Idera Pharmaceuticals, Inc. announced IMO-3100 mechanism of action data in a preclinical model of arthritis.
In this study, the improvements in disease-related parameters resulting from IMO-3100 treatment were associated with suppression of interleukin 6 and complement C3 and with induction of interleukin 10.
“Treatment with IMO-3100 showed significant reduction in arthritis symptoms compared to placebo in this study,” comments Nicola La Monica, PhD, vice president of biology, Idera Pharmaceuticals.
“Furthermore, in agreement with the intended mechanism of action, the therapeutic effect exerted by IMO-3100 was associated with decreased expression of the inflammatory proteins IL-6 and IL-1?, and increased expression of the anti-inflammatory protein IL-10.”
“In Phase 1 studies in healthy subjects, IMO-3100 was well tolerated and suppressed TLR7- and TLR9-mediated induction of cytokines including TNF-?, IFN-?, IP-10 and IL-6, consistent with the intended mechanism of action. We plan to initiate a Phase 2 clinical trial of IMO-3100 in a selected autoimmune indication by the end of this year,” says Sudhir Agrawal, D.Phil., chairman and chief executive officer of Idera.
IMO-3100 was evaluated in a preclinical model in which arthritis was induced by injection of collagen antibodies into BALB/c mice. Treatment with IMO-3100 led to dose-dependent suppression of disease development as measured by standard arthritis scoring criteria and associated histopathology. IMO-3100 treatment was associated with induction of IL-10, and increased serum levels of IL-10 were correlated with improvement in clinical scores. IMO-3100 suppressed serum levels of complement C3 and tissue deposition of complement C3 and C5a, immune system proteins that play a role in the development of inflammation. Treatment with IMO-3100 was associated with reduced messenger RNA expression of IL-1? and IL-6 compared to placebo treatment.
Release Date: June 23, 2011
Source: Idera Pharmaceuticals
Filed Under: Drug Discovery