Differential effects of FcRn antagonists on the subcellular trafficking of FcRn and albumin

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/38713534/

Research summary

This study investigates how various antagonists targeting the neonatal Fc receptor (FcRn) affect the intracellular trafficking and fate of FcRn and its ligand, albumin. The research aims to elucidate the mechanisms by which FcRn antagonists modulate albumin homeostasis, providing insights for therapeutic strategies that involve FcRn inhibition.

Key outcome of the study

The findings reveal that different FcRn antagonists have distinct effects on the subcellular trafficking pathways of FcRn and albumin. Some antagonists promote the lysosomal degradation of albumin, while others enhance its recycling to the cell surface. These differential effects have significant implications for the design and therapeutic application of FcRn inhibitors.

Mouse model

The study utilized a humanized mouse model developed in collaboration with genOway. This model expresses the human FcRn receptor, allowing for the evaluation of human-specific FcRn-antagonist interactions and their impact on albumin dynamics in a physiological context.

TARGET:
Fcgrt
Neonatal Fc receptor, FcRn

Keywords

Autoimmune diseases, Therapeutic antibodies, Protein homeostasis, Pharmacokinetics, FcRn-targeted therapy

Technical specifications

Humanized FcRn expression, Transgenic mouse model, In vivo trafficking analysis, Receptor-ligand interaction, Therapeutic modulation

Related products

Catalogue product

genO‑HSA/hFcRn

Double humanized genO‑HSA/hFcRn mouse model as a cutting-edge platform for preclinical development of HSA and FcRn-oriented therapeutics.

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