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> Insights > World Myasthenia Gravis Day | ACRO Stands with You in Protecting Muscle Health 
World Myasthenia Gravis Day is observed annually on June 15th. Myasthenia gravis (MG) is a global autoimmune disease affecting an estimated 1.5 to 2 million people worldwide. The condition is characterized by fluctuating muscle weakness that typically follows a "mild in the morning , worse in the evening" pattern—patients experience relatively milder symptoms upon waking, with progressive worsening throughout the day. Additionally, approximately 20% of MG patients may develop life-threatening myasthenic crises, posing serious threats to their health and life.
https://www.startstemcells.com/myasthenia-gravis.html
Pathogenesis and pathological features of MG
Within conventional treatment approaches, corticosteroids are commonly utilized. However, this therapy carries significant adverse effects, long-term use can lead to complications such as osteoporosis or metabolic syndrome, substantially impacting patients' quality of life and diminishing subsequent therapeutic efficacy. While intravenous immunoglobulin (IVIG) therapy demonstrates efficacy, its prohibitive cost—exceeding $10,000 per infusion—renders it financially inaccessible for many patients, limiting its widespread use. Consequently, the development of safer, more cost-effective, and accessible targeted therapies represents a pressing need within the MG treatment landscape.
ACROBiosystems has developed a comprehensive product portfolio for MG research including highly active recombinant proteins, stable cell lines, and inhibitor screening kits. Our solutions span the entire drug development continuum – from target discovery and validation, candidate drug screening and development to CMC manufacturing and quality control – accelerating the efficient translation of MG innovative therapies from foundational research to clinical implementation.
Free download: ACRO's autoimmune disease drug development solutions!
The core pathology of MG stems from an autoimmune attack on the neuromuscular junction (NMJ), where the immune system erroneously identifies the acetylcholine receptor (AChR)—a critical target at the NMJ—as a foreign antigen. This triggers the production of pathogenic IgG autoantibodies. These antibodies disrupt neuromuscular signal transmission through multiple mechanisms:
- Primarily, the antibodies act as molecular plugs by specifically binding to AChRs, blocking acetylcholine (ACh) binding sites and directly impeding neurotransmitter-receptor interaction.
- Additionally, antibodies facilitate AChR internalization and degradation via cross-linking, reducing the availability of functional receptors at the NMJ.
- Concurrently, antibody binding activates the complement cascade. Key components (C1q, C3, C5) undergo sequential activation, ultimately forming membrane attack complexes (MACs, C5b-9) at the NMJ. These molecular drills physically disrupt the postsynaptic membrane architecture, irreversibly destroying the foundation of signal transmission.
https://doi.org/10.1172/JCI179742
Structure of the NMJ
Simultaneously, the initiation and maintenance of the immune response in MG depend critically on the driving actions of key immune cells and cytokines. The core immune attack mechanism manifests as a cascade of events: pathogenic T helper 17 (Th17) cells serve as the primary drivers, B cells/plasma cells are responsible for antibody production, and the thymic microenvironment provides critical support. Specifically activated Th17 cells secrete pro-inflammatory cytokines such as interleukin-17 (IL-17), IL-21, and IL-23, driving B cell differentiation into plasma cells (the primary source of pathogenic antibodies). Concurrently, regulatory T cell (Treg) dysfunction leads to a breakdown in immune tolerance. Among the key cytokines, IL-6 promotes the sustained production of autoantibodies by plasma cells. B cell-activating factor (BAFF) and a proliferation-inducing ligand (APRIL) directly enhance the survival of B cells and plasma cells, and tumor necrosis factor-alpha (TNF-α) exacerbates inflammation and impairs neuromuscular junction function. Approximately 10-15% of patients exhibit antibody subtype variations. For instance, muscle-specific tyrosine kinase (MuSK) antibodies disrupt acetylcholine receptor (AChR) clustering. Furthermore, abnormal thymic tissue acts as a significant site of origin for the autoimmune response, constitutively expressing self-antigens (e.g., AChR) and secreting interferon-gamma (IFN-γ) and IL-1β, thereby amplifying autoimmunity. The in-depth elucidation of these mechanisms is driving a shift in MG therapeutic strategies away from non-specific immunosuppression towards precision therapies targeting specific pathways like BAFF/APRIL and the neonatal Fc receptor (FcRn).
https://doi.org/10.1172/JCI179742
Cytokine network and immune cells in MG pathogenesis and immunoregulation
MG treatment is undergoing a paradigm shift from “treating the symptoms without addressing the underlying disease” to precision targeting. Conventional therapies have long relied on broad-spectrum suppression: cholinesterase inhibitors (e.g., brompheniramine) in the symptomatic support stratum provide only transient symptomatic relief. Glucocorticoids and traditional immunosuppressive agents (such as azathioprine and tacrolimus) in the immunosuppressive stratum are associated with significant infectious and metabolic toxicity. Plasma exchange (PLEX) and intravenous immunoglobulins (IVIg) in the antibody-clearing stratum provide immediate relief but are short-lived and costly.
https://doi.org/10.2147/ITT.S377056
Targets of novel therapeutics in MG
The turning point began with the rise of targeted therapies, with market differentiation becoming prominent among approved drugs. The FcRn antagonist segment has witnessed explosive growth. Efgartigimod has expanded across multiple indications including MG and primary immune thrombocytopenia, achieving global sales of $2.2 billionin in 2024. Its subcutaneous formulation, along with rozanolixizumab (which generated $227 million in sales in 2024), is driving a revolution in dosing convenience. Johnson & Johnson's Nipocalimab received FDA approval in April 2025, becoming the first FcRn blocker to cover both anti-AChR/MuSK double-positive MG in adults and pediatric patients. It can be administered via subcutaneous injection in just 30 seconds and is projected to reach peak sales of $5 billion. Among complement inhibitors, eculizumab maintained annual revenues of $210 million, while ravulizumab gained approval in China for multiple sclerosis. Traditional intravenous immunoglobulin (IVIg), however, faced a 12% market contraction in 2023 due to competition from novel subcutaneous formulations. Chinese innovative drugs are accelerating market penetration: Telitacicept achieved domestic sales of RMB 380 million in 2023, while Junshi Biosciences' toripalimab generated RMB 447 million in Q1 2025, reflecting a 45.7% year-over-year increase and robust growth in the local market.
Pipeline development is focused on three transformative directions: dual-target/long-acting formulations, such as Povetacicept (a dual BAFF/APRIL antagonist), which achieved a 63% complete remission rate in Phase II trials for IgA nephropathy, with Phase III recruitment ongoing in China. Gefurulimab (a C5/albumin bispecific antibody) extends the dosing interval to 8 weeks. Cell therapies are redefining treatment paradigms. Phase II data for Descartes-08 (an mRNA CAR-T therapy) in myasthenia gravis showed 100% of patients demonstrating significant improvement within 9 months, without the need for chemotherapeutic conditioning or the risk of cytokine release syndrome. Mid-2024 Phase 2b results may address safety bottlenecks. Chinese pharmaceutical companies are comprehensively deploying differentiated pipelines: Shanghai Pharmaceuticals' B007 (a humanized CD20 monoclonal antibody) has entered Phase II/III trials, requiring only 5 minutes for subcutaneous administration—a 10-fold improvement in dosing efficiency compared to rituximab. Tianchen Biotech's LP-005 is the world's first C3/C5 bispecific antibody, capable of simultaneously inhibiting dual nodes of complement activation. Preclinical data indicate a 40% improvement in blocking efficiency compared to single-target agents.
Advancements in MG Drug Development (Data Source: Pharmacodia)
The treatment of MG is undergoing a revolutionary shift from "indiscriminate suppression" to "precision-guided defusing." With deepening scientific understanding of the immune system's "faulty directives," as well as enhanced policy support and capital investment in the rare disease sector, the immunological chains binding patients suffering from debilitating fatigue are being dismantled layer by layer.
ACROBiosystems has developed a comprehensive product portfolio for MG research including highly active recombinant proteins, stable cell lines, and inhibitor screening kits. Our solutions span the entire drug development continuum – from target discovery and validation, candidate drug screening and development to CMC manufacturing and quality control – accelerating the efficient translation of MG innovative therapies from foundational research to clinical implementation.
Free download: ACRO's autoimmune disease drug development solutions!
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1. Kaminski H J, Sikorski P, Coronel S I, et al. Myasthenia gravis: the future is here[J]. Journal of Clinical Investigation, 2024, 134(12): e179742. https://doi.org/10.1172/JCI179742
2. Nair S S, Jacob S. Novel immunotherapies for myasthenia gravis[J]. ImmunoTargets and therapy, 2023: 25-45. https://doi.org/10.2147/ITT.S377056
3. Huda R. Inflammation and autoimmune myasthenia gravis[J]. Frontiers in immunology, 2023, 14: 1110499. https://doi.org/10.3389/fimmu.2023.1110499
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