• A **new monoclonal antibody** targeting Myasthenia Gravis
• Helps **reduce muscle weakness and improve daily functioning**
Mechanism of action - Neonatal fragment crystallisable receptors (FcRn) play a significant role in the transport of IgG and prolonging its half-life. Nipocalimab binds to FeRn, blocks it and thereby reduces the circulating levels of IgG.
Adverse effects - Respiratory and urinary tract infections, Peripheral edema, Muscle spasms, Herpes zoster and herpes simplex
Oral infections
Why it matters:
• Patients with MG often struggle with **fatigue, mobility, and daily tasks**
• Nipocalimab provides a **targeted therapy** with better symptom control
• Early studies show **faster improvements and fewer side effects**
Could this finally change the treatment landscape for MG patients?
Dr. Anshul, this update on Nipocalimab really shows how fast neuromuscular therapeutics are advancing.
Learning about FcRn blockade here reminded me how important it is to keep ourselves constantly updated not just on new drugs, but on their mechanisms that rewrite how we think about disease management.
It’s fascinating how targeting something as specific as IgG recycling can translate into real improvements in fatigue and mobility for MG patients.
For me, this reinforces the idea that medicine evolves at the pace of curiosity and staying informed is part of patient care itself.
Thank you for your interest Susanta, So, let’s look deeper into how Nipocalimab works mechanistically,
You must be knowing that in Myasthenia Gravis (MG), the body produces pathogenic IgG autoantibodies that attack the acetylcholine receptors at the neuromuscular junction and these antibodies prevent proper nerve-to-muscle signaling, leading to muscle weakness and fatigue.
Now, under normal physiology, IgG antibodies are recycled and protected from degradation by a receptor called FcRn (Neonatal Fc Receptor). This receptor binds IgG inside cells and returns it to the bloodstream, effectively prolonging its half-life.
Nipocalimab specifically binds to FcRn and blocks this recycling pathway.
As a result, instead of being recycled, IgG including the harmful autoantibodies gets degraded.
Outcome: Reduced circulating levels of pathogenic IgG → less immune attack on acetylcholine receptors → improved neuromuscular transmission → better muscle strength and function.
Example:
Think of FcRn as a “protective recycling bin” for IgG antibodies. Nipocalimab essentially “locks” that bin, so the harmful IgG can’t be recycled and is instead discarded helping patients experience relief faster.
I hope this will give you a clear idea of the mechanism.
This is such an interesting development! The way that nipocalimab targets FcRn may revolutionize the way that MG is treated. More accurate IgG level reduction results in fewer adverse effects than general immunosuppression. Patients may finally experience faster relief from fatigue and muscle weakness, which has long been needed, if early results hold up. I’m eager to observe how this changes MG management!
Nipocalimab specifically binds to FcRn and blocks this recycling pathway.
Outcome: Reduced circulating levels of pathogenic IgG → less immune attack on acetylcholine receptors → improved neuromuscular transmission → better muscle strength and function.