Ulcerative Colitis
Ulcerative colitis (UC), an enduring inflammatory bowel disease (IBD), manifests as inflammation and the formation of ulcers in the colon and rectum. Our esteemed organization excels in offering a wide range of tailored services for the development of drugs and therapies specifically designed to address the challenges posed by ulcerative colitis.
Overview of Ulcerative Colitis
Ulcerative colitis, a type of inflammatory bowel disease, primarily affects the colon and rectum. It is characterized by persistent inflammation and ulceration of the intestinal mucosa. The development of ulcerative colitis involves intricate interactions among genetic predisposition, environmental factors, and immune system dysregulation. The disruption of immune response regulation results in an exaggerated inflammatory reaction within the colon and rectum. Key contributors to the pathogenesis include pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), as well as immune cells such as T cells and macrophages.
Fig.1 Mechanism of action of drugs for ulcerative colitis. (Segal J. P., et al., 2021)
Drug Discovery and Development for Ulcerative Colitis
The therapeutics of ulcerative colitis revolves around drug therapies that aim to induce and maintain remission, reduce inflammation, and alleviate symptoms. Aminosalicylates, such as 5-aminosalicylic acid (5-ASA), are often the first-line therapy for mild to moderate UC. They act locally in the colon and have anti-inflammatory properties. In cases of moderate to severe UC, corticosteroids like prednisolone or budesonide may be prescribed for a short duration to induce remission. Thiopurines (azathioprine, mercaptopurine) and methotrexate are examples of immunomodulators used for maintaining remission and reducing the need for corticosteroids. Moreover, anti-TNF agents, such as infliximab and golimumab, target specific inflammatory pathways to reduce inflammation and induce remission. Other biologics like vedolizumab, ustekinumab, and tofacitinib offer additional options for cases with refractory disease.
Our therapy development services encompass various stages, from target identification and validation to preclinical development. We employ cutting-edge technologies and methodologies to accelerate the drug discovery process and optimize therapeutic efficacy. If you would like to learn more about our therapeutic development solutions, please click on the links below.
Our Services
With our advanced technology platforms, we ensure that our diagnostics development services are at the forefront of innovation, including biomarker development and diagnostic kit development. In addition to diagnostics, our company specializes in the development of novel therapies for ulcerative colitis. We have expertise in the development and characterization of ulcerative colitis animal models. These models enable us to study disease mechanisms, assess drug efficacy, and explore novel therapeutic targets.
Chemically-Induced Colitis Models
By inducing colonic inflammation through the administration of chemical agents, such as dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS), we can mimic the inflammatory processes seen in UC cases.
IL-2 Knockout (KO) Models
Our IL-2 KO mouse model, which lacks the IL-2 gene, allows researchers to study the consequences of IL-2 deficiency on colonic inflammation. These mice develop colon-restricted inflammation resembling human UC, including crypt abscesses, ulcerations, and loss of goblet cells.
Gαi2 Knockout (KO) Models
The Gαi2 subunit plays a crucial role in regulating immune responses. Gαi2 KO mouse models exhibit clinical and histopathological features resembling human UC, including colonic thickening, lymphocyte and neutrophilic infiltrations, and crypt and goblet cell loss.
WASP Knockout (KO) Models
WASP is a critical regulator of actin cytoskeleton remodeling, which plays a crucial role in immune cell function. Mutations in the WASP gene lead to Wiskott-Aldrich syndrome (WAS), an immunodeficiency disorder associated with increased susceptibility to autoimmune diseases, including UC.
Mdr1a Knockout (KO) Models
Our company's Mdr1a KO model focuses on the role of the multidrug resistance protein 1 (MDR1) in UC pathogenesis. MDR1, encoded by the Mdr1a gene, is an efflux transporter responsible for the removal of various substances from cells, including drugs and toxins.
IL-7 Tg Models
The IL-7 Tg model, developed by our company, focuses on the role of interleukin-7 (IL-7) in UC pathogenesis. IL-7 is a cytokine involved in T cell development, survival, and homeostasis. Dysregulation of IL-7 signaling has been implicated in the development and progression of UC.
Through the development of cell-based models, utilizing the T84 cell line and intestinal-immunological co-cultures, we provide valuable tools to study UC pathophysiology and investigate potential therapeutic targets.
We offer a kind of ulcerative colitis organoid model enables researchers to recapitulate key aspects of UC pathophysiology, including the abnormal epithelial barrier function, immune cell infiltration, and dysregulated inflammatory responses.
Customized Disease Models
We place great value on flexibility and adaptability in scientific research. Our prestigious organization specializes in delivering customized solutions and developing disease models that are meticulously tailored to meet your specific requirements.
Our preclinical research services include drug screening, pharmacological profiling, and toxicity assessments. Through meticulous experimentation and data analysis, we generate valuable insights into the therapeutic potential of novel compounds. In addition to the aforementioned services and models, we also provide customized solutions and develop disease models that cater specifically to your unique needs. If our services have piqued your interest, please do not hesitate to contact us.
References
- Segal J. P., et al. "Ulcerative colitis: an update." Clinical Medicine 21.2 (2021): 135.
- Kucharzik T., et al. "Ulcerative colitis—diagnostic and therapeutic algorithms." Deutsches Ärzteblatt International 117.33-34 (2020): 564.