This product is an unconjugated, non-therapeutic recombinant analog of erlizumab, supplied for research use only. Erlizumab (also known as rhuMAb CD18) is a humanized anti-CD18 antibody fragment directed against the integrin beta-2 subunit (ITGB2, UniProt P05107). The research-grade analog reproduces the antigen-binding specificity of the originator molecule as a Fab (human IgG1, kappa) format, without any therapeutic intent, and is not the clinical drug; it is not for human or veterinary use. It is useful as a target-specific binding and blocking reagent for in-vitro and preclinical work: as a positive/isotype-matched control in ITGB2 detection assays, for competitive binding and epitope studies, for interrogating leukocyte integrin function (adhesion, migration, activation), for neutralization and function-blocking experiments, and as reference material during antibody-engineering or assay-development pipelines. Because it is provided as a Fab, it lacks an Fc region and therefore does not mediate Fc-dependent effector functions, which can be advantageous when studying receptor engagement in isolation. The material is offered at low endotoxin (research grade <1 EU/mg; ultra-low <0.5 EU/mg) and in bulk milligram-to-gram quantities to support scale-up and reproducibility.
ITGB2 (CD18, integrin beta-2, UniProt P05107) is the common beta subunit that pairs with distinct alpha chains to form the beta-2 (leukocyte) integrin family: LFA-1 (CD11a/CD18, alphaL beta2), Mac-1/CR3 (CD11b/CD18, alphaM beta2), p150,95/CR4 (CD11c/CD18, alphaX beta2), and CD11d/CD18. These heterodimers are expressed on leukocytes and mediate firm adhesion to endothelium, transendothelial migration, immune-synapse formation, phagocytosis, and complement-opsonized particle uptake. Key ligands include ICAM-1/2/3 and complement fragment iC3b. Beta-2 integrins undergo conformational activation ("inside-out" signaling) that switches them to high-affinity states, and they transmit "outside-in" signals upon ligand engagement. Loss-of-function mutations in ITGB2 cause leukocyte adhesion deficiency type I, characterized by impaired neutrophil recruitment and recurrent infections, underscoring the subunit's central role in leukocyte trafficking and innate immunity.