Fc-glycosylated, fully humanized anti-CTLA-4 monoclonal antibody immune checkpoint inhibitor that blocks CTLA-4 to enhance CD28-mediated T-cell priming and may deplete Tregs via ADCC/CDC.
Fully humanized anti-CTLA-4 monoclonal antibody that blocks CTLA-4 interactions to enhance CD28-mediated T-cell priming; Fc glycosylation maintains effector function enabling depletion of intratumoral regulatory T cells via ADCC/CDC.
Antibody binds CTLA-4 on Tregs and, via its Fc, recruits immune effectors to deplete them through ADCC/ADCP and complement-dependent cytotoxicity (CDC).
Investigational antibody–drug conjugate (ADC) designed to deliver a cytotoxic payload to tumor antigen–expressing cells.
Human IgG1 anti-HER3 antibody linked via a cleavable peptide linker to a DNA topoisomerase I inhibitor. After binding HER3 on tumor cells, the ADC is internalized and the payload is released to inhibit topoisomerase I, causing DNA breaks, blocking DNA replication, and inducing apoptosis in HER3-expressing cells.
ADC binds HER3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor that induces DNA breaks, blocks replication, and triggers apoptosis in HER3-expressing cells.
Intravenous Fc‑engineered anti‑CD19 monoclonal antibody that mediates ADCC and ADCP and can induce direct apoptosis of CD19+ B cells.
Fc‑engineered humanized anti‑CD19 monoclonal antibody that binds CD19 on B cells and enhances Fcγ receptor engagement to drive antibody‑dependent cellular cytotoxicity (ADCC) and antibody‑dependent cellular phagocytosis (ADCP), leading to depletion of CD19+ B cells; can also induce direct apoptosis.
Binds CD19 on B cells and engages Fcγ receptors on effector cells to mediate ADCC and ADCP, depleting CD19+ cells; can also induce direct apoptosis.
Antibody-photoabsorber conjugate targeting EGFR. After intravenous dosing, tumor sites are illuminated at 690 nm to activate the IR700 dye, causing selective tumor cell membrane damage and immunogenic cell death (photoimmunotherapy).
EGFR-targeted antibody–photoabsorber conjugate (cetuximab linked to IR700). After IV administration and binding to EGFR+ tumor cells, localized 690 nm light activates IR700, causing rapid, selective tumor cell membrane disruption and immunogenic cell death (photoimmunotherapy), enhancing antitumor immune responses.
Cetuximab–IR700 binds EGFR on tumor cells; local 690 nm light activates IR700, causing rapid membrane disruption and immunogenic cell death selectively in EGFR-expressing cells.
Allogeneic cord blood–derived natural killer cell therapy engineered to express an anti-TROP2 chimeric antigen receptor and IL-15; CAR engagement of TROP2 triggers NK cytotoxicity while IL-15 signaling sustains survival, proliferation, and in vivo persistence.
Allogeneic cord blood–derived NK cells engineered to express an anti-TROP2 chimeric antigen receptor and IL-15. CAR recognition of TROP2 on tumor cells triggers NK activation and cytotoxicity (perforin/granzyme-mediated lysis and cytokine release), while IL-15 autocrine signaling sustains NK survival, proliferation, and in vivo persistence; an inducible caspase-9 safety switch allows drug-mediated ablation if needed.
CAR-NK cells bind TROP2 on target cells, triggering NK activation and degranulation with perforin/granzyme-mediated lysis/apoptosis (with contributory cytokine effects).