Full Press Release Details
argenx to Present New Data at 2026 AAN Annual Meeting that Continue to Transform Patient Outcomes in MG and CIDP and Build Upon Strength of Pipeline
March 6, 2026, 7:00 AM CEST
Amsterdam, the Netherlands - argenx SE (Euronext & Nasdaq: ARGX), a global immunology company committed to improving the lives of people suffering from severe autoimmune diseases, will present data for VYVGART (IV: efgartigimod alfa-fcab and SC or Hytrulo: efgartigimod alfa and hyaluronidase-qvfc) and pipeline candidates empasiprubart and adimanebart at the 2026 American Academy of Neurology (AAN) Annual Meeting in Chicago from April 18-22, 2026.
Notable myasthenia gravis (MG) data supporting our pursuit of the broadest label for MG patients to be presented include:
In chronic inflammatory demyelinating polyneuropathy (CIDP), argenx will highlight results from an ADHERE post hoc analysis in treatment-na ve patients that underscore VYVGART Hytrulo's impact in this underserved population and support its use earlier in the treatment paradigm. Real-world insights will further illustrate physician approaches to transitioning patients from IVIg to VYVGART Hytrulo to support positive patient outcomes. Featured research also includes ADHERE neurofilament light chain (NfL) data from the most comprehensive dataset to date, advancing CIDP innovation by exploring this potential biomarker of disease.
Additional results from the ARGX-119 Phase 1b trial evaluating adimanebart in patients with DOK7 congenital myasthenic syndromes (CMS) will also be shared, providing proof-of-concept support based on a favorable safety profile and consistent functional improvements across multiple efficacy measures.
Details for oral and poster presentations at AAN are as follows:
| Title | Lead Author | Presentation |
| Myasthenia Gravis (MG) | ||
| Efficacy and Safety of Efgartigimod in Anti-acetylcholine Receptor Antibody-Negative Generalized Myasthenia Gravis: Initial Results of ADAPT SERON | James F. Howard Jr. | Oral Presentation #008 S14: Updates on Myasthenia Gravis Monday, April 20 2:24 p.m. CT |
| Results from the ADAPT JR Study Investigating Intravenous Efgartigimod in Juvenile Generalized Myasthenia Gravis | Abigail N. Schwaede | Oral Presentation #002 S19: Emerging Therapies in Child Neurology Monday, April 20 3:42 p.m. CT |
| Efficacy and Safety of Subcutaneous Efgartigimod PH20 Administered by Prefilled Syringe in Adults With Ocular Myasthenia Gravis: Interim Results of ADAPT OCULUS Part A | Vern C. Juel | Poster #022 P9: Neuromuscular and Clinical Neurophysiology (EMG): Myasthenia Gravis Clinical Trials Tuesday, April 21 5-6 p.m. CT |
| Sustained Clinical Efficacy and Long-term Safety of Intravenous Efgartigimod for Generalized Myasthenia Gravis: Part B of ADAPT NXT | Arjun Seth | Poster #003 P9: Neuromuscular and Clinical Neurophysiology (EMG): Myasthenia Gravis Clinical Trials Tuesday, April 21 5-6 p.m. CT |
| Long-term Safety and Efficacy of Subcutaneous Efgartigimod PH20 in Adult Participants With Generalized Myasthenia Gravis: Final Results of the ADAPT-SC+ Study | Claire Wan-Yi Huang | Poster #002 P9: Neuromuscular and Clinical Neurophysiology (EMG): Myasthenia Gravis Clinical Trials Tuesday, April 21 5-6 p.m. CT |
| Design of a Phase 2a Study to Evaluate the Safety, Efficacy, and Tolerability of Intravenous Empasiprubart as an Add-On Therapy to Intravenous Efgartigimod in Adult Participants With Generalized Myasthenia Gravis | Jeff Guptill | Poster #021 P9: Neuromuscular and Clinical Neurophysiology (EMG): Myasthenia Gravis Clinical Trials Tuesday, April 21 5-6 p.m. CT |
| Safety and Effectiveness of Efgartigimod in Japanese Patients With Generalized Myasthenia Gravis by Serological Profiles: Analysis of Post-marketing Surveillance | Hirofumi Teranishi | Poster #006 P9: Neuromuscular and Clinical Neurophysiology (EMG): Myasthenia Gravis Clinical Trials Tuesday, April 21 5-6 p.m. CT |
| Assessing Efgartigimod Dosing Patterns and Myasthenia Gravis Activities of Daily Living Outcomes in Clinical Practice: Results From a Large Patient Support Program Database in the United States | Pushpa Narayanaswami | Poster #020 P11: Neuromuscular and Clinical Neurophysiology (EMG): Myasthenia Gravis Treatments Wednesday, April 22 11:45 a.m.-12:45 p.m. CT |
| Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) | ||
| Impact of Subcutaneous Efgartigimod PH20 on Treatment-na ve Participants With Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) in the ADHERE Trial: Post Hoc Analyses | Hans Katzberg | Poster #002 P1: Neuromuscular and Clinical Neurophysiology (EMG): Autoimmune Neuropathies Sunday, April 19 8-9 a.m. CT |
| Serum NfL Z-score as a Biomarker of Disease Severity and Treatment History in the Largest CIDP Cohort to Date: Insights from the ADHERE Trial | Roger Collet Vidiella | Poster #004 P7: Neuromuscular and Clinical Neurophysiology (EMG): Peripheral Nerve Disorders Tuesday, April 21 8-9 a.m. CT |
| Physician Insights on Transitioning Patients With Chronic Inflammatory Demyelinating Polyradiculoneuropathy From Intravenous Immunoglobulin to Subcutaneous Efgartigimod PH20 | Jamie Aldridge | Poster #016 P7: Neuromuscular and Clinical Neurophysiology (EMG): Peripheral Nerve Disorders 8-9 a.m. CT |
| Characteristics of Real-world Patients With Chronic Inflammatory Demyelinating Polyradiculoneuropathy Initiating Subcutaneous Efgartigimod in United States | Nadia Zaveri | Poster #013 P7: Neuromuscular and Clinical Neurophysiology (EMG): Peripheral Nerve Disorders Tuesday, April 21 8-9 a.m. CT |
| Beyond Disability: The Burden of Fatigue in CIDP | Swapna Karkare | Poster #007 P1: Neuromuscular and Clinical Neurophysiology (EMG): Autoimmune Neuropathies Sunday, April 19 8-9 a.m. CT |
| Real-world Effectiveness and Use of Efgartigimod in Chronic Inflammatory Demyelinating Polyradiculoneuropathy: ADHERE REAL Study Design | Chafic Karam | Poster #011 P6: Neuromuscular and Clinical Neurophysiology (EMG): Peripheral Nerve and Other Neuromuscular Disorders Monday, April 20 5-6 p.m. CT |
| Empasiprubart Versus Placebo in Chronic Inflammatory Demyelinating Polyradiculoneuropathy: EMNERGIZE Phase Three Study Design | Thomas H. Brannagan | Poster #021 P1: Neuromuscular and Clinical Neurophysiology (EMG): Autoimmune Neuropathies Sunday, April 19 8-9 a.m. CT |
| Empasiprubart vs Immunoglobulin in Chronic Inflammatory Demyelinating Polyradiculoneuropathy: EMVIGORATE Phase Three Study Design | Simon Rinaldi | Poster #022 P1: Neuromuscular and Clinical Neurophysiology (EMG): Autoimmune Neuropathies Sunday, April 19 8-9 a.m. CT |
| Congenital Myasthenic Syndromes (CMS) | ||
| Phase 1b Study of the Safety, Tolerability, Pharmacokinetics, Immunogenicity, and Efficacy of ARGX-119 in Participants with DOK7 Congenital Myasthenic Syndromes | Nancy L. Kuntz | Oral Presentation #007 S32: General Neurology 1 Tuesday, April 21 4:42 p.m. CT |
| Multiple Disease Areas | ||
| Efgartigimod is a Unique FcRn Blocker That Allows IgG Reduction Without Broad Inhibition of Immune Responses | Kristin Heerlein | Poster #008 P3: Autoimmune Neurology: Inflammatory NOS 1 Sunday, April 19 5-6 p.m. CT |
More information on the data presented at the 2026 AAN Annual Meeting can be found here.
Important Safety Information
What is VYVGART (efgartigimod alfa-fcab)?
VYVGART is a prescription medicine used to treat a condition called generalized myasthenia gravis, which causes muscles to tire and weaken easily throughout the body, in adults who are positive for antibodies directed toward a protein called acetylcholine receptor (anti-AChR antibody positive).
IMPORTANT SAFETY INFORMATION
Do not use VYVGART if you have a serious allergy to efgartigimod alfa or any of the other ingredients in VYVGART. VYVGART can cause serious allergic reactions and a decrease in blood pressure leading to fainting.
VYVGART may cause serious side effects, including:
Tell your doctor if you have signs or symptoms of an infection, allergic reaction, or infusion-related reaction. These can happen while you are receiving your VYVGART treatment or afterward. Your doctor may need to pause or stop your treatment. Contact your doctor immediately if you have signs or symptoms of a serious allergic reaction.
Before taking VYVGART, tell your doctor if you:
What are the common side effects of VYVGART?
The most common side effects of VYVGART are respiratory tract infection, headache, and urinary tract infection.
These are not all the possible side effects of VYVGART. Call your doctor for medical advice about side effects. You may report side effects to the US Food and Drug Administration at 1-800-FDA-1088.
Please see the full Prescribing Information for VYVGART and talk to your doctor.
Important Safety Information
What is VYVGART HYTRULO (efgartigimod alfa and hyaluronidase-qvfc)?
VYVGART HYTRULO is a prescription medicine used to treat adults with:
It is not known if VYVGART HYTRULO is safe and effective in children.
IMPORTANT SAFETY INFORMATION
Do not take VYVGART HYTRULO if you are allergic to efgartigimod alfa, hyaluronidase, or any of the ingredients in VYVGART HYTRULO. VYVGART HYTRULO can cause serious allergic reactions and a decrease in blood pressure leading to fainting.
Before taking VYVGART HYTRULO, tell your healthcare provider about all of your medical conditions, including if you:
Tell your healthcare provider about all the medicines you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements.
VYVGART HYTRULO can cause side effects which can be serious, including:
The most common side effects of VYVGART HYTRULO include respiratory tract infection, headache, urinary tract infection, and injection site reactions.
These are not all the possible side effects of VYVGART HYTRULO. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
Please see the full Prescribing Information for VYVGART HYTRULO and talk to your doctor.
About VYVGART and VYVGART Hytrulo
VYVGART (efgartigimod alfa fcab) is a first-in-class human IgG1 antibody fragment that binds to the neonatal Fc receptor (FcRn), resulting in the reduction of circulating IgG autoantibodies. VYVGART Hytrulo is a subcutaneous combination of efgartigimod alfa (VYVGART) and recombinant human hyaluronidase PH20 (rHuPH20), Halozyme's ENHANZE drug delivery technology to facilitate subcutaneous injection delivery of biologics. VYVGART is approved for generalized myasthenia gravis (gMG) and immune thrombocytopenia (Japan only). VYVGART Hytrulo is approved for gMG and chronic inflammatory demyelinating polyneuropathy (CIDP). VYVGART Hytrulo may be marketed under different proprietary names in other regions.
About Empasiprubart
Empasiprubart (ARGX-117) is a novel humanized monoclonal antibody that binds C2 and blocks activation of both the classical and lectin pathways of the complement cascade. By blocking complement activity upstream of C3 and C5, empasiprubart has the potential to reduce tissue inflammation and cellular damage, representing a broad pipeline opportunity across multiple severe autoimmune indications. In addition to multifocal motor neuropathy, argenx is evaluating empasiprubart in delayed graft function following kidney transplant, and chronic inflammatory demyelinating polyneuropathy (CIDP).
About Adimanebart
Adimanebart (ARGX-119) is a first-in-class humanized agonist monoclonal antibody (mAb) that specifically targets and activates muscle-specific tyrosine kinase (MuSK) to promote maturation and stabilization of the neuromuscular junction (NMJ). It is a mAb derived from llamas and discovered using the argenx SIMPLE Antibody platform technology. Adimanebart is being developed for patients with neuromuscular disease, including congenital myasthenic syndromes (CMS), amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA). Adimanebart was developed through argenx's IIP program in collaboration with the world's leading key opinion leaders on MuSK and the NMJ, Professor Steven J. Burden from MGH, Professor Shohei Koide from NYU and Professor Jan Verschuuren and Associate Professor Maartje Huijbers from LUMC.
About Generalized Myasthenia Gravis (gMG)
Generalized myasthenia gravis (gMG) is a rare and chronic autoimmune disease where IgG autoantibodies disrupt communication between nerves and muscles, causing debilitating and potentially life-threatening muscle weakness. Approximately 85% of people with MG progress to gMG within 24 months, where muscles throughout the body may be affected. Patients with confirmed AChR antibodies account for approximately 85% of the total gMG population.
About Ocular Myasthenia Gravis (oMG)
Ocular myasthenia gravis (oMG) is a rare and chronic autoimmune disease characterized by muscle weakness limited to the muscles controlling the eyes and eyelids. Symptoms commonly include ptosis (drooping eyelids), diplopia (double vision), and fluctuating visual disturbance that can impair daily activities. Approximately 80% of myasthenia gravis (MG) patients initially present with ocular symptoms, and up to 92% experience ocular involvement at some point during the course of disease. While many progress to generalized myasthenia gravis (gMG), in 15-25% of patients, weakness remains restricted to the ocular muscles. oMG is driven by pathogenic IgG autoantibodies that disrupt communication at the neuromuscular junction. Despite the functional and quality-of-life burden associated with persistent ocular symptoms, there are currently no approved targeted therapies specifically for oMG. Treatment approaches often rely on symptomatic therapies and generalized immunosuppression, underscoring the need for additional therapeutic options for this distinct MG population.
About Generalized Myasthenia Gravis (gMG) without detectable AChR-Ab
Generalized myasthenia gravis (gMG) is a rare, chronic, neuromuscular autoimmune disease caused by pathogenic IgGs targeting the neuromuscular junction (NMJ), resulting in impaired neuromuscular transmission and debilitating and potentially life-threatening muscle weakness and chronic fatigue. Approximately 80% of patients with gMG have detectable antibodies against the AChR in sera, and these patients are diagnosed as AChR-Ab seropositive gMG. Approximately 20% of patients with gMG do not have detectable serum antibodies directed against AChR. These patients may have detectable autoantibodies targeting other NMJ proteins, such as muscle-specific tyrosine kinase (MuSK) and low-density lipoprotein receptor-related protein 4 (LRP4), or others. Anti-MuSK antibodies are detected in approximately 1-10% of patients with gMG, while anti-LRP4 antibodies are detected in approximately 1-5% of patients with gMG. About 10% of patients do not have any detectable autoantibodies against AChR, MuSK or LRP4. These triple seronegative patients have historically been excluded from studies and have a higher disease burden and unmet medical need compared to patients with detectable autoantibodies. Currently, there are no approved treatments available for patients with anti-LRP4 antibodies or for triple seronegative patients.
About Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP)
Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a rare and serious autoimmune disease of the peripheral nervous system. CIDP is a heterogenous disease involving different yet overlapping pathways and a varied disease course. There is increasing evidence that IgG antibodies and the complement system play a key role in the damage to the peripheral nerves. People with CIDP experience fatigue, muscle weakness and a loss of feeling in their arms and legs that can worsen over time or may come and go. These symptoms can significantly impair a person's ability to function in their daily lives. Without treatment, one-third of people living with CIDP will need a wheelchair.
About Congenital Myasthenic Syndromes (CMS)
Congenital Myasthenic Syndromes (CMS) are an ultra-rare and heterogenous group of congenital neuromuscular disorders caused by genetic defects that are essential for the integrity of the neuromuscular junction. Early age of onset and fatigable muscle weakness are considered clinical hallmarks of CMS. Muscle weakness can be debilitating and life-threatening causing difficulties in speaking or swallowing, impaired or absent mobility, proximal arm and leg weakness, and respiratory insufficiency. DOK7 variations are one of the more frequent and severe causes of CMS, accounting for approximately 24% of CMS cases. There are no approved treatments. The prevalence of CMS is estimated to be 5 per 1M (DOK7-CMS estimated to be 1.2 per 1M).
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