Autologous, gene-modified T lymphocytes expressing a chimeric antigen receptor targeting CD276 (B7-H3) for recurrent/progressive glioblastoma; intracranial (Ommaya) delivery with weekly dosing in a 3+3 escalation (5×10^6 then 1×10^7 cells). Redirects T cells independent of native TCR, activating CAR signaling (CD3ζ with costimulation), cytokine release, and perforin/granzyme-mediated cytotoxicity against CD276-positive tumor and vasculature.
Autologous T lymphocytes engineered to express a CD276 (B7-H3)-specific chimeric antigen receptor. CAR binding to CD276 on tumor cells and tumor vasculature activates CD3ζ and costimulatory signaling, driving T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxic killing independent of the native TCR.
CAR-T cells recognize CD276 on target cells, triggering CD3ζ/costimulatory signaling and T-cell cytotoxicity via perforin/granzyme release (with cytokine-mediated effects).
A T cell–engaging bispecific antibody immunotherapy that binds Claudin 18.2 on tumor cells and CD3 on T cells to redirect and activate endogenous T cells, inducing cytotoxic killing of tumor cells; administered intravenously or subcutaneously.
Affinity-optimized bispecific antibody that binds CLDN18.2 on tumor cells (bivalent, high affinity) and CD3 on T cells (monovalent, low affinity), crosslinking tumor cells and T cells to activate and expand cytotoxic T lymphocytes, triggering TCR signaling, immune synapse formation, cytokine release, and lysis of CLDN18.2-positive tumor cells with potential bystander killing.
Bispecific T‑cell engager binds CLDN18.2 on tumor cells and CD3 on T cells, crosslinking to activate CTLs and form an immune synapse, leading to perforin/granzyme-mediated lysis of CLDN18.2+ cells (with potential bystander killing).
A humanized IgG1 antibody-drug conjugate that targets B7-H3 (CD276). It is given intravenously every 3 weeks; upon binding B7-H3 on tumor cells it is internalized and releases a cytotoxic payload, and its IgG1 Fc may mediate ADCC/ADCP.
Humanized IgG1 ADC targeting B7-H3 (CD276); after binding B7-H3 on tumor cells it is internalized and releases a topoisomerase inhibitor payload that inhibits DNA topoisomerase activity, leading to replication arrest and apoptosis. The IgG1 Fc may also induce ADCC/ADCP.
HS-20093 binds B7-H3 on target cells, is internalized, and releases a topoisomerase inhibitor payload that blocks DNA replication and induces apoptosis; its IgG1 Fc can also trigger ADCC/ADCP against B7-H3–positive cells.
Hypoimmune allogeneic CD19-directed CAR T-cell therapy; genetically engineered T cells designed to evade host immune recognition and kill CD19+ B-cell malignancies.
Allogeneic T cells engineered to express an anti-CD19 chimeric antigen receptor bind CD19 on malignant B cells, triggering T-cell activation and cytotoxic killing. Hypoimmune edits—disruption of MHC class I/II and expression of CD47—reduce host immune recognition and rejection, increasing persistence and efficacy as an off-the-shelf product.
Anti-CD19 CAR T cells bind CD19 on target cells, become activated, and kill via T-cell cytotoxic pathways (perforin/granzyme release and death receptor signaling).
A biological, cell-based immunotherapy administered by intravenous infusion at 3.0×10^8 or 6.0×10^8 cells (up to three monthly infusions) for refractory colorectal or pancreatic cancer; intended to elicit immune-mediated antitumor cytotoxicity. Specific cell type/engineering and target antigens are not disclosed.
Genetically modified human T lymphocytes engineered to express a chimeric antigen receptor that recognizes two undisclosed tumor-associated antigens. Upon binding antigen on colorectal or pancreatic tumor cells, the CAR activates T-cell effector functions (cytokine release, proliferation, and perforin/granzyme-mediated lysis), producing selective immune-mediated antitumor cytotoxicity and aiming to reduce antigen-escape through dual targeting.
CAR-T cells bind the antigen via the CAR and directly lyse antigen-expressing tumor cells through perforin/granzyme-mediated cytotoxicity and T-cell effector functions.