Bispecific T-cell engager antibody (CD19xCD3) that redirects patient T cells to kill CD19-positive B-ALL blasts.
CD19xCD3 bispecific (BiTE) antibody that binds CD19 on B cells and CD3 on T cells, bridging them to form an immune synapse and redirect T‑cell cytotoxicity (perforin/granzyme) against CD19‑positive blasts, independent of MHC, leading to B‑cell depletion.
Blinatumomab links CD19 on target cells to CD3 on T cells, forming an immune synapse and inducing T‑cell perforin/granzyme–mediated killing of CD19+ cells (MHC‑independent).
Investigational monoclonal antibody targeting CCR8 on tumor-infiltrating regulatory T cells (Tregs); designed to block the CCL1–CCR8 axis and/or deplete CCR8+ Tregs to reduce immunosuppression.
Monoclonal antibody targeting CCR8 on tumor-infiltrating regulatory T cells; blocks CCL1–CCR8 signaling and may deplete CCR8+ Tregs, reducing immunosuppression in the tumor microenvironment and restoring antitumor immune responses.
Antibody binding to CCR8 on Tregs triggers Fc-mediated effector functions (ADCC/ADCP, possibly CDC), depleting CCR8+ cells; it also blocks CCL1–CCR8 signaling.
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, complement-dependent cytotoxicity, and apoptosis to reduce immune drivers of proteinuria.
Anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis, reducing pathogenic B-cell activity.
Anti-CD20 mAb binds CD20 on B cells; Fc engages effector cells for ADCC, activates complement for CDC, and can trigger direct apoptotic signaling in target cells.
Autologous gene-modified T-cell therapy using a T-cell Antigen Coupler (TAC) that binds CLDN18.2 on tumors and activates endogenous TCR/CD3 signaling; administered as a single IV infusion.
Autologous T cells are genetically engineered to express a T-cell Antigen Coupler (TAC) that binds CLDN18.2 on tumor cells and engages the endogenous TCR/CD3 complex, triggering physiologic TCR signaling to activate, proliferate, and mediate cytotoxic killing of CLDN18.2-expressing tumor cells.
Engineered TAC T cells bind CLDN18.2 on target cells and engage endogenous TCR/CD3, activating CTL effector functions (perforin/granzyme and Fas–FasL) to kill CLDN18.2-expressing cells.
An anti-CD33 antibody–drug conjugate that targets CD33-positive myeloblasts and delivers the cytotoxic agent calicheamicin to induce DNA double-strand breaks.
Anti-CD33 monoclonal antibody–drug conjugate that binds CD33 on myeloblasts, is internalized, and releases the cytotoxic payload calicheamicin in lysosomes; calicheamicin binds the DNA minor groove and induces double‑strand breaks, leading to apoptosis of CD33-positive cells.
Anti-CD33 antibody-drug conjugate binds CD33, is internalized, and releases calicheamicin that induces DNA double-strand breaks, triggering apoptosis of CD33-positive cells.