Idera Pharmaceuticals, Inc. (Nasdaq: IDRA) announced today the presentation of 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 (IL-6) and complement C3 and with induction of interleukin 10 (IL-10). The presentation (#T65), entitled "Treatment with IMO-3100, a novel TLR7 and TLR9 dual antagonist, inhibits disease development in a mouse model of collagen antibody-induced arthritis (CAIA)," is being made at the Annual Meeting of the Federation of Clinical Immunology Societies (FOCIS) held June 23-26, 2011 in Washington, D.C. IMO-3100 is an antagonist of Toll-like Receptor (TLR) 7 and TLR9 and is in clinical development for the treatment of autoimmune diseases.
"Treatment with IMO-3100 showed significant reduction in arthritis symptoms compared to placebo in this study," commented Nicola La Monica, Ph.D., 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-1β, and increased expression of the anti-inflammatory protein IL-10."
"IMO-3100 provides a novel mechanism of action for the treatment of selected autoimmune diseases and has shown encouraging activity in preclinical models of arthritis, lupus, psoriasis and hyperlipidema," said Sudhir Agrawal, D.Phil., Chairman and Chief Executive Officer of Idera. "In Phase 1 studies in healthy subjects, IMO-3100 was well tolerated and suppressed TLR7- and TLR9-mediated induction of cytokines including TNF-α, IFN-α, 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."
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