Human CD16a (176F) Protein (In Vivo Grade, Ultra-Low Endotoxin) (ICH3014)

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This is a recombinant human CD16a (FcgammaRIIIa) protein carrying the 176F allotypic variant (the low-affinity F allele at position 158/176 depending on numbering convention), expressed in human embryonic kidney (HEK) 293 cells to preserve mammalian glycosylation. It is supplied as an ultra-low-endotoxin, in-vivo-grade reagent for research use only (RUO), manufactured to <0.5 EU/mg so it is suitable for endotoxin-sensitive functional, cell-based, and in-vivo work as well as biophysical assays. HEK293 expression yields a correctly folded, glycosylated ectodomain appropriate for studying Fc-Fc receptor interactions. The protein is validated for SPR, BLI, and ELISA, making it well suited to measuring antibody Fc-binding affinity, ranking Fc-engineered or afucosylated antibody variants, characterizing therapeutic mAb effector potential, and epitope/competition studies. Being the F (lower-affinity) allotype, it is particularly useful for allotype-stratified affinity comparisons alongside the V (higher-affinity) variant. Bulk milligram-to-gram quantities support assay development, screening campaigns, and reagent-intensive workflows. CD16a (FcgammaRIIIa, encoded by FCGR3A; UniProt P08637) is a low-to-intermediate affinity activating Fc receptor for IgG, expressed chiefly on natural killer (NK) cells, monocytes/macrophages, and some gammadelta T cells. On NK cells it is the principal trigger of antibody-dependent cellular cytotoxicity (ADCC): engagement of IgG-opsonized targets clusters CD16a, signaling through associated ITAM-bearing adaptors (FcRgamma and/or CD3zeta) to drive degranulation and cytokine release. A well-characterized allotypic polymorphism (V158F, also written as 176 in some mature-protein numbering) modulates IgG affinity, with the valine (V) allotype binding IgG1/IgG3 more tightly than the phenylalanine (F) allotype; this variation influences clinical responses to therapeutic antibodies such as rituximab. Afucosylation of the antibody Fc N-glycan markedly increases CD16a binding and ADCC, a property exploited in engineered therapeutics. The 176F variant here represents the lower-affinity allotype.