-- Data Published in Journal of
Neuroinflammation --
Omeros Corporation (NASDAQ: OMER) today announced results from
its OMS721 complement program. OMS721 is Omeros’ lead antibody
targeting mannan-binding lectin-associated serine protease-2
(MASP-2). In well-established animal models of ischemic brain
injury or stroke, MASP-2 deficiency or inhibition significantly
limited brain infarct size and protected against functional loss.
The results of the studies were recently published in the Journal
of Neuroinflammation (Orsini et al., Mannan binding
lectin-associated serine protease-2 (MASP-2) critically contributes
to post-ischemic brain injury independent of MASP-1, J.
Neuroinflammation 2016, 13:213) and can be accessed online
at http://link.springer.com/article/10.1186/s12974-016-0684-6.
The studies were conducted collaboratively in the laboratories
of Prof. Wilhelm Schwaeble at the University of Leicester and of
Dr. Maria-Grazia De Simoni, head of the Laboratory of Inflammation
and Nervous System Diseases, IRCCS-Istituto di Ricerche
Farmacologiche Mario Negri. Focal brain ischemia was induced in
wild-type (WT) mice and in mice deficient for MASP-2 by transient
middle cerebral artery occlusion (tMCAO). Forty-eight hours after
ischemia, histopathologic damage to brain tissue and functional
neurological deficits were assessed. All surgical procedures and
assessments were performed by investigators blinded to the
experimental conditions. MASP-2-deficient mice, compared to WT
mice, had significantly reduced infarct volumes (19 percent
reduction, p < 0.05) and significantly lower neurological
deficits (44 percent [p < 0.05] and 39 percent
[p < 0.01] reductions for general and focal functional
deficits, respectively). Consistent results were seen with a
derivative of Omeros’ lead human MASP-2 antibody OMS721 modified
for improved activity in mice and administered in three doses, two
prior to and the third following ischemia. Compared to an isotype
control antibody, the OMS721 derivative decreased infarct volume by
20 percent (p < 0.05) and reduced general (46 percent, p <
0.01) and focal (45 percent, p < 0.01) neurological deficits. In
an additional model of stroke in which brain ischemia is induced by
three-vessel occlusion, MASP-2-deficient mice were again protected
against ischemic brain damage as evidenced by a 31 percent
reduction (p < 0.01) in infarct volume. Immunohistochemical and
morphologic analyses further demonstrated the protective effects of
MASP-2 inhibition on brain tissue during stroke. Additional studies
are planned to define further the therapeutic window for OMS721 in
stroke.
“The data clearly identify MASP-2, the effector enzyme of the
lectin pathway, as a primary driver in ischemic brain tissue
injury,” said Prof. Dr. Eberhard Weihe, director of the Institute
of Anatomy and Cell Biology and head of the department of molecular
neuroscience at Philipps-University, Marburg. “The strength and
consistency of the data in these studies across infarct size,
functional outcomes and other histopathological assessments suggest
an important role for OMS721, a highly selective MASP-2 inhibitor,
in protecting the brain, heart, kidney and other organs from the
damage of ischemic injury. Certainly the ability to preserve both
cerebral tissue and associated neurological function would
represent a major advance in the acute management of stroke
patients.”
Omeros currently is conducting a Phase 3 clinical program
evaluating OMS721 in atypical hemolytic uremic syndrome as well as
Phase 2 programs assessing the drug in hematopoietic stem cell
transplant-associated thrombotic microangiopathy, in thrombotic
thrombocytopenic purpura and in IgA nephropathy and other
complement-related renal diseases.
About Omeros’ MASP Program
Omeros controls the worldwide rights to MASP-2 and all
therapeutics targeting MASP-2, a novel pro-inflammatory protein
target involved in activation of the complement system, which is an
important component of the immune system. The complement system
plays a role in the inflammatory response and becomes activated as
a result of tissue damage or microbial infection. MASP-2 appears to
be unique to, and required for the function of, one of the
principal complement activation pathways, known as the lectin
pathway. Importantly, inhibition of MASP-2 does not appear to
interfere with the antibody-dependent classical complement
activation pathway, which is a critical component of the acquired
immune response to infection and is associated with a wide range of
autoimmune disorders. Adults who are genetically deficient in one
of the proteins that activate MASP-2 do not appear to be
detrimentally affected by the deficiency. Omeros has received both
orphan drug status and fast track designation from the U.S. FDA for
its lead human MASP-2 antibody OMS721. Omeros has an ongoing Phase
3 clinical program for OMS721 in atypical hemolytic uremic
syndrome, an ongoing Phase 2 program targeting hematopoietic stem
cell transplant-associated thrombotic microangiopathy as well as
thrombotic thrombocytopenic purpura and another ongoing Phase 2
program targeting complement-related renal diseases. An
investigator-requested compassionate use program for OMS721 is also
underway. OMS721 has demonstrated no safety concerns in human
trials or chronic toxicity studies. In addition to potential
intravenous administration, Omeros plans to commercialize OMS721
initially for one or more therapeutic indications as a subcutaneous
injection. In addition to its antibodies, Omeros is developing
small molecules targeting MASP-2.
Omeros also has identified MASP-3 as the protein essential to
the activation of the alternative pathway of complement (APC). APC
inhibitors are thought to have preventive or therapeutic effects
across a broad range of diseases including hemolytic uremic
syndrome (HUS), atypical HUS, paroxysmal nocturnal hemoglobinuria,
traumatic brain injury, arthritis, wet age-related macular
degeneration, ischemia-reperfusion injury, transplant-related
complications and other immune-related disorders. In its OMS906
program, Omeros is developing both antibody and small molecules to
block MASP-3. Through its growing intellectual property position,
Omeros exclusively controls inhibitors of the protein activator of
the alternative pathway (MASP-3) and, with its OMS721 program,
inhibitors of the effector enzyme of the lectin pathway (MASP-2),
allowing the company to target with unprecedented precision
diseases caused by dysregulation of one or both of these
pathways.
About Omeros Corporation
Omeros is a biopharmaceutical company committed to discovering,
developing and commercializing both small-molecule and protein
therapeutics for large-market as well as orphan indications
targeting inflammation, coagulopathies and disorders of the central
nervous system. Part of its proprietary PharmacoSurgery® platform,
the company’s first drug product, OMIDRIA® (phenylephrine and
ketorolac injection) 1%/0.3%, was broadly launched in the U.S. in
April 2015 for use during cataract surgery or intraocular lens
(IOL) replacement to maintain pupil size by preventing
intraoperative miosis (pupil constriction) and to reduce
postoperative ocular pain. In the European Union, the European
Commission has approved OMIDRIA for use in cataract surgery and
lens replacement procedures to maintain mydriasis (pupil dilation),
prevent miosis (pupil constriction), and to reduce postoperative
eye pain. Omeros has clinical-stage development programs focused
on: complement-related thrombotic microangiopathies;
complement-mediated glomerulopathies; Huntington’s disease and
cognitive impairment; addictive and compulsive disorders; and
preventing problems associated with urologic surgical procedures.
In addition, Omeros has a proprietary G protein-coupled receptor
(GPCR) platform, which is making available an unprecedented number
of new GPCR drug targets and corresponding compounds to the
pharmaceutical industry for drug development, and a platform used
to generate antibodies.
Forward-Looking Statements
This press release contains forward-looking statements within
the meaning of Section 27A of the Securities Act of 1933 and
Section 21E of the Securities Exchange Act of 1934, which are
subject to the “safe harbor” created by those sections for such
statements. All statements other than statements of historical fact
are forward-looking statements, which are often indicated by terms
such as “anticipate,” “believe,” “could,” “estimate,” “expect,”
“goal,” “intend,” “look forward to,” “may,” “plan,” “potential,”
“predict,” “project,” “should,” “will,” “would” and similar
expressions and variations thereof. Forward-looking statements are
based on management’s beliefs and assumptions and on information
available to management only as of the date of this press release.
Omeros’ actual results could differ materially from those
anticipated in these forward-looking statements for many reasons,
including, without limitation, risks associated with product
commercialization, Omeros’ unproven preclinical and clinical
development activities, regulatory oversight, intellectual property
claims, competitive developments, litigation and the risks,
uncertainties and other factors described under the heading “Risk
Factors” in the company’s Quarterly Report on Form 10-Q filed with
the Securities and Exchange Commission on August 9, 2016. Given
these risks, uncertainties and other factors, you should not place
undue reliance on these forward-looking statements, and the company
assumes no obligation to update these forward-looking statements,
even if new information becomes available in the future.
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version on businesswire.com: http://www.businesswire.com/news/home/20160908005593/en/
Cook Williams Communications, Inc.Jennifer Cook Williams,
360-668-3701Investor and Media Relationsjennifer@cwcomm.org
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