Polyclonal IgG biologic immunosuppressant targeting T lymphocytes, administered pre-transplant to prevent GVHD. Depletes and modulates T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; inhibits T-cell activation/proliferation and trafficking; may reduce antigen-presenting cell activity and inflammatory cytokine signaling.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; also suppresses T-cell activation/proliferation and trafficking and dampens APC activity and inflammatory cytokine signaling to prevent GVHD.
ATLG antibodies bind CD45 on T cells and deplete them via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional induction of apoptosis.
Polyclonal IgG biologic immunosuppressant targeting T lymphocytes, administered pre-transplant to prevent GVHD. Depletes and modulates T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; inhibits T-cell activation/proliferation and trafficking; may reduce antigen-presenting cell activity and inflammatory cytokine signaling.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; also suppresses T-cell activation/proliferation and trafficking and dampens APC activity and inflammatory cytokine signaling to prevent GVHD.
Polyclonal antibodies bind T‑cell antigens including CD45/CD45RA, triggering complement-dependent cytotoxicity and Fc-mediated ADCC, with additional apoptosis induction, directly depleting CD45RA+ T cells.
Polyclonal IgG biologic immunosuppressant targeting T lymphocytes, administered pre-transplant to prevent GVHD. Depletes and modulates T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; inhibits T-cell activation/proliferation and trafficking; may reduce antigen-presenting cell activity and inflammatory cytokine signaling.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; also suppresses T-cell activation/proliferation and trafficking and dampens APC activity and inflammatory cytokine signaling to prevent GVHD.
Polyclonal anti–T-cell IgG binds CD45RO on T cells and triggers complement-dependent cytotoxicity and Fc receptor–mediated ADCC, inducing apoptosis/lysis.
An anti-HER2 antibody–drug conjugate (also known as RC48-ADC) consisting of a humanized IgG1 anti-HER2 antibody linked via a valine–citrulline linker to the cytotoxic payload monomethyl auristatin E (MMAE). It binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; may also exert Fc-mediated effects.
Anti-HER2 IgG1 antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and—via a protease-cleavable valine–citrulline linker—releases monomethyl auristatin E (MMAE), which inhibits tubulin polymerization to induce G2/M arrest and apoptosis; the IgG1 may also engage Fc-mediated effector functions (e.g., ADCC).
The ADC binds HER2 on tumor cells, is internalized, and releases MMAE via a cleavable linker to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the IgG1 Fc can also mediate ADCC against HER2+ cells.
Autologous, fully human anti-CD19 chimeric antigen receptor T-cell (CAR-T) therapy that targets and depletes CD19+ B-lineage cells to reduce pathogenic autoantibodies and B cell–driven inflammation.
Autologous T cells are lentivirally engineered to express a fully human anti‑CD19 CAR (CD8α hinge/transmembrane, CD28 costimulatory, CD3ζ signaling). After infusion, the CAR-T cells recognize CD19 on B-lineage cells, become activated, expand, and mediate cytolytic killing, depleting CD19+ B cells to reduce pathogenic autoantibodies and B cell–driven inflammation.
Anti-CD19 CAR-T cells bind CD19 on B-lineage cells, become activated, and kill targets via T-cell cytolytic pathways (perforin/granzyme-mediated apoptosis and Fas–FasL), leading to lysis of CD19+ cells.