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.
YES
DIRECT
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).
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.
NO
INDIRECT
Polatuzumab vedotin targets CD79b on B cells; after internalization it releases MMAE, which binds beta-tubulin and blocks microtubule polymerization, causing G2/M arrest and apoptosis in CD79b+ cells. Tubulin expression alone is not sufficient for targeting or 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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
Bispecific CD3xCD20 engagement redirects T cells to CD20+ cells, forming an immune synapse and inducing perforin/granzyme-mediated apoptosis.