MOG Antibody Disease (MOGAD)
MOG antibody disease (MOGAD) stands as an autoimmune-rooted condition that leads to demyelination within the central nervous system. At Protheragen, our dedicated researchers and scientists bring a wealth of specialized experience in the pathology and treatment of MOGAD. Fueled by a resolute commitment to the patient community, we are focused on creating next-generation therapies that directly target the disease's mechanisms, striving to fill the current void in effective treatments.
Introduction to MOG Antibody Disease (MOGAD)
MOG antibody disease, or MOGAD, is a separate type of neuroinflammatory disorder where the body produces autoantibodies against myelin oligodendrocyte glycoprotein MOG, resulting in damage to the myelin sheath within the central nervous system CNS. In practice, MOGAD commonly shows up as optic neuritis, transverse myelitis, or symptoms resembling acute disseminated encephalomyelitis ADEM, especially in pediatric cases. Current estimates put the yearly worldwide incidence of MOGAD at 1.6 to 4.8 cases for every million individuals.
Fig.1 MOG antibody disease (MOGAD) pathogenesis. (Gklinos P, Dobson R., 2024)
Pathogenesis of MOG Antibody Disease (MOGAD)
MOG antibody disease (MOGAD) stems mainly from IgG1 antibodies that target myelin oligodendrocyte glycoprotein (MOG). These antibodies latch onto MOG found on oligodendrocytes and myelin sheaths, setting off complement cascades, microglial uptake through Fc receptors, and inflammatory demyelination throughout the central nervous system. In contrast to multiple sclerosis, the axons here are preserved to a greater degree. Additional T-cell activity and genetic risk factors, such as the HLA-DRB1*15 haplotype, help shape the disease course.
Fig.2 Management of MOG antibody disease (MOGAD). (Wynford-Thomas R, et al., 2019)
Therapeutic Development for MOG Antibody Disease (MOGAD)
| Drug Names | Mechanism of Action | Targets | NCT Number | Research Phase |
| Rozanolixizumab | Humanized monoclonal antibody that inhibits the neonatal Fc receptor (FcRn), reducing circulating IgG levels including pathogenic MOG-IgG | Neonatal Fc Receptor (FcRn) | NCT05063162 | Phase III |
| Satralizumab | IL-6 receptor inhibitor that reduces inflammation and B-cell activation | Interleukin-6 Receptor (IL-6R) | NCT05271409 | Phase III |
| Tocilizumab | Monoclonal antibody targeting IL-6 receptor; modulates immune responses and reduces inflammation | Interleukin-6 Receptor (IL-6R) | NCT06452537 | Early research |
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
To enhance the management of MOG antibody disease (MOGAD), Protheragen provides integrated services spanning diagnostic and therapeutic development. Centered on the range of molecular pathways that underpin MOGAD, we commit to formulating novel, targeted treatments that meet pressing clinical gaps. Our specialists produce precise disease models that rigorously characterize the safety, effectiveness, and mechanistic dynamics of candidate therapies.
Therapeutic Development Services
By Mechanism of Action
Disease Model Development Services
In Vitro Model Development
- Experimental Autoimmune Encephalomyelitis (EAE) Model: The model is induced by immunizing rodents with a MOG peptide, typically the MOG35-55 peptide, in combination with an adjuvant.
- Other Models
At Protheragen, we are dedicated to supporting the development of innovative therapies through comprehensive preclinical research services. Our expertise spans pharmacodynamics (PD), pharmacokinetic (PK) and toxicology studies, ensuring a thorough evaluation of your therapeutic candidates. If you are interested in our services, please feel free to contact us for more details and quotation information of related services.
References
- Gklinos P, Dobson R. Myelin oligodendrocyte glycoprotein-antibody associated disease: an updated review of the clinical spectrum, pathogenetic mechanisms and therapeutic management[J]. Antibodies, 2024, 13(2): 43.
- Wynford-Thomas R, Jacob A, Tomassini V. Neurological update: MOG antibody disease[J]. Journal of neurology, 2019, 266(5): 1280-1286.