Autologous adoptive cell therapy comprising patient-derived tumor-reactive T cells isolated from bladder tumors, expanded ex vivo with IL-2 and anti-CD3 stimulation, and administered intravesically to treat high-grade non-muscle-invasive urothelial carcinoma.
Autologous tumor-infiltrating lymphocytes (TIL) are isolated from the patient’s bladder tumor, activated and expanded ex vivo with IL-2 and anti-CD3, then administered intravesically. These non-engineered T cells recognize tumor antigens via their native TCRs and mediate cytotoxicity (perforin/granzyme) and cytokine release (e.g., IFN-γ), increasing local anti-tumor immunity within the bladder.
Tumor-reactive TILs use native TCRs to recognize the tumor antigen peptide presented by HLA-DQ (pMHC II) and directly kill the presenting cells via perforin/granzyme cytotoxicity (and Fas-FasL).
Autologous T lymphocytes genetically modified ex vivo to express a chimeric antigen receptor targeting CD123 (IL-3 receptor alpha); infused once post-lymphodepletion to induce targeted cytotoxicity via CAR-mediated activation, proliferation, cytokine release, and perforin/granzyme-dependent killing of CD123+ malignant cells.
Autologous T cells are engineered ex vivo to express a CD123-specific chimeric antigen receptor. After infusion, CAR engagement of CD123 activates the T cells, driving proliferation, cytokine release, and targeted killing of CD123-positive malignant cells via perforin/granzyme and death-receptor pathways, independent of the native TCR.
Anti-CD123 CAR T cells recognize CD123 on target cells and, upon CAR activation, kill them via T‑cell cytotoxicity (perforin/granzyme release and death‑receptor/apoptotic pathways).
Humanized anti-HER2 IgG1 monoclonal antibody that inhibits HER2 signaling and dimerization, promotes receptor downregulation, and mediates ADCC via Fcγ receptor–bearing NK cells.
Humanized anti-HER2 IgG1 monoclonal antibody that binds HER2, blocks receptor dimerization and downstream signaling, promotes receptor internalization/downregulation, and triggers antibody-dependent cellular cytotoxicity via Fc gamma receptor–bearing NK cells, inhibiting proliferation of HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on target cells and its Fc region engages Fcγ receptors on NK cells (and other effectors) to trigger antibody‑dependent cellular cytotoxicity (ADCC), killing HER2-expressing cells; complement-mediated cytotoxicity may also contribute.
An intravenous, glycoengineered type I anti‑CD20 monoclonal antibody immunotherapy that selectively binds CD20 on B cells and depletes them primarily via enhanced antibody‑dependent cellular cytotoxicity, with contributions from complement‑dependent cytotoxicity and apoptosis; targets pre‑B and mature CD20+ B lymphocytes (sparing plasma cells) to reduce antigen presentation, costimulation, and proinflammatory cytokine signaling in multiple sclerosis.
Glycoengineered type I anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B lymphocytes and depletes them primarily via enhanced antibody‑dependent cellular cytotoxicity, with additional complement‑dependent cytotoxicity and apoptosis; spares plasma cells and reduces B‑cell antigen presentation, costimulation, and proinflammatory cytokine signaling.
Ublituximab binds CD20 on B cells and induces killing via Fc-mediated antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Fourth-generation dual-target autologous chimeric antigen receptor T cells engineered to recognize CD19 on B cells and BCMA (TNFRSF17) on plasmablasts/plasma cells, inducing cytolytic depletion of autoreactive B-lineage cells to reduce autoantibody production.
Autologous fourth-generation CAR T cells engineered to recognize CD19 and BCMA activate upon antigen binding and mediate cytolytic killing of B cells, plasmablasts, and plasma cells, thereby depleting autoreactive B-lineage populations and reducing autoantibody production.
BCMA-targeted CAR-T cells bind BCMA on plasmablasts/plasma cells, become activated, and kill them via perforin/granzyme-mediated cytolysis and death-receptor pathways (e.g., Fas/FasL).