Ankylosing Spondylitis
Ankylosing spondylitis (AS) is a chronic inflammatory disorder characterized by its predominant impact on the spine, resulting in pain, stiffness, and limited mobility. At our esteemed organization, we proudly lead the way in pioneering the development of groundbreaking drug and therapy solutions for AS.
Introduction to Ankylosing Spondylitis
Ankylosing spondylitis is a chronic inflammatory condition that primarily affects the axial skeleton, leading to gradual stiffness of the spine and reduced mobility. Inflammation is commonly observed in the sacroiliac joints, spine, and peripheral joints.
While the exact cause of ankylosing spondylitis remains somewhat elusive, genetic factors, particularly the presence of human leukocyte antigen-B27 (HLA-B27), have been identified as significant contributors. Research has demonstrated a strong association between the HLA-B27 gene and ankylosing spondylitis, with approximately 90-95% of patients possessing this genetic marker. The interaction between HLA-B27 and the immune system is believed to trigger abnormal immune responses, resulting in persistent inflammation within the affected joints. Furthermore, alterations in the gut microbiome, the involvement of innate-like lymphoid cells, mechanical stress, and autoimmune processes are considered to be additional factors contributing to the development of ankylosing spondylitis.
Fig.1 Ankylosing spondylitis and its complications. (You H., et al., 2020)
Drug Discovery and Development for Ankylosing Spondylitis
To date, several targets have been identified for the development of therapeutics against AS, including cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-17 (IL-17), and interleukin-23 (IL-23), which play a crucial role in promoting inflammation and bone erosion in AS. Specifically, multiple inhibitors, such as JAK inhibitors, TNF-α inhibitors, and IL-17A inhibitors, have been developed to modulate immune responses and reduce inflammation in AS. Moreover, cell-based therapies hold great promise in the field of regenerative medicine for AS. Mesenchymal stem cells (MSCs) have immunomodulatory properties and the potential to reduce inflammation and promote tissue repair.
As a pioneer company in preclinical drug discovery and development, our company is actively involved in the design and development of multiple therapeutics against AS. To learn more about how we can assist you, please click the links below.
Our Services
At our company, we take pride in providing a wide range of services to accelerate the development process of diagnostics and therapies for ankylosing spondylitis (AS). Currently, our services span a full package of preclinical drug discovery and development services to evaluate the efficacy, safety, and mechanism of action of potential AS therapies. Particularly, we employ a multidisciplinary approach, integrating in vitro assays, animal models, and molecular analysis to ensure robust and reliable results.
Animal Models
Transgenic Model Development
- Murine Progressive Ankylosis (MPA) Model
At our company, we specialize in the development and utilization of the murine progressive ankylosis model for AS research. In this model, mice are genetically modified to have a deficiency in the progressive ankylosis gene (Ank), resulting in spontaneous inflammation and progressive ankylosis of the joints.
- Human Leukocyte Antigen-B27 (HLA-B27) Transgenic Model
The association between AS and the human leukocyte antigen-B27 (HLA-B27) gene variant is well-established. Our company offers cutting-edge HLA-B27 transgenic model development services. Through the precise integration of the HLA-B27 gene into animal models, we replicate the genetic susceptibility observed in AS cases.
Induced Disease Model Development
- Proteoglycan Aggrecan (PG)-Induced Arthritis (PGIA) Model
Our skilled researchers employ meticulous techniques to induce joint inflammation and closely monitor disease progression in these models. In this model, mice are injected with aggrecan, a key component of cartilage, which triggers an immune response and subsequent joint inflammation.
- Versican-Induced Ankylosing Spondylitis Model
Versican, a large chondroitin sulfate proteoglycan, is injected into the joints of mice, leading to immune activation and subsequent joint inflammation. Our company is at the forefront of versican-induced model development for AS research.
In Vitro Models
Cell-Based Model Development
- Primary Cell Cultures
Primary cell cultures derived from patient samples provide a valuable tool for studying the cellular and molecular processes involved in AS. Our company specializes in isolating and culturing various cell types, such as fibroblasts, chondrocytes, and immune cells, from AS patients. These primary cell cultures can be used to investigate the inflammatory response, cytokine production, and cellular interactions associated with the disease.
Organoid Model Development
- Three-Dimensional (3D) HA/β-TCP Scaffold Model
Three-dimensional (3D) scaffold models, such as those utilizing Hydroxyapatite (HA) and beta-tricalcium phosphate (β-TCP), provide a biomimetic environment that closely resembles the native bone microenvironment. At our company, we specialize in the development of 3D HA/β-TCP scaffold models for studying AS. Our team of experts utilizes advanced fabrication techniques to create scaffolds with tailored properties, such as pore size, porosity, and mechanical strength.
Our company is dedicated to providing one-stop preclinical drug discovery and development services for global researchers. In addition to the services and models listed above, we also provide customized services and disease model development services to meet your specific needs. If you are interested in our services, please don't hesitate to contact us.
References
- Wang H., et al. "Drug treatment of ankylosing spondylitis and related complications: an overlook review." Annals of Palliative Medicine 9.4 (2020): 2279285-2272285.
- Perrotta F. M., et al. "Therapeutic targets for ankylosing spondylitis–recent insights and future prospects." Open Access Rheumatology: Research and Reviews (2022): 57-66.