Autologous T cells engineered to express a chimeric antigen receptor targeting CD19, administered as a single IV infusion after lymphodepletion to deplete CD19+ B-lineage cells and modulate humoral autoimmunity.
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor recognize and bind CD19 on B-lineage cells, triggering T-cell activation, proliferation, and cytotoxic killing (perforin/granzyme). This results in deep depletion of CD19+ B cells (including naive, memory, and plasmablasts), reducing autoantibody production and B cell–mediated immune activation after lymphodepletion and a single IV infusion.
CD19-specific CAR-T cells bind CD19 on target cells and kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, with possible Fas/FasL signaling).
Therapeutic monoclonal antibody targeting CCR8 on tumor-infiltrating regulatory T cells, engineered for enhanced ADCC to selectively deplete CCR8+ Tregs and reduce intratumoral immunosuppression.
HC006 is a monoclonal antibody that binds CCR8 on tumor-infiltrating regulatory T cells and is Fc-engineered for enhanced ADCC, recruiting FcγR-expressing effector cells (e.g., NK cells) to selectively deplete CCR8+ Tregs in the tumor microenvironment, thereby reducing intratumoral immunosuppression and promoting antitumor immunity.
Anti-CCR8 mAb binds CCR8 on Tregs; its Fc engages FcγR on NK cells (and other effectors) to trigger ADCC (and ADCP), leading to depletion of CCR8+ cells.
An intravenous CD19-directed antibody–drug conjugate (ADC), also known as MT-2111. A humanized anti-CD19 monoclonal IgG that binds CD19 on malignant B cells, is internalized, and releases a pyrrolobenzodiazepine (PBD) dimer payload (tesirine) via a cleavable linker to create DNA crosslinks and induce apoptosis.
Humanized anti-CD19 monoclonal antibody binds CD19 on B cells, is internalized, and via a cleavable linker releases a pyrrolobenzodiazepine (PBD) dimer payload (tesirine) that forms DNA minor-groove interstrand crosslinks (N2-guanine), blocking DNA replication and inducing apoptosis in CD19-expressing tumor cells.
Anti-CD19 ADC binds CD19, is internalized, and releases a PBD dimer (tesirine) via a cleavable linker that forms DNA interstrand crosslinks, blocking replication and inducing apoptosis in CD19+ cells.
Fully human IgG1 monoclonal antibody immunotherapy that selectively binds CD20 on B lymphocytes and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, while sparing stem cells and plasma cells; suppresses B cell–mediated antigen presentation, T-cell costimulation, cytokine production, and autoantibody-driven inflammation relevant to MS.
Fully human IgG1 monoclonal antibody targeting CD20 on B lymphocytes; induces B-cell depletion via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, sparing stem cells and plasma cells, thereby reducing antigen presentation, T-cell costimulation, cytokine release, and autoantibody-driven inflammation.
Ofatumumab binds CD20 on B cells and induces complement-dependent lysis and Fc-mediated ADCC (with apoptosis), directly depleting CD20+ cells.
Type II, glycoengineered anti-CD20 monoclonal antibody that depletes CD20+ B cells via enhanced ADCC and direct cell death; used as pre-treatment to mitigate CRS.
Glycoengineered, humanized type II anti‑CD20 IgG1 that binds CD20 on B cells; afucosylated Fc increases FcγRIIIa binding to enhance ADCC (and ADCP) and induces direct, caspase‑independent cell death, leading to depletion of CD20+ B cells.
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages Fc-gammaRIIIa on effector cells to trigger potent ADCC and ADCP, and it also induces direct, caspase-independent cell death of CD20+ cells.