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Myasthenia Gravis (MG)

Myasthenia Gravis (MG)

Myasthenia gravis (MG) imposes a substantial socioeconomic burden due to chronic disability, high treatment costs, and 10-20% mortality risk during myasthenic crises. At Protheragen, we focus on developing novel therapeutics and building accurate animal models to accelerate preclinical studies of potential therapies for MG. Our expertise ensures that client's research receives the most reliable and relevant support, accelerating their drug development journey.

Introduction to Myasthenia Gravis (MG)

Myasthenia gravis (MG) is a chronic autoimmune neuromuscular disorder characterized by fatigable muscle weakness due to impaired synaptic transmission at the neuromuscular junction (NMJ). The disease manifests with hallmark symptoms such as ptosis, diplopia, dysphagia, and proximal limb weakness, which worsen with physical activity and improve with rest. MG affects approximately 20 per 100,000 individuals, with higher incidence in women under 40 and men over 60.

Pathogenesis of myasthenia gravis. Fig.1 Pathogenesis of myasthenia gravis (MG). (Gomez F, et al., 2023)

Pathogenesis of Myasthenia Gravis (MG)

The pathogenesis of myasthenia gravis (MG) is primarily driven by autoantibody-mediated disruption of neuromuscular transmission, with most cases (85%) involving anti-acetylcholine receptor (AChR) antibodies that block, degrade, or complement-mediated destroy postsynaptic AChRs, impairing muscle activation. In MuSK-MG (5-8%), antibodies against muscle-specific kinase (MuSK) disrupt AChR clustering, while LRP4 antibodies (1-2%) interfere with agrin-MuSK signaling. Thymic abnormalities contribute to immune dysregulation by fostering autoreactive B-cells.

Schematic diagram of agrin secretion from the presynaptic membrane and its interaction with Lrp4. Fig.2 Diagram depicting the secretion of agrin from the presynaptic membrane and its interaction with Lrp4. (Dresser L, et al., 2021)

Therapeutic Development for Myasthenia Gravis (MG)

Drug Names Mechanism of Action Targets NCT Number Research Phase
Human normal immunoglobulin G Provides passive immunity; modulates immune response, suppresses antibody production and complements Multiple immune pathways; Fc receptors NCT02774239 Approved
HBM9161 FcRn antagonist; accelerates degradation of pathogenic IgG autoantibodies Neonatal Fc receptor (FcRn) NCT04346888 Phase II
HN2301 Selective complement C5 inhibitor; prevents formation of membrane attack complex (MAC) Complement component C5 NCT06965309 Phase I/II
CNP-106 Autologous tolerogenic cell therapy; designed to induce antigen-specific immune tolerance Autoreactive T cells specific to AChR/MuSK NCT06106672 Phase Ib/IIa

Disclaimer: Protheragen focuses on providing preclinical research services. This table is for information exchange purposes only. This table is not a treatment plan recommendation. For guidance on treatment options, please visit a regular hospital.

Our Services

Protheragen specializes in providing cutting-edge diagnostic and therapeutic development services for rare neuroinflammatory diseases, including myasthenia gravis (MG). We focus on creating advanced disease models to better understand MG pathogenesis, and we utilize innovative blood-brain barrier (BBB) models to enhance the delivery and efficacy of therapeutic compounds. Through our comprehensive approach, we aim to accelerate the development of accurate diagnostic kits and effective treatments tailored to MG.

Therapeutic Development Services

By Molecule Types

At Protheragen, we address critical challenges in myasthenia gravis (MG) therapeutics through integrated, mechanism-driven drug development platforms, accelerating precision treatments from target identification to preclinical validation.

By Mechanism of Action

Specializing in precision-engineered neuroimmunotherapies, our research focuses on disrupting the autoimmune pathogenesis of myasthenia gravis (MG) through targeted molecular interventions that restore neuromuscular synaptic function.

Disease Model Development Services

  • Experimental Autoimmune Myasthenia Gravis (EAMG) Model, induced by immunizing animals with acetylcholine receptors (AChRs), is a widely used model.
  • MuSK-EAMG Model involves immunization with MuSK protein, mimicking a rare form of MG associated with anti-MuSK antibodies.

Focusing on preclinical research, Protheragen offers comprehensive pharmacodynamic (PD), pharmacokinetic (PK), and toxicology study services to support the development and regulatory approval of potential therapies. If you are interested in our services, please feel free to contact us for more details and quotation information of related services.

References

  1. Gomez F, Mehra A, Ensrud E, et al. COVID-19: a modern trigger for Guillain-Barre syndrome, myasthenia gravis, and small fiber neuropathy[J]. Frontiers in Neuroscience, 2023, 17: 1198327.
  2. Dresser L, Wlodarski R, Rezania K, et al. Myasthenia gravis: epidemiology, pathophysiology and clinical manifestations[J]. Journal of clinical medicine, 2021, 10(11): 2235.
For research use only. Not intended for any clinical use.

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