Antibody–drug conjugate targeting CD79b that delivers the microtubule inhibitor MMAE to B cells, causing mitotic arrest and apoptosis.
Anti-CD79b antibody-drug conjugate linked via a protease-cleavable linker to MMAE (a microtubule inhibitor). After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
The anti-CD79b ADC binds CD79b on B cells, is internalized, and releases MMAE via protease cleavage; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target cells.
Inhaled monobactam antibiotic used in cystic fibrosis to treat chronic Pseudomonas aeruginosa infection.
Monocyclic beta-lactam (monobactam) antibiotic that selectively binds and inhibits penicillin-binding protein 3 (PBP-3), blocking peptidoglycan cross-linking and bacterial cell wall synthesis, leading to cell lysis and death. Resistant to many beta-lactamases; active primarily against aerobic gram-negative bacteria, including Pseudomonas aeruginosa. Inhaled formulation is used in cystic fibrosis for chronic P. aeruginosa infection.
Aztreonam binds bacterial PBP3 (FtsI) and blocks peptidoglycan cross-linking, disrupting cell wall synthesis and causing osmotic lysis and death of the bacteria.
Anti‑CD20 monoclonal antibody that mediates ADCC/CDC and can induce direct apoptosis of B cells.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B cells and depletes CD20‑positive cells via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and direct induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC (e.g., NK cells), complement-dependent cytotoxicity (CDC), and can directly trigger apoptosis.
A humanized IgG1 monoclonal antibody (Ocrevus) targeting CD20 on B cells; depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis to reduce B-cell antigen presentation and pro-inflammatory cytokines in multiple sclerosis.
Humanized IgG1 monoclonal antibody targeting CD20 on B cells; induces antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis to deplete CD20+ B cells, reducing B-cell antigen presentation and pro-inflammatory cytokine production.
CD20+ B cells are opsonized by the anti-CD20 IgG1, leading to Fc-mediated ADCC by NK cells/macrophages and complement-dependent cytotoxicity (CDC); antibody crosslinking can also induce apoptosis.
Antibody–drug conjugate targeting CD30; the anti-CD30 monoclonal antibody is internalized and releases MMAE, a microtubule-disrupting agent, leading to mitotic arrest and apoptosis (may also mediate ADCC).
Anti-CD30 antibody-drug conjugate that binds CD30 on tumor cells, is internalized, and undergoes linker cleavage to release monomethyl auristatin E (MMAE). MMAE inhibits tubulin polymerization, leading to G2/M mitotic arrest and apoptosis; the antibody may also mediate ADCC.
The anti-CD30 ADC binds CD30, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; the Fc can also mediate ADCC.