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Idera Pharmaceuticals Present New Data That Show Toll-like Receptor Antagonists Inhibit Inflammasome Activation and Suppress

  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

Top-line data from Phase 2 study of IMO-3100 in psoriasis anticipated by year

Business Wire

CAMBRIDGE, Mass. -- October 30, 2012

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.

About the Inflammasome and Interleukin 1 beta

Activation of the inflammasome, an intracellular complex that regulates the
release of proinflammatory cytokines such as IL-1β in response to exogenous
pathogens and endogenous danger signals, is influenced by specific TLR
signaling. Inflammasome is a multi-protein complex, and its components include
NLRP3 and AIM2 for recognition of cellular nucleic acids. Evidence from
studies involving human genetics, human ex vivo mononuclear cell responses,
and in vivo and in vitro murine models confirms the importance of the
inflammasome and interleukin-1β in the pathogenesis of several inflammatory

Since the discovery and cloning of IL-1β, this critical proinflammatory
mediator implicated in many diseases has been a focus of the pharmaceutical
industry. The first successful biologic in this class was a recombinant form
of the IL-1 receptor antagonist (RA), a natural inhibitor of IL-1β-mediated
inflammation. At least three additional IL-1-targeted biologics have been
developed, including a recombinant protein with high affinity for IL-1β and
two humanized monoclonal antibodies. [Curr Allergy Asthma Rep. 2010 July;
10(4): 229–235.]

About TLRs and Idera's Pipeline

Toll-like Receptors (TLRs) play a key role in inflammation and immunity. Of
the 10 human TLRs identified to date, Idera is developing compounds targeted
to TLRs 3, 7, 8, and 9, which are expressed in different cells and serve
unique functions. Using its chemistry-based approach, Idera has created novel
drug candidates that modulate immune responses through either activation or
inhibition of specific TLRs. Inhibition of specific TLRs may be useful in
treating autoimmune disorders, such as systemic lupus erythematosus (SLE),
psoriasis, and rheumatoid arthritis, by blocking the induction of multiple
cytokines and signaling pathways. Idera's lead clinical candidates for
application in autoimmune diseases are IMO-3100, an antagonist of TLR7 and
TLR9, and IMO-8400, an antagonist of TLRs 7, 8, and 9.

A characteristic of autoimmune diseases such as SLE and psoriasis is the
production of immune complexes with self-nucleic acids. These abnormal immune
complexes activate TLRs 7, 8, and 9 and induce multiple cytokines that cause
further damage to the body's own tissues and organs, thereby releasing more
self-nucleic acids. Thus, a pathologic amplification cycle is established,
promoting disease maintenance and progression. In preclinical models of
several autoimmune diseases, IMO-3100 and IMO-8400 inhibited TLR-mediated
immune responses, broke the cycle of disease maintenance and progression
through decreases in Th1, Th17 and inflammasome pathways, and led to
improvements in multiple measures of disease.

About Idera Pharmaceuticals, Inc.

Idera Pharmaceuticals applies its proprietary Toll-like receptor (TLR) drug
discovery platform which has created immunomodulatory drug candidates and has
a clinical development program in autoimmune diseases. Additionally, Idera has
a collaboration with Merck & Co. for the use of TLR-targeted candidates as
vaccine adjuvants. The Company is also advancing its gene-silencing
oligonucleotide (GSO) technology for the purpose of inhibiting the expression
of disease-promoting genes. For more information, visit

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,
including whether Idera’s cash resources will be sufficient to fund the
Company’s continuing operations and the further development of the Company’s
autoimmune disease program; whether results obtained in preclinical studies
and early clinical trials, such as the results from the preclinical 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 will be able to license any of its TLR target candidates on a
timely basis or at all; whether the Company's collaboration with Merck & Co,
Inc., 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; 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 quarter ended June 30, 2012 which important factors are incorporated
herein by reference. Idera disclaims any intention or obligation to update any
forward-looking statements.


Idera Pharmaceuticals, Inc.
Lou Arcudi, 617-679-5517
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