Preclinical data from Idera's autoimmune and inflammatory disease program presented at 74th ACR

Idera Pharmaceuticals, Inc. (Nasdaq: IDRA) today announced two presentations of preclinical data from its autoimmune and inflammatory disease program at the 74^th Annual Scientific Meeting of the American College of Rheumatology (ACR) in Atlanta, Georgia. One presentation is entitled "IMO-3100, a Toll-like Receptor (TLR) Antagonist, Suppresses TLR7- and TLR9-mediated Immune Responses in Non-human Primates" (#856). IMO-3100 is an antagonist of TLR7 and TLR9 and Idera's lead drug candidate being developed for the treatment of autoimmune and inflammatory diseases. The other presentation is entitled "Peripheral Blood Mononuclear Cells and Plasmacytoid Dendritic Cells from Healthy Human Females Exhibit Altered TLR7-Mediated Immune Responses Compared to Males" (#862). Both presentations are begin given by Idera scientists.

“Peripheral Blood Mononuclear Cells and Plasmacytoid Dendritic Cells from Healthy Human Females Exhibit Altered TLR7-Mediated Immune Responses Compared to Males”

"In the study of IMO-3100, once-weekly doses of IMO-3100 in non-human primates led to sustained suppression of TLR7- and TLR9-mediated immune responses over four weeks of treatment, which confirmed the intended mechanism of action of IMO-3100 with multiple dosing," commented Tim Sullivan, Ph.D., Vice President, Development Programs and Alliance Management of Idera Pharmaceuticals. "We recently completed a multiple-dose clinical trial of IMO-3100 in healthy subjects and intend to analyze the data by the end of the year and present the results at a scientific meeting in the first half of 2011."

In one of the preclinical studies presented today, IMO-3100 suppressed immune responses mediated through TLR7 and TLR9, reducing the production of cytokines such as TNF- α, IL-6, IP-10 and IFN-α in cells isolated from blood samples. TLR7- and TLR9-mediated immune responses remained suppressed by weekly IMO-3100 administration throughout the four-week treatment period. The secretion of cytokines began to rebound to pre-dose levels two weeks after the last dose of IMO-3100. Importantly, IMO-3100 did not affect TLR4-mediated responses, confirming its specific activity as an antagonist of TLR7 and TLR9.

The other preclinical study evaluated the differences between female and male healthy human subjects in the TLR-mediated immune responses of isolated blood cells. The data demonstrate that blood cells from healthy females produce higher levels of pro-inflammatory cytokines in response to TLR7 stimulation than do blood cells from healthy male subjects.