
Human FcRn TR-FRET Detection Kit
Item | Cat# | Price |
TR-FRET Detection Kit | Inquiry | |
Compound Test Services | CT-001 | $1,050 per 384w plate (Up To 16 cpds Dose) |
Product Description
The neonatal Fc receptor (FcRn) is widely expressed in various tissues and binds IgG in a pH‑dependent manner, protecting IgG from degradation, prolonging its serum half‑life, and mediating maternal IgG transplacental transport. FcRn maintains IgG homeostasis; its dysregulation leads to autoimmune diseases or hypogammaglobulinemia. FcRn‑targeting drugs (e.g., efgartigimod) treat autoimmune diseases by accelerating pathogenic IgG clearance, underscoring its critical role in antibody homeostasis and immunotherapy.
Screeningbio’s TR-FRET Human FcRn Binding Assay Kit can be used to screen for IgGs that bind to Human FcRn, and is suitable for half‑life evaluation of antibody drug candidates as well as high‑throughput screening of FcRn inhibitors. This kit is a competitive immunoassay developed using TR‑FRET technology, characterized by simplicity, rapidity, high accuracy, and good reproducibility.
The basic principle of this method is as follows: a pre‑complexed conjugate of Streptavidin conjugated to TR‑FRET Solar Eu*1 and Human FcRn protein binds to Human IgG conjugated to TR‑FRET LA*2, bringing the Solar Eu donor and LA acceptor into close proximity. Upon excitation by an external light source, fluorescence resonance energy transfer occurs between the donor and acceptor. The binding level between FcRn and Human IgG can be determined by measuring the signal intensity at a specific wavelength (665 nm). Free Human IgG or proteins with a human Fc tag in the sample compete with Human IgG‑LA for the binding sites on FcRn, and the TR‑FRET signal intensity is inversely proportional to the concentration of free Human IgG or proteins with a human Fc tag in the sample.
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Target Background
The neonatal Fc receptor (FcRn) is widely expressed in various tissues and binds IgG in a pH‑dependent manner, protecting IgG from degradation, prolonging its serum half‑life, and mediating maternal IgG transplacental transport. FcRn maintains IgG homeostasis; its dysregulation leads to autoimmune diseases or hypogammaglobulinemia. FcRn‑targeting drugs (e.g., efgartigimod) treat autoimmune diseases by accelerating pathogenic IgG clearance, underscoring its critical role in antibody homeostasis and immunotherapy.
