Autologous CD19/CD20-directed chimeric antigen receptor (CAR) T-cell therapy; patient T cells are genetically engineered to express CARs targeting CD19 and CD20 on B cells to mediate cytotoxic killing of lymphoma cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor recognizing CD19 and CD20 on B cells; antigen binding activates CAR signaling to expand and activate the T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with on-target depletion of normal B cells.
CAR T cells engineered to target CD19 bind the antigen and, upon CAR signaling, kill CD19+ cells via perforin/granzyme release (and death receptor pathways), leading to apoptosis/lysis.
Anti‑CD20 monoclonal IgG1 antibody that depletes CD20‑positive B cells via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis.
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (CDC), and induction of apoptosis.
An intravenous mRNA–lipid nanoparticle therapy that delivers mRNA to the liver to produce a bispecific T-cell engager targeting GPC3-positive hepatocellular carcinoma cells and activating endogenous T cells for tumor cell killing.
Intravenous lipid nanoparticles deliver mRNA to the liver, where it is translated into a bispecific T-cell engager that binds GPC3 on hepatocellular carcinoma cells and engages endogenous T cells, activating them to mediate cytotoxic killing of GPC3-positive tumor cells.
An expressed bispecific T‑cell engager binds GPC3 on tumor cells and CD3 on T cells, forming a cytolytic synapse that activates T cells to kill GPC3+ cells via perforin/granzyme-mediated apoptosis.
Autologous gene-modified T cells engineered to express a chimeric antigen receptor targeting CD19 on B cells, leading to T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant CD19+ B cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting CD19 on B cells. Binding to CD19 triggers MHC-independent T-cell activation and co-stimulation, leading to T-cell expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant CD19+ B cells (with on-target depletion of normal B cells).
Anti-CD19 CAR-T cells recognize CD19 on target cells, triggering T-cell activation and perforin/granzyme-mediated cytotoxic killing (MHC-independent).
Investigational CLDN18.2-targeted antibody-drug conjugate that binds claudin 18.2 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death; may also engage immune effector functions.
CLDN18.2-targeted monoclonal antibody linked via a cleavable linker to MMAE; after binding CLDN18.2 on tumor cells and internalization, releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc region may engage immune effector functions.
ADC binds CLDN18.2, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; Fc region may also trigger ADCC/CDC.