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Idera Pharmaceuticals Presents Preclinical Data from its Autoimmune Disease Program at the 74th Annual Scientific Meeting of the American College of Rheumatology

CAMBRIDGE, Mass.--(BUSINESS WIRE)--Nov 9, 2010 - Idera Pharmaceuticals, Inc. (Nasdaq: IDRA) today announced two presentations of preclinical data from its autoimmune and inflammatory disease program at the 74th 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.

“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.

These presentations are now available on the Company's website,

About IMO-3100

IMO-3100, an antagonist of TLR7 and TLR9, is a lead drug candidate in development to treat autoimmune and inflammatory diseases. Independent research studies suggest that pro-inflammatory cytokines characteristic of autoimmune disease are induced through activation of TLR7 and TLR9. IMO-3100 is designed to block production of multiple pro-inflammatory cytokines induced through TLR7 and TLR9. In contrast, many current autoimmune disease treatments aim to block the activity of individual cytokines. IMO-3100 has demonstrated potent activity in reducing pathologic and immunologic manifestations in preclinical mouse models of diseases such as lupus, rheumatoid arthritis, psoriasis and hyperlipidemia. IMO-3100 is currently being evaluated in a Phase 1 clinical program.

About Idera Pharmaceuticals, Inc.

Idera Pharmaceuticals is developing drug candidates that act by modulating immune responses through specific Toll-like Receptors (TLRs). TLRs, a family of immune system receptors and the immune system's first line of defense, recognize pathogens and initiate an immune response. Idera's DNA and RNA chemistry expertise has generated a pipeline of compounds designed to interact with specific TLRs for a broad range of diseases. Through its internal pipeline and collaborative alliances, Idera has established a portfolio of TLR-targeted therapeutic candidates for infectious diseases, autoimmune and inflammatory diseases, cancer, and respiratory diseases, and for use as vaccine adjuvants.

Idera Forward Looking Statements

This press release contains forward-looking statements concerning Idera Pharmaceuticals, Inc. that involve a number of risks and uncertainties. For this purpose, any statements contained herein that are not statements of historical fact may be deemed to be forward-looking statements. Without limiting the foregoing, the words "believes," "anticipates," "plans," "expects," "estimates," "intends," "should," "could," "will," "may," and similar expressions are intended to identify forward-looking statements. There are a number of important factors that could cause Idera's actual results to differ materially from those indicated by such forward-looking statements; whether results obtained in preclinical studies such as the studies referred to in this release will be indicative of results obtained in future clinical trials; whether products based on Idera's technology will advance into or through the clinical trial process on a timely basis or at all and receive approval from the United States Food and Drug Administration or equivalent foreign regulatory agencies; whether, if the Company's products receive approval, they will be successfully distributed and marketed; whether the Company's collaborations will be successful; whether the patents and patent applications owned or licensed by the Company will protect the Company's technology and prevent others from infringing it; whether Idera's cash resources will be sufficient to fund the Company's operations; and such other important factors as are set forth under the caption "Risk Factors" in Idera's Quarterly Report on Form 10-Q for the three months ended September 30, 2010, which important factors are incorporated herein by reference. Idera disclaims any intention or obligation to update any forward-looking statements.


Contact: Idera Pharmaceuticals, Inc.
Teri Dahlman, 617-679-5519
MacDougall Biomedical Communications
Chris Erdman, 781-235-3060



Posted: November 2010