Autologous, second-generation bispecific CAR T-cell therapy targeting CD19 and CD20; utilizes CD3 zeta signaling and 4-1BB costimulation to enhance T-cell activation, expansion, and persistence; administered as a single IV infusion after lymphodepletion for relapsed/refractory large B-cell lymphoma.
Autologous T cells engineered with a second-generation bispecific CAR that recognizes CD19 and CD20 on B-cell malignancies. Antigen binding activates CD3 zeta signaling to drive T-cell cytotoxicity, while the 4-1BB costimulatory domain enhances expansion and persistence, leading to depletion of malignant (and normal) B cells and helping prevent antigen-escape relapse.
CAR T cells recognize CD20 on B cells, triggering CD3ζ signaling with 4-1BB costimulation and inducing cytolysis via perforin/granzyme (and Fas–FasL), killing CD20-positive cells.
Autologous, gene-modified BCMA-directed CAR T-cell therapy (Carvykti; cilta-cel) that targets BCMA-expressing myeloma cells.
Autologous T cells are gene-modified ex vivo to express a BCMA-directed chimeric antigen receptor with dual-epitope binders and a 4-1BB costimulatory domain. After infusion, these CAR T cells recognize BCMA on malignant plasma cells, become activated, proliferate, release cytokines, and mediate perforin/granzyme-dependent cytolysis of BCMA-expressing myeloma cells.
BCMA-targeted CAR T cells recognize BCMA on target cells and kill them via T-cell cytotoxicity, primarily perforin/granzyme-mediated lysis after CAR activation.
Anti-CD33 antibody-drug conjugate that delivers calicheamicin to CD33+ AML cells, causing DNA double-strand breaks.
Anti-CD33 monoclonal antibody-drug conjugate that binds CD33 on AML blasts, is internalized, and releases calicheamicin; the payload binds the DNA minor groove and induces double-strand breaks, leading to cell death.
The anti‑CD33 ADC binds CD33, is internalized, and releases calicheamicin intracellularly; the payload binds DNA’s minor groove causing double‑strand breaks and apoptosis of CD33+ cells.
Anti-CD33 antibody-drug conjugate that delivers calicheamicin to CD33+ AML cells, causing DNA double-strand breaks.
Anti-CD33 monoclonal antibody-drug conjugate that binds CD33 on AML blasts, is internalized, and releases calicheamicin; the payload binds the DNA minor groove and induces double-strand breaks, leading to cell death.
After CD33-mediated internalization, calicheamicin is released and binds the DNA minor groove, inducing double‑strand breaks that trigger apoptosis and cell death.