Myasthenia gravis is an autoimmune disease in which immunoglobulin G (IgG) 
autoantibodies are formed against the nicotinic acetylcholine receptor (AChR) or 
other components of the neuromuscular junction. Though effective treatments are 
currently available, many commonly used therapies have important limitations and 
alternative therapeutic options are needed for patients. A novel treatment 
approach currently in clinical trials for myasthenia gravis targets the neonatal 
Fc receptor (FcRn). This receptor plays a central role in prolonging the 
half-life of IgG molecules. The primary function of FcRn is salvage of IgG and 
albumin from lysosomal degradation through the recycling and transcytosis of IgG 
within cells. Antagonism of this receptor causes IgG catabolism, resulting in 
reduced overall IgG and pathogenic autoantibody levels. This treatment approach 
is particularly intriguing as it does not result in widespread immune 
suppression, in contrast to many therapies in routine clinical use. Experience 
with plasma exchange and emerging phase 2 clinical trial data of FcRn 
antagonists provide proof of concept for IgG lowering in myasthenia gravis. Here 
we review the IgG lifecycle and the relevance of IgG lowering to myasthenia 
gravis treatment and summarize the available data on FcRn targeted therapeutics 
in clinical trials for myasthenia gravis.