Myasthenia Gravis Treatments

Treatment Overview

Treatment Options: Surgery

  • Thymectomy

Treatment Options: Medicine

Acetylcholinesterase inhibitors

  • Mestinon® (pyridostigmine bromide)
  • Regonol® (pyridostigmine bromide)

Corticosteroids and other immunosuppressants

  • Prednisone
  • Imuran® (azathioprine)
  • CellCept® (mycophenolate mofetil)
  • Cyclosporin

Targeted treatments

B-cell directed treatments

  • Rituximab

Neonatal Fc receptor blockers

  • Vyvgart® (efgartigimod alfa-fcab)
  • Vyvgart® Hytrulo (efgartigimod alfa and hyaluronidase-qvfc)
  • Rystiggo® (rozanolixizumab-noli)

Complement inhibitors

  • Soliris® (eculizumab)
  • Ultomiris® (ravulizumab-cwvz)
  • Zilbrysq® (zilucoplan)

Intravenous immunoglobulin

Subcutaneous immunoglobulin

  • Hizentra® (immunoglobulin)

Therapeutic plasma exchange

References

Treatment Overview

Myasthenia gravis (pronounced `my˖ĕs˖`thēēn˖ē˖ă `grăv˖ĭs), is a rare, chronic, autoimmune disorder affecting the signals between the nerves and the muscles (at the neuromuscular junction) which causes the muscles to feel weak and easily tired. People with the condition may experience flare-ups, followed by periods of improvement in their symptoms.1,2Whilst there is no known cure for myasthenia gravis, treatment development is advancing,1-3 and there are several treatments that can help to improve symptoms..1,2,4 While symptom improvement and even remission can occur without treatment, every case of myasthenia gravis is unique.1 You and your doctor will decide on a treatment plan specific to your needs. 

In preparation for your visit to your doctor, you may find it helpful to read the current myasthenia gravis treatment guidelines. The myasthenia gravis treatment guidelines provide a set of recommendations about the various treatment options available for the condition and were developed by myasthenia gravis experts over several years. As new treatments are developed and as our knowledge of the condition improves, the guidelines are updated with leadership from the MGFA’s Medical Advisory Committee members and international disease experts. You can view the guidelines that were published in 2016, titled ‘International Consensus Guidance for Management of Myasthenia Gravis’ and the latest update of the guidelines that were re-published in 2020, titled ‘International Consensus Guidance for Management of Myasthenia Gravis Update 2020’ here:5,6

There are several treatment options that can improve your strength, help to keep the symptoms of myasthenia gravis under control and may improve your quality of life. As everyone’s experience of myasthenia gravis is different, this may include a variety of treatments, and sometimes emergency treatment if your symptoms get worse.1,4,7 We will discuss in more detail the established and new treatments that continue to give hope to people with myasthenia gravis, their family and their caregivers.

As with any treatment, the medications for treating myasthenia gravis have a risk of side effects. The common side effects that you might experience include nausea, diarrhea, high blood pressure and an increased risk of getting infections.3 If your doctor suggests a specific medication to manage your myasthenia gravis symptoms, they will discuss the side effects of that particular medication in more detail.

The information presented here is based on therapies approved in the US. Treatment availability in other countries may differ according to local approvals. 

Treatment Options: Surgery

Thymectomy

Thymectomy is the surgical removal of the thymus gland.7 The thymus gland is in the middle of your upper chest, behind your breastbone.8 This gland is associated with our immune system and the production of antibodies. The thymus helps with the development of T cells (a type of white blood cell that is associated with our immune response). T cells are involved in the production of antibodies and can produce abnormal antibodies that cause autoimmune conditions such as myasthenia gravis. The thymus is most active in early childhood up until puberty, after which it gradually shrinks and does not play an important role.1,8

The thymus gland is known, however, to play a role in myasthenia gravis. Many people with the condition may develop:1

  • Enlarged size of the thymus gland (hyperplasia)
  • A tumor of the thymus gland (thymoma) 

If there is a dysfunction in the thymus, it could lead to a change in T-cell development and therefore the production of antibodies including abnormal antibodies that are responsible for the symptoms of myasthenia gravis.1

Thymectomy can be carried out if you have myasthenia gravis with or without thymus abnormalities. If you do not have a thymoma, the surgery may be recommended early on in your treatment pathway to improve your symptoms in the long-term and is strongly recommended if you have a thymoma.5,6 The surgery can help to improve your muscle weakness and the number of medications needed or may even provide remission of your symptoms.9 Following thymectomy, you may not experience improvements immediately, and the amount of improvement that you experience may differ compared to other people treated with thymectomy. However, there is evidence to suggest that patients who have a thymectomy have less severe symptoms and may require a lower dose of corticosteroids over time.7

Treatment Options: Medicine

Acetylcholinesterase inhibitors

For a muscle to function normally, acetylcholine attaches to acetylcholine receptors, producing a signal between the nerve and the muscle which causes the muscle to contract. In myasthenia gravis, abnormal autoantibodies block the attachment of acetylcholine to its receptors which affects the signals between the nerves and muscles, causing muscle weakness.1,2

Acetylcholinesterase is an enzyme that is responsible for breaking down acetylcholine.1 Acetylcholinesterase inhibitors prevent this breakdown, meaning that there is more acetylcholine available to bind to the receptors. This in turn increases the signals between the muscle and nerves and improves muscle activation.7,9 Acetylcholinesterase inhibitors are often part of the initial treatment for myasthenia gravis, and one of the most used drugs is pyridostigmine bromide.5

Mestinon® (pyridostigmine bromide)

Mestinon® (ICN Pharmaceuticals Inc) comes in two forms, fast-acting 60 mg tablets, long-lasting slow-release 180 mg capsules known as Timespan®, which deliver pyridostigmine bromide over 12 hours. You may expect to take Mestinon® tablets multiple times per day.10

Regonol® (pyridostigmine bromide)

The acetylcholinesterase inhibitor, pyridostigmine bromide, is also available as an injection, under the brand name Regonol® (Sandoz Inc).11 Regonol® is given as an intravenous injection (an injection into a vein) and is sometimes used as an alternative to Mestinon® if you cannot take tablets by mouth, or in certain emergency situations.9,12

Corticosteroids and other immunosuppressants

A corticosteroid is a medicine that acts as an immunosuppressant, which means that it reduces the action of our immune system.13 While the immune system is usually helpful in fighting infection, in myasthenia gravis there is a disruption to the balance of how the immune system works.1 This disruption causes the production of abnormal antibodies, for example, acetylcholine receptor (AChR) and muscle-specific tyrosine kinase (MuSK) antibodies. These abnormal antibodies attach to or block the acetylcholine receptors and cause changes to the neuromuscular junction. This leads to problems with the communication between the nerves and muscles and in turn, muscle weakness.1,2

Immunosuppressants reduce the action of the immune system by reducing the creation of certain white blood cells called T cells and B cells that are involved in your body’s immune response and produce antibodies.13,14 By reducing the action of the immune system, these medicines reduce the number of abnormal antibodies that are produced. Therefore, there are fewer abnormal antibodies to attach to and block your body’s acetylcholine receptors and less change to the neuromuscular junction. This helps the communication between the muscles and the nerves and increases muscle activation.13

Corticosteroids or other immunosuppressants are usually the next lines of treatment if treatment beyond acetylcholinesterase inhibitors is needed.5,9 Corticosteroids can be very effective for many people, with 7–8 out of every 10 people on steroids seeing marked improvement in their symptoms.9 However, like all medicines, they have several side effects.9 Other types of immunosuppressants that are not classified as steroids are currently used in treating myasthenia gravis and can also produce marked improvements in symptoms.9,13

Prednisone

Prednisone is a common type of corticosteroid used in the treatment of many conditions including myasthenia gravis. This type of corticosteroid works by acting on the glucocorticoid receptors in our body to help reduce the action of the immune system.13

Prednisone is a tablet taken by mouth. Usually, your doctor will prescribe a low dose of prednisone, and will then gradually increase the dose until your symptoms are controlled. You may expect to notice an improvement in your symptoms within 2 weeks, with the most improvement over the first 4–8 weeks. As every case of myasthenia gravis is different, you may be asked to take prednisone on alternate days, or to reduce the dose gradually so that you are only taking as much as you need to control your symptoms. The side effects that you may experience, particularly if you take prednisone for a prolonged time, include high blood pressure, weight gain, stomach ulcers, infections, and mood changes.9 For a full list of side effects, please speak to your doctor and see the leaflet inside your medicine packet.

Imuran® (azathioprine)

Imuran® (Sebela Pharmaceuticals Inc) is a non-steroidal immunosuppressant (an immunosuppressant that is not a steroid) that is also used in the treatment of myasthenia gravis, amongst other conditions.15 When Imuran® breaks down in the body, it prevents the white blood cells that are involved in our immune system from multiplying.9

Imuran® is a tablet taken by mouth once or twice a day.9,15 It can take 4–6 months before you start to notice an improvement in your symptoms. Your doctor may advise you to take Imuran® by itself or alongside a corticosteroid, depending on your other medications, conditions and the severity of your symptoms.5,9 The side effects that you may experience include flu-like symptoms, nausea (feeling sick) and low white blood cell levels which may cause an infection. Long-term use of Imuran® can sometimes affect your liver, pancreas or bone marrow and may increase your chance of getting certain types of cancer including skin cancer.9,15 For a full list of side effects, please speak to your doctor and see the leaflet inside your medicine packet.

CellCept® (mycophenolate mofetil)

CellCept® (Roche) is another non-steroidal immunosuppressant that reduces T-cell and B-cell (white blood cells involved in our immune response) production.16 CellCept® achieves this by reducing the production of a chemical called guanosine, which is one of the building blocks for cells and is important for cells to multiply. Without guanosine, there are fewer T cells and B cells produced, our immune system activity is reduced, thereby reducing the number of abnormal antibodies.9

CellCept® is usually taken by mouth as a liquid or tablet and may be prescribed alone or Cyclosporinalongside a corticosteroid.5,9,16

Cyclosporin

Cyclosporin is a type of immunosuppressant called a calcineurin inhibitor. This medicine reduces the immune system response by blocking a protein called calcineurin in T cells. This prevents the activation of certain genes and the production of key immune system signals. As a result, the immune system is less active, producing less antibodies.13

Cyclosporin is taken as a tablet by mouth, usually twice a day.7,9 As with Imuran® and CellCept®, cyclosporin may be prescribed alone or with a corticosteroid.5

Targeted treatments

B-cell directed treatments

B-cells are a type of white blood cell that has an important role in making antibodies and the immune response thought to cause the symptoms of myasthenia gravis. Treatments that target B-cells are thought to reduce this immune response and the levels of abnormal antibodies that can cause myasthenia gravis symptoms.2,7,14

Rituximab

Rituximab is a monoclonal antibody (an antibody that is made in a laboratory and has a specific target) that targets and attacks B-cells. As B-cells play a part in producing the abnormal antibodies responsible for the symptoms of myasthenia gravis, this may improve the symptoms of myasthenia gravis.7,9,14

You may be prescribed rituximab if you have myasthenia gravis with MuSK antibodies and have not had improvement with other treatments.6 If you are prescribed this medication, you will receive it as an intravenous infusion (a drip that is inserted into a vein) in cycles.9

Neonatal Fc receptor blockers

The neonatal Fc receptor helps to extend the life of immunoglobulin G antibodies. In myasthenia gravis, the abnormal antibodies responsible for the symptoms of myasthenia gravis are primarily types of immunoglobulin G antibodies. These abnormal antibodies block acetylcholine from binding to its receptor, resulting in changes to the neuromuscular junction and affecting the signals between the nerves and muscles, ultimately causing the symptoms associated with myasthenia gravis, including muscle weakness.2

Neonatal Fc receptor blockers attach to and block the neonatal Fc receptor, reducing the levels of immunoglobulin G antibodies, including the abnormal antibodies responsible for myasthenia gravis symptoms.2

Here are the neonatal Fc receptor blockers approved in the US:

Vyvgart® (efgartigimod alfa-fcab)

Vyvgart® (argenx) is a medicine that uses a fragment of an immunoglobulin G antibody to attach to and block the neonatal Fc receptor. This causes a reduction in immunoglobulin G antibodies, including the abnormal antibodies that are responsible for the symptoms of myasthenia gravis.14,17

Vyvgart® has been approved by the US Food and Drug Administration (FDA) to be used as a treatment for adult patients with generalized myasthenia gravis who are anti-AChR antibody positive (they have abnormal AChR antibodies). If you are prescribed Vyvgart®, you will receive the medicine as an intravenous infusion (a drip that is inserted into a vein) in cycles. Each cycle is 4 weeks long and cycles will be repeated at varying intervals depending on your symptoms. During each cycle, you will receive one infusion per week (four infusions per cycle). Each infusion lasts 1 hour.17

Vyvgart® Hytrulo (efgartigimod alfa and hyaluronidase-qvfc)

The FDA have also approved Vyvgart® Hytrulo (argenx) for the treatment of adults with myasthenia gravis who are anti-AChR antibody positive. Similar to Vyvgart®, the medicine also uses a fragment of an immunoglobulin G antibody to attach to and block the neonatal Fc receptor, but is given as a subcutaneous injection (an injection under the skin) by a healthcare professional. The injection takes 30–90 seconds and is also delivered in treatment cycles. One cycle consists of one injection each week for 4 weeks (four injections per cycle).18

You can find more information about Vyvgart® and Vyvgart® Hytrulo treatment via the following links: 

Rystiggo® (rozanolixizumab-noli)

RYSTIGGO® (Rozanolixizumab-noli), manufactured by UCB, an injection for subcutaneous infusion, is a humanized IgG4 monoclonal antibody that binds to the neonatal Fc receptor (FcRn), resulting in the reduction of circulating IgG1,4.  It is the only FDA-approved treatment in adults for both anti-AChR and anti-MuSK antibody-positive gMG, the two most common subtypes of gMG. If you are prescribed RYSTIGGO®, you will receive the drug via subcutaneous infusion (a drip given underneath the skin) by a healthcare professional in treatment cycles. One cycle consists of a subcutaneous infusion once a week for 6 weeks. 

For more information on Rystiggo®, you can view: 

Complement inhibitors

An important part of our immune system is a pathway called the complement pathway.14 While this pathway typically plays a beneficial role, it can become overactive in individuals with myasthenia gravis, and other auto-immune conditions, causing changes to the neuromuscular junction and the acetylcholine receptors3. This means that acetylcholine cannot bind to its receptors, which affects the signals between the muscles and nerves and results in muscle weakness3. Complement inhibitors can reduce activation of the complement pathway by blocking certain complement proteins, including C5. Through its targeted mechanism of action, zilucoplan binds to C5 with high affinity and specificity, preventing its cleavage to C5a and C5b, thus inhibiting complement mediated damage to the neuromuscular junction 2.

Due to the increased risk of serious meningococcal infections, all complement inhibitors are available only through a REMS (Risk Evaluation Mitigation Strategy) program4,5. REMS is a drug safety program that the Food and Drug Administration (FDA) may require for medications with serious safety concerns to ensure the benefits of the medication outweigh its risks4.  

  1. https://www.ucb-usa.com/zilbrysq-prescribing-information.pdf
  2. Howard JF Jr, et al. Safety and efficacy of zilucoplan in patients with generalized myasthenia gravis (RAISE): a randomized, double-blind, placebo-controlled, phase 3 study. Lancet Neurol. 2023;22(5):395-406. 
  3. Howard JF Jr. Myasthenia gravis: the role of complement at the neuromuscular junction. Ann N Y Acad Sci. 2018 Jan;1412(1):113-128. doi: 10.1111/nyas.13522. Epub 2017 Dec 21. PMID: 29266249.
  4. https://zilbrysqrems.com/
  5. https://www.fda.gov/drugs/drug-safety-and-availability/risk-evaluation-and-mitigation-strategies-re

Here are the complement inhibitors approved in the US:

Soliris® (eculizumab)

Soliris® (Alexion AstraZeneca Rare Disease) is a monoclonal antibody (an antibody that is made in a laboratory and has a specific target) that inhibits the complement pathway by targeting the C5 complement protein. While we do not fully understand how Soliris® improves the symptoms of myasthenia gravis, it may prevent the complement pathway from causing damage to the neuromuscular junction and the resulting muscle weakness experienced by people with the condition.21

Soliris® has been approved by the FDA as a treatment for generalized myasthenia gravis in adult patients who are anti-AChR antibody positive (they have abnormal AChR antibodies). If you are prescribed Soliris®, you will receive the medicine as an intravenous infusion (a drip into a vein) once a week for the first 5 weeks and then once every 2 weeks after this. A possible serious side effect of Solaris® is meningococcal sepsis (when bacteria and their toxins circulate in the blood and damage the organs). It is therefore important that you are vaccinated against meningococcal bacteria before receiving Solaris®.21 For a full list of side effects, please speak to your doctor and see the leaflet inside your medicine packet.

You can find more information about Soliris® treatment via the following links: 

Ultomiris® (ravulizumab-cwvz)

Ultomiris® (Alexion AstraZeneca Rare Disease) is another complement inhibitor that targets the C5 complement protein to reduce activation of the complement pathway.22 It is also a monoclonal antibody, but has a slightly different structure than Soliris®, meaning that the drug lasts longer in the body.23

Ultomiris® has been approved by the FDA to treat adults with generalized myasthenia gravis who are anti-AChR antibody-positive (they have abnormal AChR antibodies).1,22 If you are prescribed Ultomiris®, you will receive the medicine via intravenous infusion (a drip into your vein). You will receive an initial dose, then another dose 2 weeks later, followed by one dose every 4–8 weeks. A possible serious side effect of Ultomiris® is meningococcal sepsis (when bacteria and their toxins circulate in the blood and damage the organs). It is therefore important that you are vaccinated against meningococcal bacteria before receiving Ultomiris®.22 For a full list of side effects, please speak to your doctor and see the leaflet inside your medicine packet.

You can find out more information about Ultomiris® treatment by following the links: 

Zilbrysq® (zilucoplan)

ZILBRYSQ® (zilucoplan), manufactured by UCB, is approved by the U.S. Food and Drug Administration (FDA) and currently available for the treatment of generalized myasthenia gravis (gMG) in adult patients who are anti-acetylcholine receptor (AChR) antibody-positive1. ZILBRYSQ® is the first and only once-daily, subcutaneous, self-administered peptide inhibitor of complement component 5 (C5 inhibitor)1. If you are prescribed ZILBRYSQ®, you will be taught how to administer the medicine at home via a subcutaneous injection into your abdomen, thighs or upper arms (only if someone else is giving you the injection) once a day1, 24,25.  

Intravenous immunoglobulin

Your body’s immune system naturally produces antibodies called immunoglobulins to help fight infection and disease. Intravenous immunoglobulin is a treatment that uses these antibodies from donations of plasma (a part of our blood). This treatment increases the levels of immunoglobulins in your blood and results in multiple effects on different aspects of the immune system, including reducing the levels of abnormal antibodies responsible for the symptoms of myasthenia gravis.26

Intravenous immunoglobulin is used as a short-term treatment in an emergency, if other treatments are not working or when a quick improvement in strength is needed, for example before surgery. This treatment is also commonly used if you experience a severe relapse of symptoms or if you develop severe weakness in your breathing muscles(myasthenic crisis).5 If you need intravenous immunoglobulin, it will be given to you via an intravenous infusion (a drip containing the immunoglobulins). The intravenous infusion can be given over a period of 2–5 days for emergency treatment or every 3–6 weeks as a maintenance treatment, and is typically given in a hospital or clinic setting.7,9 After treatment with intravenous immunoglobulins, improvement in your symptoms can be temporary and you may therefore need repeated treatments.9

Subcutaneous immunoglobulin

A new, less-invasive method of receiving immunoglobulins is being investigated as a treatment for myasthenia gravis. This type of treatment is known as subcutaneous (under the skin) immunoglobulin. While there are studies that show the benefits and safety of subcutaneous immunoglobulin in patients with myasthenia gravis, it has not yet been approved for treating people with myasthenia gravis.14,27

Hizentra® (immunoglobulin)

Hizentra® (CSL Behring) is an example of subcutaneous immunoglobulin that has been approved by the FDA for the treatment of other neurological and primary immunodeficiency conditions but has not yet been approved for the treatment of myasthenia gravis. In this method of delivering immunoglobulins, rather than receiving a drip through a vein, you would receive the medication via subcutaneous infusion; up to eight needles placed under the skin at different points on your body. A typical subcutaneous infusion may only take 1–2 hours and can be done at home.27

Therapeutic plasma exchange

Therapeutic plasma exchange, also known as plasmapheresis, is a treatment that takes your blood and separates the different components to remove the blood plasma that contains the abnormal antibodies responsible for myasthenia gravis symptoms. The blood is then returned with a replacement plasma that does not contain the abnormal antibodies. The procedure is carried out using needles that are inserted into your veins or a port (a small device installed beneath the skin that allows medication to be delivered into your bloodstream).9,28,29 With fewer abnormal antibodies, the signals between the nerves and muscles are improved resulting in greater muscle activation.1

Plasma exchange is used as a short-term treatment in an emergency, if other treatments are not working or when a quick improvement in strength is needed, for example before surgery. As your body will continue to produce abnormal antibodies, repeated plasma exchange treatments may be needed.5

References

1. Dresser L, Wlodarski R, Rezania K, et al. Myasthenia gravis: epidemiology, pathophysiology and clinical manifestations. J Clin Med 2021; 10: 2235.

2. DeHart-McCoyle M, Patel S, Du X. New and emerging treatments for myasthenia gravis. BMJ Med 2023; 2: e000241.

3. Gilhus NE, Tzartos S, Evoli A, et al. Myasthenia gravis. Nat Rev Dis Primers 2019; 5: 30.

4. Vanoli F, Mantegazza R. Current drug treatment of myasthenia gravis. Curr Opin Neurol 2023; 36: 410-415.

5. Sanders DB, Wolfe GI, Benatar M, et al. International consensus guidance for management of myasthenia gravis. Neurology 2016; 87: 419–425.

6. Narayanaswami P, Sanders DB, Wolfe G, et al. International consensus guidance for management of myasthenia gravis: 2020 update. Neurology 2021; 96: 114–122.

7. Farmakidis C, Pasnoor M, Dimachkie MM, et al. Treatment of myasthenia gravis. Neurol Clin 2018; 36: 311–337.

8. Miller J. The function of the thymus and its impact on modern medicine. Science 2020; 369.

9. Alhaidar MK, Abumurad S, Soliven B, et al. Current treatment of myasthenia gravis. J Clin Med 2022; 11: 1597.

10. Mestinon US Prescribing Information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2001/15193s18lbl.pdf. Accessed on January 2024.

11. Regonol US Prescribing Information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2004/17398s015lbl.pdf. Accessed on January 2024.

12. Katz NK, Barohn RJ. The history of acetylcholinesterase inhibitors in the treatment of myasthenia gravis. Neuropharmacology 2021; 182: 108303.

13. Sanders DB, Evoli A. Immunosuppressive therapies in myasthenia gravis. Autoimmunity 2010; 43: 428–435.

14. Schneider-Gold C, Gilhus NE. Advances and challenges in the treatment of myasthenia gravis. Ther Adv Neurol Disord 2021; 14: 17562864211065406.

15. Imuran US Prescribing Information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/016324s039lbl.pdf. Accessed on January 2024.

16. CellCept US Prescribing Information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/050722s021,050723s019,050758s019,050759s024lbl.pdf. Accessed on January 2024.

17. Vyvgart US Prescribing Information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2021/761195s000lbl.pdf. Accessed on January 2024.

18. Vyvgart Hytrulo US Prescribing Information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/761304s000lbl.pdf. Accessed on January 2024.

19. NCI Dictionary of Cancer Terms: Humanized monoclonal antibody. https://www.cancer.gov/publications/dictionaries/cancer-terms/def/humanized-monoclonal-antibody. Accessed on February. 2024.

20. Rystiggo US PI. https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/761286s000lbl.pdf. Accessed on November 2023.

21. Solaris US Prescribing Information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/125166s047s048lbl.pdf. Accessed on January 2024.

22. Ultomiris US Prescribing Information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/761108s000lbl.pdf. Accessed on January 2024.

23. Röth A, Rottinghaus ST, Hill A, et al. Ravulizumab (ALXN1210) in patients with paroxysmal nocturnal hemoglobinuria: results of 2 phase 1b/2 studies. Blood Adv 2018; 2: 2176-2185.

24. Zilbrysq US Prescribing Information. https://www.ucb-usa.com/zilbrysq-prescribing-information.pdf. Accessed on January 2024.

25. Howard JF, Jr., Bresch S, Genge A, et al. Safety and efficacy of zilucoplan in patients with generalised myasthenia gravis (RAISE): a randomised, double-blind, placebo-controlled, Phase 3 study. Lancet Neurol 2023; 22: 395–406.

26. Dalakas MC, Meisel A. Immunomodulatory effects and clinical benefits of intravenous immunoglobulin in myasthenia gravis. Expert Rev Neurother 2022; 22: 313–318.

27. Hizentra US Prescribing Information. https://www.fda.gov/vaccines-blood-biologics/approved-blood-products/hizentra. Accessed on January 2024.

28. Ipe TS, Davis AR, Raval JS. Therapeutic plasma exchange in myasthenia gravis: A systematic literature review and meta-analysis of comparative evidence. Front Neurol 2021; 12: 662856.

29. Osman C, Jennings R, El-Ghariani K, et al. Plasma exchange in neurological disease. Pract Neurol 2020; 20: 92–101.