MG Patients on Efgartigimod Still Respond to Vaccinations

Efgartigimod does not impair the ability of patients with myasthenia gravis (MG) to generate new specific immunoglobin G (IgG) responses, regardless of the timing of vaccinations, a new study published in Autoimmunity found.

These findings suggest that efgartigimod treatment has no effect on long-lived plasma cells and that protective antibody levels obtained via vaccination can be maintained even during efgartigimod treatment.

These findings are important because the effect of efgartigimod on existing protective antibody titers and the body’s ability to mount an immune response after vaccination were unclear.

In the present study, a team of researchers led by Kevin L. Winthrop, MD, MPH, from the Division of Infectious Disease, Oregon Health and Science University in Portland analyzed data from 3 clinical trials.

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Two of these included a randomized, double-blind, placebo-controlled phase 3 trial of efgartigimod in patients with generalized MG and its extension. The researchers assessed patients’ vaccine-specific responses by measuring changes in IgG titers of patients who were vaccinated against influenza, pneumococcus, or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) during the trials.

They found that efgartigimod treatment reduced the levels of protective anti-tetanus toxoid, anti-varicella zoster virus, and anti-pneumococcal capsular polysaccharide antibodies and total IgG. However, the levels of the first 2 antibodies stayed above minimally protective thresholds for most patients. Once treatment with efgartigimod was stopped, levels of protective antibodies returned to baseline values.

IgG responses to influenza, pneumococcus, and SARS-CoV-2 were also present while patients were on efgartigimod therapy.

The authors concluded that efgartigimod treatment did not impair patients’ ability to generate new specific IgG responses, regardless of the timing of vaccinations.

Efgartigimod, marketed under the brand name Vyvgart^®, is a human IgG1-derived Fc fragment that binds to the neonatal Fc receptor, thereby promoting IgG removal and reduction in circulation.