CD79b-directed antibody-drug conjugate that delivers monomethyl auristatin E (MMAE), a microtubule inhibitor.
CD79b-targeted monoclonal antibody linked via a protease-cleavable linker to monomethyl auristatin E (MMAE). After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis of CD79b-positive malignant B cells.
The ADC binds CD79b on B cells, is internalized, and releases MMAE via a cleavable linker to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis of CD79b-positive cells.
An investigational antibody–drug conjugate (ADC) consisting of a monoclonal antibody linked to a camptothecin-derived topoisomerase I inhibitor. It binds a tumor-associated surface antigen on SCLC cells, is internalized, and releases the payload to cause DNA damage and tumor cell death, with potential bystander effect.
Monoclonal antibody targets a tumor-associated surface antigen on SCLC cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload that induces DNA damage and tumor cell death, with potential bystander killing of neighboring tumor cells.
ADC binds the antigen on SCLC cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that causes DNA damage, leading to tumor cell death (with potential bystander killing).
Anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and mediates B‑cell depletion via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
Binds CD20 on B cells and induces killing via Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity (CDC), and apoptosis upon crosslinking.
Autologous gene-modified T lymphocytes expressing a CAR targeting CSPG4, incorporating an inducible caspase-9 safety switch; mediates HLA-independent killing of CSPG4-positive tumor cells.
Autologous T cells genetically engineered to express a CAR targeting CSPG4; upon antigen engagement they activate and kill CSPG4-positive tumor cells in an HLA-independent manner via cytotoxic effector pathways. The construct includes an inducible caspase-9 safety switch enabling on-demand ablation of the CAR-T cells to manage severe toxicity.
CAR-T cells bind CSPG4 on target cells via the CAR, become activated, and kill the bound cells through HLA-independent cytotoxic effector pathways (perforin/granzyme release and death-receptor signaling).
Subcutaneous bispecific T‑cell–engaging antibody (CD3xCD20) that redirects cytotoxic T cells to CD20+ B cells, inducing immune synapse formation and perforin/granzyme-mediated apoptosis.
Bispecific CD3xCD20 antibody that binds CD3 on T cells and CD20 on B cells, redirecting cytotoxic T cells to CD20+ B cells to form an immune synapse and induce perforin/granzyme-mediated apoptosis.
Bispecific CD3xCD20 engagement redirects T cells to CD20+ cells, forming an immune synapse and inducing perforin/granzyme-mediated apoptosis.