Anti-CD20 monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive B lymphocytes via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity, and can induce apoptosis via CD20 crosslinking.
Fully human anti-CD20 IgG1 monoclonal antibody (brand: Kesimpta) administered subcutaneously; binds a membrane-proximal CD20 epitope and depletes CD20+ B cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis; spares stem cells and plasma cells and reduces antigen presentation and pro-inflammatory cytokines (e.g., IL-6, GM-CSF).
Fully human IgG1 anti‑CD20 monoclonal antibody that binds a membrane‑proximal CD20 epitope on B cells and depletes CD20+ B cells via complement‑dependent cytotoxicity, antibody‑dependent cellular cytotoxicity, and apoptosis; spares stem cells and plasma cells, reducing antigen presentation and pro‑inflammatory cytokines.
Binds CD20 on B cells and triggers complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity (via Fc-engaged effector cells), with additional induction of apoptosis.
Humanized anti-CD20 IgG1 monoclonal antibody administered subcutaneously; depletes CD20+ B cells mainly via ADCC and apoptosis, with less CDC activity compared with ofatumumab.
Humanized anti-CD20 IgG1 monoclonal antibody that binds CD20 on pre-B to mature B cells and depletes them primarily via antibody-dependent cellular cytotoxicity (ADCC) and apoptosis, with lower complement-dependent cytotoxicity; spares stem cells and plasma cells, reducing antigen presentation and proinflammatory cytokines.
Anti-CD20 IgG1 binds CD20 on B cells and triggers their depletion via Fc-mediated ADCC (NK cells/macrophages), with some complement-dependent cytotoxicity and apoptosis.
IGM-2323; an intravenously administered bispecific IgM monoclonal antibody (T-cell engager) that binds CD20 on B cells and CD3 on T cells to redirect T-cell cytotoxicity and activate complement, depleting CD20+ B cells to reduce pathogenic autoantibody production in SLE.
Imvotamab is a bispecific IgM antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to redirect T-cell cytotoxicity against CD20+ B cells. Its multivalent IgM format confers high-avidity CD20 binding and strong complement activation, inducing complement-dependent cytotoxicity in addition to T-cell–mediated killing, resulting in depletion of CD20+ B cells and reduction of pathogenic autoantibody production.
Imvotamab bridges CD3+ T cells to CD20+ cells to trigger T‑cell–mediated killing (perforin/granzyme apoptosis) and, via its IgM format, activates complement to induce complement-dependent cytotoxicity (CDC) of CD20-expressing cells.
A fully humanized IgG1 antibody–drug conjugate targeting B7-H3 (CD276). Upon binding to B7-H3 on tumor cells, it is internalized and releases a cytotoxic payload, leading to selective killing of B7‑H3–expressing cells.
Fully humanized IgG1 ADC targeting B7-H3 (CD276); upon binding to B7-H3 on tumor cells, the complex is internalized and releases a cytotoxic payload, selectively killing B7-H3–expressing tumor cells.
The ADC binds B7-H3 on tumor cells, is internalized, and releases a cytotoxic payload inside the cell, leading to target-cell death (e.g., via DNA damage or microtubule disruption).