West Midlands Academic Health Science Network has supported a new spinout company to develop a breakthrough in the treatment of rheumatoid arthritis.
University of Birmingham Enterprise announced the formation of a new spinout company, Viatem Ltd to coincide with the presentation of new research showing that synthetic PEPITEM (Peptide Inhibitor of Trans-Endothelial Migration) can prevent or delay the onset of rheumatoid arthritis (RA) in animal models of disease, and restore regulation of white blood cell migration in human tissues.
RA is an autoimmune disease that affects over 20 million people worldwide. It results in extensive damage to joints and causes significant disability. Currently there is no curative treatment.
Viatem has been funded via the WMAHSN’s SME Innovation Fund in collaboration with Mercia Fund Management, a leading investment business in UK innovation. The fund aims to help build and support healthcare start-ups across the West Midlands.
Viatem is located in the BioHub Birmingham, the University of Birmingham’s bioincubator. The University of Birmingham is shareholder in the company, which has also received funding from Innovate UK and the University of Birmingham’s Enterprising Birmingham Fund.
PEPITEM is a naturally occurring protein that controls a key chemical pathway involved in the recruitment of immune cells into inflamed tissues.
About PEPITEM and the adiponectin pathway
The adiponectin pathway was discovered by a research group led by Professor Ed Rainger of the Institute of Cardiovascular Sciences at the University of Birmingham and described in their seminal paper in Nature Medicine in 2015.
The pathway modulates the migration of T-cells (white blood cells) from the blood stream into body tissues, and PEPITEM is its key regulator.
PEPITEM is a potential novel therapeutic for T-cell mediated inflammatory diseases:
· In response to adiponectin, B-cells release PEPITEM
· PEPITEM binds to cadherin 15 on EC
· Triggering formation and secretion of S1P via SPSN2
· S1P binds S1PR1 on T-cells inhibiting their migration.