Glycoengineered type II anti-CD20 IgG1 monoclonal antibody; induces potent ADCC and direct cell death.
Humanized, glycoengineered type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells; afucosylated Fc increases affinity for FcgammaRIIIa, driving potent antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis, and directly induces caspase-independent cell death, leading to depletion of malignant CD20+ B cells.
Obinutuzumab binds CD20 on B cells; its afucosylated Fc strongly engages FcγRIIIa on NK cells and macrophages to drive ADCC and phagocytosis, and it also triggers direct, caspase-independent cell death of CD20+ cells.
Type I anti-CD20 monoclonal antibody; mediates ADCC and complement-dependent cytotoxicity.
Type I anti-CD20 chimeric IgG1 monoclonal antibody that binds CD20 on B cells and mediates antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and phagocytosis, resulting in depletion of CD20-positive B cells.
Rituximab binds CD20 on B cells and recruits immune effectors to kill via ADCC and antibody-dependent phagocytosis, and activates complement for CDC, depleting CD20+ cells.
Anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric IgG1 monoclonal antibody targeting CD20 on B cells; induces B‑cell depletion via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and direct apoptosis.
Anti‑CD20 antibody binding triggers complement-dependent cytotoxicity, Fc-mediated ADCC by NK cells/macrophages, and can induce apoptosis via CD20 crosslinking.
Autologous gene‑modified T cells engineered with a mesothelin‑targeted CAR; co‑expresses a CD40 agonist and a T‑cell costimulatory agonist to enhance activation, proliferation, persistence, and APC licensing.
Autologous gene‑modified T cells expressing a mesothelin‑targeted CAR that recognizes MSLN on tumor cells and mediates T‑cell activation and cytotoxicity; co‑expression of a CD40 agonist licenses/activates antigen‑presenting cells, and a T‑cell costimulatory agonist augments T‑cell activation, proliferation, and persistence to enhance antitumor efficacy.
MSLN‑CAR T cells bind mesothelin on target cells and directly induce killing via T‑cell effector mechanisms (perforin/granzyme release and death‑receptor pathways), with co‑stimulatory/CD40 agonism enhancing activity.
Tebentafusp (IMCgp100) is a bispecific ImmTAC T‑cell engager with an affinity‑enhanced TCR that binds the gp100 (PMEL) peptide presented by HLA‑A*02:01 on melanoma cells and an anti‑CD3 domain that recruits and activates T cells, inducing TCR/CD3 signaling, cytokine release, immune synapse formation, and tumor cell lysis.
A soluble ImmTAC that uses an affinity‑enhanced TCR to bind the gp100 (PMEL) peptide presented by HLA‑A*02:01 on melanoma cells and an anti‑CD3 domain to recruit and activate polyclonal T cells, crosslinking tumor cells and T cells to trigger TCR/CD3 signaling, cytokine release, immune synapse formation, and cytotoxic killing of gp100‑expressing tumor cells.
An ImmTAC with an affinity-enhanced TCR binds the gp100 peptide–HLA-A*02:01 complex on target cells and its anti-CD3 domain engages T cells, forming an immune synapse that activates T cells to kill the bound target cell via perforin/granzyme-mediated cytolysis (and related T cell effector mechanisms).