Anti-CD20 chimeric monoclonal antibody; depletes B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Anti-CD20 antibody binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP; it can also induce apoptosis of CD20+ cells.
Anti-CD79b antibody–drug conjugate delivering MMAE; internalization releases a microtubule inhibitor causing G2/M arrest and apoptosis.
Anti-CD79b monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE; binding to CD79b on B cells triggers internalization and intracellular release of MMAE, which inhibits tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
ADC binds CD79b on B cells, is internalized, linker is cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis of the target-expressing cells.
ImmTAC bispecific (IMC‑F106C): affinity‑enhanced PRAME‑specific TCR fused to anti‑CD3 scFv that binds PRAME peptide presented by HLA‑A*02:01 on tumor cells and recruits/activates T cells via CD3 to kill PRAME+ cells.
ImmTAC bispecific composed of an affinity‑enhanced PRAME‑specific TCR fused to an anti‑CD3 scFv; binds PRAME peptide presented by HLA‑A*02:01 on tumor cells and simultaneously engages CD3 on T cells, activating and redirecting polyclonal T cells to kill PRAME‑positive cells.
Affinity‑enhanced TCR binds PRAME peptide–HLA‑A*02:01 on tumor cells while anti‑CD3 engages T cells, forming an immune synapse and triggering T‑cell–mediated killing (perforin/granzymes, apoptosis) of PRAME/HLA‑A*02:01–positive cells.
An antibody-drug conjugate (ADC) comprising a humanized anti-CLDN18.2 monoclonal antibody linked via a cleavable linker to a cytotoxic payload (DDDXD), with a drug–antibody ratio of 8; administered IV every 3 weeks (0.5–5.0 mg/kg). It binds CLDN18.2 on tumor cells, is internalized, and releases the cytotoxic agent intracellularly to kill cancer cells.
Humanized anti‑CLDN18.2 monoclonal antibody conjugated via a cleavable linker to a cytotoxic payload. Binds CLDN18.2 on tumor cells, is internalized, linker is cleaved in lysosomes, releasing the payload that induces DNA damage and kills CLDN18.2‑expressing cells, with potential bystander killing of adjacent tumor cells.
ADC binds CLDN18.2, is internalized, linker cleaved in lysosomes, releasing a cytotoxic payload that induces DNA damage and kills the target-expressing cell (with possible bystander effect).
A conditionally active biologic (CAB) bispecific T‑cell engager antibody that simultaneously binds EpCAM on tumor cells and CD3 on T cells to redirect and activate cytotoxic T cells against EpCAM-expressing cancer cells; designed for conditional activation within the tumor microenvironment.
Conditionally active bispecific antibody that binds EpCAM on tumor cells and CD3 on T cells; in the acidic tumor microenvironment it becomes activated to recruit and activate cytotoxic T cells, forming an immune synapse and inducing T cell–mediated killing of EpCAM‑expressing cancer cells while aiming to limit systemic toxicity.
A bispecific T‑cell engager binds EpCAM on tumor cells and CD3 on T cells (activated in the acidic TME), forming immune synapses that activate cytotoxic T cells to kill EpCAM+ cells via perforin/granzyme-mediated cytolysis.