-- Data Published in Journal of Neuroinflammation --
SEATTLE--(BUSINESS WIRE)--Sep. 8, 2016--
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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Source: Omeros Corporation
Cook Williams Communications, Inc.
Jennifer Cook Williams,
360-668-3701
Investor and Media Relations
jennifer@cwcomm.org
