The amount of circulating IgG decreases and therefore prevents the acetylcholine receptors from being degraded by the autoantibodies that are responsible for the myasthenia gravis. Pharmacokinetics
The drug is mainly metabolized via proteolytic enzymes. The termination half-life of Efgartigimod alfa is 80 to 120 hours. Side effects
Side effects of efgartigimod alfa include respiratory tract infections, headache, urinary tract infection, numbness and tingling and muscle pain. Society and culture
Legal status
The U.S. Food and Drug Administration (FDA) granted the application for efgartigimod alfa fast track and orphan drug designations. The FDA granted the approval of Vyvgart to Argenx BV.On 23 June 2022, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for the medicinal product Vyvgart, intended for the treatment of anti‑acetylcholine receptor (AChR) antibody positive generalized myasthenia gravis. The applicant for this medicinal product is Argenx. Efgartigimod alfa was approved for medical use in the European Union in August 2022. Names
Efgartigimod alfa is the international nonproprietary name (INN). References
This article incorporates public domain material from the United States Department of Health and Human Services. Further reading
Howard JF, Bril V, Vu T, Karam C, Peric S, Margania T,  et al. (July 2021). "Safety, efficacy, and tolerability of efgartigimod in patients with generalised myasthenia gravis (ADAPT): a multicentre, randomised, placebo-controlled, phase 3 trial". Lancet Neurol. 20 (7): 526–536. doi:10.1016/S1474-4422(21)00159-9. hdl:10067/1859580151162165141. PMID 34146511. S2CID 235456637. External links
"Efgartigimod alfa". Drug Information Portal. U.S. National Library of Medicine.
With the onset of apnea, low pressure develops in the airspace of the lungs because more oxygen is absorbed than CO2 is released. With the airways closed or obstructed, this will lead to a gradual collapse of the lungs and suffocation. However, if the airways are open, any gas supplied to the upper airways will follow the pressure gradient and flow into the lungs to replace the oxygen consumed. If pure oxygen is supplied, this process will serve to replenish the oxygen stored in the lungs and resume sufficient ventilation. The uptake of oxygen into the blood will then remain at the usual level, and the normal functioning of the organs will not be affected. A detriment to this hyperoxygenation is the occurrence of nitrogen washout, which can lead to absorption atelectasis.However, no CO2 is removed during apnea. The partial pressure of CO2 in the airspace of the lungs will quickly equilibrate with that of the blood. As the blood is loaded with CO2 from the metabolism without a way to remove it, more and more CO2 will accumulate and eventually displace oxygen and other gases from the airspace. CO2 will also accumulate in the tissues of the body, resulting in respiratory acidosis. Under ideal conditions (i.e., if pure oxygen is breathed before onset of apnea to remove all nitrogen from the lungs, and pure supplemental oxygen is insufflated), apneic oxygenation could theoretically be sufficient to provide enough oxygen for survival of more than one hours duration in a healthy adult.