Many of the newer MG treatments are biologics or biologic type therapies.
“What distinguishes these treatments is their precision: The new treatments target one part of the immune system, so they are much more tailored in their approach,” says Becker.
Instead of broadly suppressing immune function, these therapies focus on key steps in the autoimmune process such as antibody production, antibody recycling, or immune-mediated damage at the neuromuscular junction.
FcRn Blockers Lower Harmful Antibodies
FcRn blockers reduce levels of harmful antibodies that drive myasthenia gravis.
These medications target the neonatal Fc receptor (FcRn), a protein that normally helps recycle IgG antibodies. Blocking FcRn accelerates the breakdown of these antibodies, including those that attack the neuromuscular junction and cause symptoms of MG.
Examples include:
- efgartigimod alfa (Vyvgart)
- rozanolixizumab (Rystiggo)
- nipocalimab-aahu (Imaavy)
“FcRn inhibitors are considered more immunomodulatory rather than immunosuppressive; they modulate how your immune system reacts,” says Becker.
Because of this, they may carry a lower risk of infection compared with broader immunosuppressive therapies — though infection risk with traditional treatments remains relatively low when appropriately managed, he adds.
Complement Inhibitors Help Prevent Muscle Damage
Another class of therapies targets the complement system — part of the immune response that contributes to damage at the neuromuscular junction.
In acetylcholine receptor (AChR) antibody–positive MG, complement activation plays a key role in weakening the connection between nerves and muscles. Complement inhibitors block a protein called C5, helping prevent this damage.
Examples include:
- eculizumab (Soliris)
- ravulizumab (Ultomiris)
- zilucoplan (Zilbrysq)
“Complement inhibition decreases the degree that immune activation damages your neuromuscular junction,” says Becker.
Because this pathway is specific to certain antibody types, these medications are primarily used in people with AChR-positive MG. This is because complement activation plays a central role in AChR-antibody–positive MG but not in all MG subtypes.
B-Cell–Targeting Therapy
Another strategy focuses on B cells, a type of white blood cell that produces antibodies to fight infection.
Rituximab (Rituxan) targets CD20, a protein found on B cells. By reducing these cells, it can lower the production of harmful antibodies over time.
Although not FDA-approved specifically for MG, rituximab is used off-label, particularly in certain subtypes of MG, such as MuSK-positive MG, or in cases that don’t respond to other treatments.
“B-cell depleting therapy focuses on your B cells while leaving your T cells intact,” Dr. Becker says. T cells are another type of white blood cell that help to protect against both infection and cancer.
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