Idera Pharmaceuticals Present New Data That Show Toll-like Receptor Antagonists Inhibit Inflammasome Activation And Suppress Induction Of Interleukin 1 Beta In Autoimmune Disease Models

Idera Pharmaceuticals, Inc. (NASDAQ: IDRA) today announced new data from preclinical studies showing that selective inhibition of Toll-like Receptors (TLRs) 7, 8, and 9, which play a key role in inflammation and immunity, also resulted in inhibition of inflammasome activation and induction of Interleukin 1 beta (IL-1β), a pro-inflammatory cytokine that has been shown to be involved in Behçet's disease, non-infectious uveitis, cardiovascular disease, and other auto-inflammatory diseases. The data were presented during the 8 th Annual Meeting of the Oligonucleotide Therapeutics Society being held October 28-31, 2012 in Boston.

“We are pleased that in the preclinical studies, in addition to controlling the induction of multiple cytokines such as TNF-α, IL-12, IL-6, and IL-17 and the consequent downstream signaling, our approach to blocking TLR-mediated pathways also led to decreased production of inflammasome components and suppression of IL-1β in disease models,” said Dr. Timothy Sullivan, VP of Development Programs at Idera. “These new data provide further support for our focus on autoimmune diseases, where the inflammasome plays a fundamental role in inflammatory and immune responses. Our clinical development program in autoimmune diseases includes an ongoing Phase 2 study of IMO-3100 in psoriasis, with top-line data expected before the end of 2012, and a planned Phase 1 clinical study of IMO-8400, a candidate initially targeted for the treatment of lupus.”

In a mouse model of IL-23-induced psoriasis, the inflammasome components NLRP3 and AIM2 were up-regulated and IL-1β was increased compared to control animals. Treatment with an antagonist of TLRs 7, 8, and 9 led to suppression of NLRP3, AIM2, and IL-1β in these animals. In mouse models of NZBW/F1 lupus-prone mice and collagen antibody-induced arthritis, NLRP3 was up-regulated and IL-1β was induced compared to control animals. Treatment with an antagonist of TLRs 7, 8, and 9 led to the suppression of NLRP3 and IL-1β in these animals.

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