binding to B7-H3 on tumor cells, the ADC is internalized and releases a topoisomerase inhibitor payload that inhibits topoisomerase activity (primarily Topo I), blocking DNA replication and inducing cell-cycle arrest and apoptosis; the IgG1 Fc may also engage immune effector functions (e.g., ADCC/ADCP).
HS-20093 ADC binds B7-H3 on target cells, is internalized, and releases a topoisomerase I inhibitor that blocks DNA replication causing cell-cycle arrest and apoptosis; its IgG1 Fc can also trigger ADCC/ADCP against B7-H3–positive cells.
Patient-derived T cells genetically engineered to express an anti-CD5 chimeric antigen receptor that binds CD5 on malignant T cells and activates CAR-mediated cytotoxicity (CD3zeta/costimulatory signaling), leading to killing of CD5+ tumor cells with expected on-target depletion of normal CD5+ T cells.
Autologous patient T cells are genetically engineered to express a CD5-directed chimeric antigen receptor. Upon binding CD5 on malignant T cells, the CAR transmits activation signals (CD3ζ with costimulatory domains), triggering T-cell cytotoxicity (perforin/granzyme) and elimination of CD5+ tumor cells, with expected on-target depletion of normal CD5+ T cells.
CD5 CAR T cells bind CD5 on target cells, activating CAR signaling and T-cell cytotoxicity (perforin/granzyme-mediated lysis/apoptosis) to kill CD5+ cells.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting B-cell antigens (CD19 and/or CD22 for B-ALL/B-NHL or BCMA for multiple myeloma) and to co-express interleukin-15 (IL-15) to enhance T-cell activation, proliferation, survival, and persistence for antitumor cytotoxicity.
Autologous T lymphocytes are engineered to express a chimeric antigen receptor targeting B‑cell antigens (CD19 and/or CD22, or BCMA). Antigen engagement triggers CAR/CD3ζ signaling, leading to T‑cell activation and cytotoxic killing of tumor cells via perforin/granzymes and cytokine release. Co‑expressed IL‑15 delivers autocrine IL‑15R–JAK/STAT signaling that enhances T‑cell activation, proliferation, survival, and persistence, improving antitumor efficacy.
CAR T cells bind CD19 on target cells; CAR/CD3ζ signaling activates T-cell cytotoxicity, leading to perforin/granzyme-mediated apoptosis (with possible Fas/FasL), augmented by IL-15-enhanced activation and persistence.