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Mechanism of Action

RYSTIGGO® is a humanised monoclonal antibody that inhibits binding of IgG to FcRn1,2
gMG pathophysiology

Immunoglobin G (IgG) autoantibodies target key proteins involved in signal transmission at the neuromuscular junction (NMJ), impairing synaptic and muscle function. By facilitating autoantibody recycling in endothelial cells, the neonatal Fc receptor (FcRn) is a key driver of gMG pathogenesis.1-5

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Rystiggo MoA_gMG pathophysiology.
With RYSTIGGO®

RYSTIGGO® binds FcRn with a high affinity, preventing pathogenic autoantibodies binding and thereby allowing their degradation. This results in a reduction in the concentration of autoantibodies at the NMJ and promotes receptor survival.1-5

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With Rystiggo

 

Abbreviations

Ab, antibody; AChR, acetylcholine receptor; FcRn, neonatal Fc receptor; gMG, generalised myasthenia gravis; IgG, Immunoglobulin G; MOA, mechanism of action; MuSK, muscle-specific tyrosine kinase; NMJ, neuromuscular junction.

 

 

References

1. RYSTIGGO® (rozanolixizumab) Approved Product Information

2. Zhu L-N, et al. Neural Regen Res. 2023;18(8):1637–1644.

3. Smith B, et al. MAbs. 2018;10(7):1111–1130.

4. Gable KL, Guptill JT. Front Immunol. 2020;10:3052.

5. Wolfe GI, et al. J Neurol Sci. 2021;15:430:118074.

 

PBS information: Not listed on the PBS for the treatment of generalised myasthenia gravis

Please review the full Product Information before prescribing RYSTIGGO®. The full Product Information is available from UCB Australia here.


This medicinal product is subject to additional monitoring in Australia. This will allow quick identification of new safety information. Healthcare professionals are asked to report any suspected adverse events at www.tga.gov.au/reporting-problems.

 

AU-RZ-2500081

Date of preparation: December 2025