Based on a decade of cutting-edge bench research and the completion of a challenging, yet ultimately successful drug campaign, Creative Biolabs concentrates on promoting the understanding of drug development breakthroughs in treating autoimmune diseases. We are dedicated to providing integrated solutions for Vogt-Koyanagi-Harada (VKH) syndrome drug discovery in unprecedented ways. In our company, our scientists specializing in VKN syndrome studies will work with you to develop the most appropriate strategy that will offer reproducible data for your research.
VKH syndrome is a rare autoimmune disease that affects most tissues and organs in the human body, such as the eyes, skin, brain, and ears. The common symptoms of VKN diseases include headache, nausea, alopecia, white hair, as well as loss of vision. In general, the early stages of VKN disease symptoms are headache and dizziness. After a few weeks, inflammation in the eyes can lead to blindness or hearing loss and eventually changes in eye and skin color. Small yellow nodules appear in parts of the retina and smooth white patches appear on the skin. Pilot studies have demonstrated that abnormal immune responses and genetic factors may be the main causes of VKN diseases, but the exact cause is still not known. Also, VKH disease is more prevalent in 30 to 40-year-old northern Europe, Spain, and American Indians.
VKH disease, a type of T-cell-mediated autoimmune inflammatory disease, is characterized as a bilateral non-necrotizing granulomatous panuveitis. It affects many body systems involving the eyes, ears, skin, and nervous system. Currently, a wide variety of treatment strategies, including steroid drugs and antibody drugs, have been generated for improving the clinical outcomes of VKN syndrome therapy. Among them, systemic corticosteroids and immunosuppressive drugs have been regarded as the standard method for the management of VKN diseases. The data have indicated that the combined therapy of immunosuppressive drugs with steroids is effective in preventing inflammatory responses and improving the patient's vision. However, no suitable drug has been developed for addressing a range of permanent problems associated with VKN disease, such as hearing defects, hair loss, and visual impairments.
Fig.1 Immunogenetic mechanisms contributing to VKH disease pathogenesis.1
By continuing to grow in response to the requirements of our clients, Creative Biolabs has established a comprehensive VKN syndrome drug development platform and offers a series of antibody development services. For instance, we have generated several antibodies against the tyrosinase-related protein (TRP), potential antigens specific to VKN disease, and tested the efficacy of these antibodies in preclinical. The results have shown that newly discovered anti-TRP1 and TRP2 antibodies provide a unique and completely novel approach for the inhibition of VKN disease-causing pathways simultaneously.
Besides, Creative Biolabs is also in a unique position to pursue the discovery of a new class of cell therapies for the treatment of VKN diseases. In the past few years, chimeric antigen receptor (CAR) T cells have become the most popular option for treating various liquid tumors. By using the same idea of modifying T cells to target diseased cells, scientists at Creative Biolabs have established new CAR T cells to delete harmful T cells that are essential for VKN disease development and function.
Creative Biolabs is recognized as the world leader for providing the most diverse portfolio of drug development services for VKN syndrome research. We are very proud of providing high-quality, omnidirectional VKN syndrome drug development services to remove the difficulties of your projects. For more information, please feel free to contact us or send us an inquiry.
Reference
For Research Use Only | Not For Clinical Use
Creative Biolabs is a world-leading CRO that is skilled in developing novel therapies,
especially in antibody and cell therapy for autoimmune diseases.
Copyright © 2024 Creative Biolabs. All Rights Reserved.