Guillain-Barré Syndrome (GBS)
Therapeutic challenges in Guillain-Barré syndrome (GBS) include rapid disease progression requiring timely intervention and heterogeneity in patient responses to standard therapies. At Protheragen, we are committed to advancing the understanding and management of GBS through cutting-edge therapeutic development and disease modeling services. Our goal is to provide end-to-end solutions for the entire process from GBS therapeutic research to commercialization.
Introduction to Guillain-Barré Syndrome (GBS)
Guillain-Barré syndrome (GBS) is an acute, immune-mediated polyneuropathy characterized by rapid-onset muscle weakness, areflexia, and sensory disturbances, often progressing to paralysis. With an incidence of 1-2 cases per 100,000 annually, GBS represents a neurological emergency requiring prompt intervention. The disease typically follows a monophasic course, peaking within 2-4 weeks, unlike its chronic counterpart, CIDP.
Fig.1 Pathophysiology of COVID-19 related Guillain-Barré syndrome (GBS). (Valaparla V L, et al., 2024)
Pathogenesis of Guillain-Barré Syndrome (GBS)
The pathogenesis of Guillain-Barré syndrome (GBS) is primarily driven by molecular mimicry, where microbial antigens trigger cross-reactive autoantibodies against peripheral nerve components, particularly gangliosides. These autoantibodies activate complement cascades, leading to formation of membrane attack complexes (C5b-9) that disrupt nodes of Ranvier and induce either demyelination or direct axonal injury. Concurrent T-cell infiltration and pro-inflammatory cytokine release exacerbate nerve damage, while genetic factors influence disease susceptibility and severity.
Fig.2 Immunopathological mechanisms involved in Guillain-Barré syndrome (GBS). (Shastri A, et al., 2023)
Therapeutic Development for Guillain-Barré Syndrome (GBS)
| Drug Names | Mechanism of Action | Targets | NCT Number | Research Phase |
| Imlifidase | IgG-degrading enzyme (cleaves IgG antibodies) | IgG antibodies | NCT03943589 | Phase II |
| Efgartigimod | FcRn antagonist (reduces IgG autoantibodies) | Neonatal Fc receptor (FcRn) | NCT06885762 | Phase III |
| ANX005 | Anti-C1q monoclonal antibody (inhibits complement) | Complement C1q | NCT04035135 | Phase Ib |
| Crovalimab | Anti-C5 monoclonal antibody (complement inhibitor) | Complement C5 | NCT05494619 | Phase III |
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
Recognizing the complexity of diagnosing and treating Guillain-Barré syndrome (GBS), Protheragen is committed to building a team of experts to provide cutting-edge diagnostic and therapeutic development solutions. Our commitment lies in providing a variety of customized therapy development services to meet the diverse research needs of our customers. We also excel in generating precise disease models that are carefully engineered to replicate the unique features of GBS.
Therapeutic Development Services
By Mechanism of Action
Disease Model Development Services
In Vitro Model Development
- Experimental Autoimmune Neuritis (EAN) Model
- Campylobacter jejuni Induced Model
- Rabbit Anti-GalC Model
- FcγRIIB-KO Mouse Model
- L31 Mouse Model
- Other Models
At Protheragen, we are committed to supporting the development of innovative therapeutics through comprehensive preclinical research services, including pharmacodynamics (PD), pharmacokinetic (PK) and toxicology studies. Our customized approach addresses the unique challenges of your studies and helps you optimize your drug candidates for commercial success. If you are interested in our services, please feel free to contact us for more details and quotation information of related services.
References
- Valaparla V L, Rane S P, Patel C, et al. Guillain–Barre syndrome and link with COVID-19 infection and vaccination: a review of literature[J]. Frontiers in Neurology, 2024, 15: 1396642.
- Shastri A, Al Aiyan A, Kishore U, et al. Immune-mediated neuropathies: pathophysiology and management[J]. International journal of molecular sciences, 2023, 24(8): 7288.