Bullous Pemphigoid
Bullous pemphigoid (BP) is a prevalent autoimmune subepidermal blistering disorder that accounts for approximately 80% of subepidermal immunobullous cases. As a professional and well-known CRO, our company provides comprehensive services in the diagnostics, therapeutics, animal models, and preclinical research of bullous pemphigoid.
Overview of Bullous Pemphigoid
Bullous pemphigoid is an autoimmune disorder characterized by the presence of autoantibodies targeting proteins located at the dermal-epidermal junction. These autoantibodies mainly recognize two basal keratinocyte hemidesmosomal proteins, BP antigen 230 (BPAG1) and BP antigen 180 (BPAG2 or type XVII collagen). The binding of autoantibodies to their target antigens triggers an inflammatory response, leading to complement activation, mast cell activation, and subsequent release of inflammatory cells that cause damage to the dermal-epidermal junction.
Fig.1 Aging-related mechanisms that induce bullous pemphigoid (BP). (Moro F., et al., 2020)
Drug Discovery and Development for Bullous Pemphigoid
The therapeutics of bullous pemphigoid depend on the severity of the disease and the individual characteristics. In cases of extensive disease, systemic corticosteroids, particularly prednisone, are recommended. Immunosuppressive therapy becomes necessary when corticosteroids fail to control the disease or are contraindicated. Alternative agents such as azathioprine, mycophenolate mofetil, methotrexate, chlorambucil, and cyclophosphamide can be considered. For therapeutic-resistant cases, intravenous immunoglobulin (IVIG), anti-CD20 (rituximab), or omalizumab have shown promising results.
At our company, we strive to contribute to the development of effective therapies for bullous pemphigoid. Below is a showcase of our diverse therapeutic development platform. If you are interested, you can click on the link below to learn more.
Small Molecule Drug
Probiotics Therapy
Therapeutic Antibody
Cell Therapy
Gene Therapy
Therapeutics Development
Our Services
Our company conducts rigorous preclinical studies to evaluate the safety, efficacy, and pharmacokinetics properties of potential therapeutic agents for bullous pemphigoid. Through animal models and in vitro assays, we assess the impact of drug candidates on disease progression, immune response modulation, and adverse effects, providing crucial data for further development.
Rabbit Cornea Models
One of the major advantages of rabbit cornea model is its transparency, which allows for easy observation of inflammatory changes. By injecting pathogenic antibodies into the cornea, we can closely monitor the development of blisters, inflammation, and other disease-related manifestations.
Neonatal Mouse Injection Models
Intraperitoneal injection in neonatal mice has proven to be a successful approach in modeling autoimmune diseases, such as pemphigus vulgaris and pemphigus foliaceus. However, the development of a reliable bullous pemphigoid animal model using this method has presented challenges.
By incorporating patient-derived cells, optimizing co-culture systems, and employing advanced genetic manipulation techniques, we strive to provide you with the most relevant and reliable model for your research.
Our company excels in the development and characterization of organoid models for BP therapy research. Whether utilizing patient-derived cells or pluripotent stem cells, our team of experts can generate organoids that faithfully represent the disease phenotype.
In addition to the aforementioned range of services and models, we also specialize in tailoring customized solutions and developing disease models that precisely align with your distinctive requirements. At the same time, we are committed to advancing the field of bullous pemphigoid diagnostics by providing innovative and reliable services. Should our array of services capture your interest, we warmly encourage you to reach out to us without hesitation.
Reference
- Moro F., et al. "Bullous pemphigoid: trigger and predisposing factors." Biomolecules 10.10 (2020): 1432.