Functionally blocking anti-human junctional adhesion molecule-like (JAML) antibodies for the treatment of inflammatory diseases, such as inflammatory bowel disease, rheumatoid arthritis, and skin or eye inflammatory diseases.
Binds with higher affinity and specificity than currently available JAM antibodies based on comparative analyses.
Approximately 1.4 million individuals in the US and 2.2 million individuals in Europe have inflammatory bowel disease, which includes both Crohn?s disease and ulcerative colitis. There is currently no cure for inflammatory bowel disease and existing therapies must be taken for the remainder of the patient?s life. Examples of available therapeutics include corticosteroids, immunosuppressants, and monoclonal antibodies. Unfortunately, about 50 percent of patients do not benefit from these treatments, indicating a considerable unmet need for new, more effective therapies.
Junctional adhesion molecules (JAMs) are a family of glycoproteins important in the control of vascular permeability and leukocyte transmigration across endothelial-cell surfaces. JAMs play a vital role in epithelial inflammation by regulating leukocyte transmigration and barrier function. Binding of JAML to its ligand Coxsackie and adenovirus receptor (CAR) provides T-cell co-stimulation leading to cellular proliferation and cytokine and growth factor production in the skin. Several monoclonal Abs have been produced that specifically bind JAML but not other JAMs. However, no antibodies have been produced that potently inhibit JAML-CAR binding. According to comparative analyses, these JAML antibodies bind with much higher affinity and specificity than currently available JAM antibodies and inhibit JAM-L mediated effects on CAR function.
- Antibody binds JAM with great affinity and completely inhibits its function in vitro.
- In vivo studies are currently underway.
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