Autologous, gene-modified chimeric antigen receptor T-cell (CAR-T) therapy engineered to express a dual-target CAR recognizing CD19 and CD22 on B-lineage cells; CAR signaling (CD3ζ with costimulation) activates T-cell cytotoxicity and cytokine release to eliminate malignant B lymphoblasts, with dual targeting intended to reduce antigen-escape relapse in relapsed/refractory B-ALL.
Autologous T cells are gene-modified to express a dual-target chimeric antigen receptor recognizing CD19 and CD22 on B-lineage cells. Antigen engagement triggers CAR signaling (CD3ζ with costimulation), inducing T-cell cytotoxicity and cytokine release to eliminate malignant B lymphoblasts; dual targeting is intended to reduce antigen-escape relapse and leads to on-target B-cell depletion.
CD19-expressing cells are recognized by the CD19-directed CAR on the infused T cells, which then kill targets via cytotoxic granule release (perforin/granzyme) and death-receptor pathways, leading to lysis/apoptosis of CD19+ cells.
Autologous, gene-modified chimeric antigen receptor T-cell (CAR-T) therapy engineered to express a dual-target CAR recognizing CD19 and CD22 on B-lineage cells; CAR signaling (CD3ζ with costimulation) activates T-cell cytotoxicity and cytokine release to eliminate malignant B lymphoblasts, with dual targeting intended to reduce antigen-escape relapse in relapsed/refractory B-ALL.
Autologous T cells are gene-modified to express a dual-target chimeric antigen receptor recognizing CD19 and CD22 on B-lineage cells. Antigen engagement triggers CAR signaling (CD3ζ with costimulation), inducing T-cell cytotoxicity and cytokine release to eliminate malignant B lymphoblasts; dual targeting is intended to reduce antigen-escape relapse and leads to on-target B-cell depletion.
CAR-T cells recognize CD22 via the engineered CAR, triggering CD3ζ/costimulatory signaling and T-cell activation, leading to perforin/granzyme-mediated lysis (and Fas/FasL, cytokines) of CD22+ cells.
Humanized IgG1 monoclonal antibody targeting HER2/ERBB2; binds HER2 on tumor cells to inhibit receptor dimerization and downstream PI3K/AKT/MAPK signaling, and engages Fcγ receptors to elicit antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing cells.
Trastuzumab binds HER2 and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate ADCC against HER2+ cells; may also trigger complement (CDC).
A Trop-2-directed antibody-drug conjugate (aliases: PBI-410, GQ1010). A monoclonal antibody binds Trop-2 (TACSTD2) on epithelial tumor cells, is internalized, and delivers a cytotoxic payload to kill Trop-2–expressing cancer cells.
A Trop-2-targeted monoclonal antibody binds TACSTD2 on tumor cells, is internalized, and releases a camptothecin analog via a cleavable linker to inhibit topoisomerase I, blocking DNA replication and inducing cell cycle arrest and apoptosis in Trop-2–expressing cancer cells.
An anti–TROP-2 antibody-drug conjugate binds TROP-2, is internalized, and releases a camptothecin analog that inhibits topoisomerase I, blocking DNA replication and triggering cell-cycle arrest and apoptosis in TROP-2–expressing cells.
An intravenous anti-GD2 IgG1 monoclonal antibody that binds GD2 on neuroblastoma cells and induces antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity.
Naxitamab is an IgG1 monoclonal antibody that binds the GD2 antigen on neuroblastoma cells and mediates tumor cell killing primarily through antibody-dependent cellular cytotoxicity (via NK cells and macrophages) and complement-dependent cytotoxicity, leading to immune-mediated lysis of GD2-expressing cells.
Anti-GD2 IgG1 binds GD2 on target cells and engages immune effectors via Fc to induce antibody-dependent cellular cytotoxicity and activates complement for complement-dependent cytotoxicity, leading to lysis of GD2-positive cells.