Vogt-Koyanagi-Harada (VKH) Disease
The key therapeutic challenge in Vogt-Koyanagi-Harada (VKH) disease lies in achieving long-term immune control without steroid dependence while preventing irreversible ocular and cutaneous complications in this chronic, relapsing autoimmune disorder. With our deep expertise in VKH therapy development, Protheragen is well positioned to provide tailored solutions and comprehensive support to facilitate your journey from VKH therapy research to commercialization.
Introduction to Vogt-Koyanagi-Harada (VKH) Disease
Vogt-Koyanagi-Harada (VKH) disease is a rare, multisystem autoimmune disorder characterized by bilateral granulomatous panuveitis with extraocular manifestations affecting melanocyte-rich tissues, including the skin, meninges, and inner ear. First described as a distinct clinical entity in the early 20th century, VKH primarily affects pigmented populations (Asian, Hispanic, Native American) with a female predominance (2:1 ratio).
Fig.1 Molecular mimicry, remnant epitopes and infections in VKH disease, as an example of autoimmunity. (Abu El-Asrar A M, et al., 2021)
Pathogenesis of Vogt-Koyanagi-Harada (VKH) Disease
Vogt-Koyanagi-Harada (VKH) disease is primarily driven by autoimmune targeting of melanocytes, where genetically susceptible individuals (HLA-DRB1*04:05/DQ4 carriers) develop T-cell-mediated responses against tyrosinase peptides, leading to cross-reactive attack on ocular, cutaneous, and auditory melanin-containing tissues. This process involves Th1/Th17 cytokine dominance (IFN-γ, IL-17) and blood-ocular barrier disruption, with potential triggers including viral infections (e.g., EBV) in predisposed hosts.
Therapeutic Development for Vogt-Koyanagi-Harada (VKH) Disease
| Drug Names | Mechanism of Action | Targets | Research Phase |
| Cyclosporine | Calcineurin inhibitor that blocks T-cell activation by inhibiting NFAT (nuclear factor of activated T-cells) signaling | Calcineurin phosphatase, NFAT pathway | Approved |
| Tacrolimus | Potent calcineurin inhibitor that suppresses IL-2 production and T-cell proliferation | FKBP12-calcineurin complex | Approved |
| Bevacizumab | Monoclonal antibody that binds VEGF-A, reducing vascular permeability and angiogenesis | Vascular endothelial growth factor A (VEGF-A) | Early clinical stage |
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
As a preclinical research service provider for Vogt-Koyanagi-Harada (VKH) disease, Protheragen provides end-to-end diagnostic and therapeutic development solutions. We excel in building physiologically relevant models, including in vitro models, animal models, and specialized blood-brain barrier (BBB) models, to enable comprehensive biomarker discovery, target validation, and CNS drug efficacy optimization.
Therapeutic Development Services
By Mechanism of Action
Disease Model Development Services
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At Protheragen, we offer comprehensive pharmacodynamic (PD), pharmacokinetic (PK), and toxicology research services to support the development and regulatory approval of potential therapies for Vogt-Koyanagi-Harada (VKH) disease. If you are interested in our services, please feel free to contact us for more details and quotation information of related services.
Reference
- Abu El-Asrar A M, Van Damme J, Struyf S, et al. New perspectives on the immunopathogenesis and treatment of uveitis associated with Vogt-Koyanagi-Harada disease[J]. Frontiers in Medicine, 2021, 8: 705796.