Researchers have shown that a novel antibody has greater activity and potentially fewer side effects than existing biological therapies for conditions such as rheumatoid arthritis (RA), psoriasis, and inflammatory bowel disease (IBD).
The antibody, called Ab-IPL-IL-17, targets a specific section of signalling proteins IL-17A and IL-17F which play a central role in sustaining inflammation during onset and progression of autoimmune diseases.
Research published in the Annals of Rheumatic Diseases identifies the sequence, and reports the results of animal, cell and tissue studies that demonstrate the effectiveness of Ab-IPL-IL-17, and its potential clinical benefit for people with RA and IBD.
The paper was authored by Dr Asif Iqbal from the University of Birmingham and Professor Francesco Maione, Head of ImmunoPharma Lab from the University of Naples Federico II.
In cell studies, Ab-IPL-IL-17 showed potent activity, significantly decreasing the production of cyto-chemokines and reducing white blood cell migration in tissues primed for inflammation.
Mouse studies evaluating the activity of Ab-IPL-IL-17 against existing anti-IL-17 therapies (secukinumab, ixekizumab and bimekizumab) showed Ab-IPL-IL-17 does not trigger unwanted immune responses, reduce the numbers of platelets, or increase the numbers of lymphocytes (white blood cells) in the blood.
Further studies in mouse models of arthritis showed that therapeutic administration of Ab-IPL-IL-17 is as effective at halting disease progression and triggering resolution as the gold-standard current treatment for RA, infliximab.
Finally, the researchers conducted proof-of-concept studies that tested the response of tissues donated by patients with RA and IBD to Ab-IPL-IL-17. In RA, the results strongly suggested that Ab-IPL-IL-17 specifically inhibits the pro-inflammatory actions of chronically inflamed fibroblasts within the rheumatoid joint.
In IBD, Ab-IPL-IL-17 was able to deplete plasma IL-17A in samples obtained from treatment naïve IBD patients, indicating its potential to alleviate pathological pro-inflammatory changes in this disease.
Edited by Diana Spencer, Senior Digital Content Editor, Drug Discovery World