Anti–IL-5Rα monoclonal antibody that induces antibody-dependent cellular cytotoxicity to deplete eosinophils and basophils.
Afucosylated humanized monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα). By binding IL-5Rα on eosinophils and basophils, it enhances FcγRIIIa-mediated antibody-dependent cellular cytotoxicity (ADCC), leading to rapid depletion of these cells and consequent suppression of IL-5–driven type 2 inflammation.
YES
DIRECT
Benralizumab binds IL-5Ralpha on eosinophils/basophils and, via its afucosylated Fc, engages Fc-gamma RIIIa on NK cells to trigger ADCC, depleting IL-5Ralpha+ cells.
Anti–IL-5Rα monoclonal antibody that induces antibody-dependent cellular cytotoxicity to deplete eosinophils and basophils.
Afucosylated humanized monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα). By binding IL-5Rα on eosinophils and basophils, it enhances FcγRIIIa-mediated antibody-dependent cellular cytotoxicity (ADCC), leading to rapid depletion of these cells and consequent suppression of IL-5–driven type 2 inflammation.
NO
INDIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and engages CD16a on NK cells via its afucosylated Fc to trigger ADCC, killing IL-5Rα+ targets. CD16a-expressing cells are effectors, not killed.
An anti-HER2 antibody–drug conjugate (RC48, DV) in which a humanized anti‑HER2 monoclonal antibody is linked to the microtubule inhibitor monomethyl auristatin E (MMAE); after binding HER2 on tumor cells and internalization, it releases MMAE to disrupt microtubules, causing G2/M arrest and apoptosis with a potential bystander effect.
Anti-HER2 monoclonal antibody linked to the microtubule inhibitor MMAE; after binding HER2 and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis, with potential bystander killing.
YES
DIRECT
An anti‑HER2 ADC binds HER2 on tumor cells, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis (with possible bystander killing).
An anti-HER2 antibody–drug conjugate (RC48, DV) in which a humanized anti‑HER2 monoclonal antibody is linked to the microtubule inhibitor monomethyl auristatin E (MMAE); after binding HER2 on tumor cells and internalization, it releases MMAE to disrupt microtubules, causing G2/M arrest and apoptosis with a potential bystander effect.
Anti-HER2 monoclonal antibody linked to the microtubule inhibitor MMAE; after binding HER2 and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis, with potential bystander killing.
NO
INDIRECT
Disitamab vedotin targets HER2 on tumor cells; after HER2-mediated internalization, the linker releases MMAE, which binds the vinca site on beta-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis (with possible bystander killing). Beta-tubulin expression alone is not the selective target of this ADC.
Allogeneic, donor-derived gene-modified chimeric antigen receptor T-cell (CAR-T) product targeting mesothelin (MSLN); designed as an off-the-shelf CAR-T therapy that binds MSLN on tumor cells and induces T-cell activation and cytotoxic killing.
Allogeneic, gene-modified T cells expressing a chimeric antigen receptor that binds mesothelin (MSLN) on tumor cells, activating CAR signaling to induce T-cell effector functions and cytotoxic killing (perforin/granzyme release and cytokine secretion) independent of the native TCR.
YES
DIRECT
CAR-T cells bind mesothelin on target cells, triggering T-cell effector functions (perforin/granzyme-mediated lysis and apoptosis, ± Fas–FasL) leading to direct killing.