An antibody-drug conjugate (fully human IgG1) targeting CD205/Ly75 that delivers a cytotoxic payload to CD205-high tumor cells, enabling direct tumor cell killing and potential immune activation.
Fully human IgG1 antibody targeting CD205/Ly75 linked via a cleavable SPDB linker to the maytansinoid DM4. Upon CD205 binding and internalization, intracellular proteases cleave the linker to release DM4, which binds tubulin and disrupts microtubule dynamics, inhibiting mitosis and causing tumor cell death; may also promote immune activation through antigen uptake.
NO
INDIRECT
The ADC binds CD205 on target cells, is internalized, and releases DM4; DM4 then binds β‑tubulin to disrupt microtubules and induce mitotic cell death. β‑tubulin itself is not the targeted antigen; killing occurs only after CD205-mediated delivery.
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
YES
DIRECT
Polyclonal anti-thymocyte IgG binds TCR/CD3 (including TCRα) on T cells and induces complement-mediated lysis and Fc-dependent ADCC; cross-linking can also trigger apoptosis, depleting TCRα-expressing cells.
Hypoimmune, allogeneic CD19-directed CAR T-cell therapy engineered to evade host immune rejection and deplete CD19+ B-lineage cells to reset humoral immunity in autoimmune disease.
Allogeneic T cells engineered with an anti‑CD19 chimeric antigen receptor recognize and kill CD19+ B‑lineage cells (naive/memory B cells and plasmablasts), depleting pathogenic B cells to reset humoral immunity. The product is rendered 'hypoimmune' by disrupting MHC class I/II and overexpressing CD47 to evade host immune rejection and enhance persistence.
YES
DIRECT
Anti‑CD19 CAR T cells bind CD19 on B-lineage cells, become activated, and lyse target cells via perforin/granzyme release and death receptor–mediated apoptosis.
Anti‑CD20 monoclonal antibody that depletes CD20+ B cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and induction of apoptosis, reducing malignant B‑cell populations.
YES
DIRECT
Binds CD20 on B cells and triggers Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity (CDC), and can induce apoptosis upon CD20 crosslinking.
Rituximab‑abbs biosimilar; anti‑CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis.
Anti-CD20 monoclonal antibody (rituximab-abbs) that binds CD20 on B lymphocytes and depletes CD20+ B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis.
YES
DIRECT
Anti-CD20 mAb binds CD20 on B cells and kills via Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity (CDC), and can trigger apoptosis upon CD20 ligation.