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.
NO
INDIRECT
SHR-A2009 binds HER3 on tumor cells, is internalized, and releases a topoisomerase I–inhibiting payload that causes DNA damage and apoptosis. Cells expressing only DNA topoisomerase I are not specifically targeted; killing depends on HER3 binding.
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.
YES
DIRECT
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.
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.
NO
INDIRECT
Tafasitamab binds CD19 on B cells; its Fc engages Fcγ receptors on NK cells/macrophages to trigger ADCC/ADCP that kills CD19+ cells. FcγR-expressing cells act as effectors and are not targeted or killed by the drug.
Anti-CD47 IgG4 monoclonal antibody that blocks the CD47–SIRPα 'don’t-eat-me' signal to promote macrophage phagocytosis of malignant myeloid cells.
Humanized IgG4 monoclonal antibody against CD47 that blocks the CD47–SIRPα checkpoint, removing the “don’t‑eat‑me” signal on tumor cells. This enables macrophage phagocytosis (via pro‑phagocytic cues such as calreticulin) and can enhance downstream anti‑tumor T‑cell responses.
YES
INDIRECT
Blocking CD47–SIRPα removes the “don’t‑eat‑me” signal, enabling macrophage-mediated phagocytosis (ADCP) of CD47+ cells; can also augment downstream T‑cell killing.
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.
YES
DIRECT
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.