Glycoengineered chimeric IgG1 anti-CD20 monoclonal antibody (Briumvi) that selectively depletes CD20+ pre-B and mature B lymphocytes via enhanced antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), reducing B-cell antigen presentation, proinflammatory cytokine secretion, and pathogenic antibody production to dampen CNS neuroinflammation in multiple sclerosis.
Glycoengineered anti‑CD20 IgG1 monoclonal antibody that binds CD20 on pre‑B and mature B cells and depletes them via enhanced antibody‑dependent cellular cytotoxicity (ADCC) and complement‑dependent cytotoxicity (CDC), thereby reducing B‑cell antigen presentation, proinflammatory cytokine release, and pathogenic antibody production to dampen CNS neuroinflammation in multiple sclerosis.
Anti-CD20 mAb binds CD20 on B cells and triggers Fc-mediated ADCC (e.g., NK cells/macrophages) and complement-dependent cytotoxicity (CDC), leading to lysis/apoptosis of CD20+ cells.
Antibody–drug conjugate targeting TROP-2; an anti–TROP-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor) that delivers cytotoxic payload to TROP-2–expressing tumor cells causing DNA damage and cell death.
Anti–TROP-2 monoclonal antibody (hRS7) conjugated to SN-38 (topoisomerase I inhibitor). The antibody binds TROP-2 on tumor cells, is internalized, and the linker is cleaved to release SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA breaks, inhibition of DNA replication, and apoptosis.
ADC binds TROP-2 on target cells, is internalized, and releases SN-38; SN-38 inhibits topoisomerase I, causing DNA damage and apoptosis of TROP-2-positive cells.
An antibody-drug conjugate targeting Trop-2 that delivers the topoisomerase I inhibitor SN-38 to induce DNA damage and cytotoxicity.
Humanized anti-TROP2 monoclonal antibody linked to SN-38. Upon TROP2 binding and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I, stabilizes TOP1-DNA complexes, causes DNA breaks, blocks DNA replication, and induces apoptosis.
The ADC binds TROP2 on target cells, is internalized, and releases SN-38 intracellularly; SN-38 inhibits topoisomerase I, causing DNA breaks and apoptosis in TROP2-expressing cells.
Autologous T lymphocytes genetically engineered to express a T-cell receptor specific for an HPV16 E7 peptide presented by HLA-A*02:01; infused to recognize and kill E7-positive tumor cells.
Autologous T lymphocytes genetically engineered to express an HLA-A*02:01–restricted T-cell receptor specific for an HPV16 E7 peptide. Upon encountering E7–HLA complexes on tumor cells, the TCR-T cells activate via TCR signaling and mediate cytotoxic killing through perforin/granzyme release and cytokine secretion, eliminating E7-positive cancer cells.
Engineered TCR-T cells recognize the HPV16 E7 peptide–HLA-A*02:01 complex via their TCR and kill target cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis) after activation.
Autologous, gene-modified cellular therapy (CD19-directed CAR-T; relma-cel, JWCAR029) made from the patient’s T cells; administered as a single fixed dose of 1×10^8 CAR+ T cells to target and kill CD19+ B-cell lymphoma cells; expected on-target effect includes B-cell aplasia.
Autologous T cells genetically modified to express a CD19-directed chimeric antigen receptor; after infusion, the CAR binds CD19 on B cells, activating and expanding the T cells to release cytotoxic mediators and kill CD19+ lymphoma cells, with on-target B-cell aplasia.
CD19-directed CAR T cells bind CD19 on target B cells, become activated, and directly kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).