Omeros Announces Positive OMS721 Data in Model of Thrombotic Microangiopathy

 Omeros Announces Positive OMS721 Data in Model of Thrombotic Microangiopathy

-- Support Advancing Initial Clinical Indication of Atypical Hemolytic Uremic
Syndrome --

PR Newswire

SEATTLE, April 2, 2013

SEATTLE, April 2, 2013 /PRNewswire/ -- Omeros Corporation (NASDAQ: OMER) today
announced positive data using OMS721, the lead human monoclonal antibody in
Omeros' mannan-binding lectin-associated serine protease-2 (MASP-2) program,
in a well-established animal model of thrombotic microangiopathy (TMA), a
disorder that occurs in the microcirculation (e.g., venules and capillaries)
of the body's organs, most commonly the kidney and brain. Omeros expects to
submit a European Clinical Trial Application (CTA) this quarter to initiate
clinical trials evaluating OMS721. The lead indication planned for OMS721
clinical trials is atypical hemolytic uremic syndrome (aHUS), a rare but
life-threatening form of TMA.

Omeros controls the worldwide rights to MASP-2 and all therapeutics targeting
MASP-2, a novel pro-inflammatory protein involved in activation of the
complement system – an important component of the immune system. The
complement system plays a role in the inflammatory response to tissue damage
or microbial infection. OMS721 selectively inhibits MASP-2, blocking the
lectin pathway of the complement system while leaving intact the classical
pathway, or the acquired immune response to infection. The Company has
conducted a series of preclinical studies that suggest that MASP-2 inhibition
may have a preventive or therapeutic effect in the treatment of aHUS, HUS, wet
age-related macular degeneration (AMD), paroxysmal nocturnal hemoglobinuria
(PNH), transplant-related complications, ischemia-reperfusion injury, and
other immune-related disorders.

The studies reported today were conducted to support the planned initial
indication for OMS721 – aHUS. In this well-established model, thrombus (blood
clot) formation is induced in microvessels following phototoxic injury of the
vessel wall. Using intravital microscopy, a high-resolution imaging technique
that allows direct visualization of dynamic biological processes in the
microcirculation in live animals, the effects of OMS721 on thrombus formation
were assessed. Specifically, the study evaluated OMS721's ability to delay the
time to onset of thrombus formation and to complete occlusion of the blood
vessel. 100 percent of isotype-antibody control animals versus 71 percent of
OMS721-treated animals showed thrombus formation, with the initiation of
thrombus formation delayed approximately three-fold in the OMS721-treated
group relative to control (a median of 19.0 vs. 6.8 minutes; p=0.0097). Eighty
percent of control-treated animals showed complete occlusion within the
observation period while only 43 percent of those treated with OMS721 occluded
completely. Median time to complete occlusion was 18.0 minutes for control and
38.0 minutes for the OMS721-treated animals (p=0.0036).

"These data are impressive," stated Markus Sperandio, M.D., professor of
cardiovascular physiology and microvascular disorders at the
Walter-Brendel-Center of Experimental Medicine, Munich, Germany, where he
conducted the TMA studies evaluating OMS721. "OMS721 looks like a promising
agent to prevent thrombus formation in the microcirculation. We are planning
additional studies to refine the dosing and timing of administration of OMS721
in models across a wide range of thrombotic disorders."

"We are pleased with these results and are excited to initiate the clinical
program for OMS721," stated Gregory A. Demopulos, M.D., chairman and chief
executive officer of Omeros. "The current treatment options for aHUS are
limited and, when compared to those options, we believe that OMS721 carries
marked advantages that will translate to significant patient benefits. We are
eager to evaluate the drug product in aHUS patients, and we remain on track to
begin Phase 1 clinical trials mid-year."

About Atypical Hemolytic Uremic Syndrome (aHUS)

Atypical Hemolytic Uremic Syndrome (aHUS) is a chronic, very rare,
life-threatening disease. The condition has the hallmarks of a thrombotic
microangiopathy and manifests as hemolytic anemia, thrombocytopenia and renal
impairment. aHUS differs from HUS in that an infectious etiology, i.e., E.
coli or streptococcal infection, is absent. Dysregulation of the complement
system lies at the heart of aHUS pathogenesis, and genetic abnormalities in
complement genes have been identified in greater than 60 percent of all aHUS
patients. It is thought that certain precipitating factors are needed to
trigger aHUS in a genetically predisposed individual. Many of the potential
precipitating factors are linked to endothelial cell activation, stress or
injury; all of these processes activate the lectin pathway. If untreated, most
aHUS patients die or develop end-stage renal disease within one year of
diagnosis. Current treatment options include plasma therapy and eculizumab,
which have limitations in terms of feasibility, safety and patient

About Omeros' MASP-2 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 its abnormal function is associated
with a wide range of autoimmune disorders. MASP-2 is generated by the liver
and is then released into the circulation. Adult humans who are genetically
deficient in one of the proteins that activate MASP-2 do not appear to be
detrimentally affected by the deficiency. Therefore, Omeros believes that it
may be possible to deliver MASP-2 antibodies systemically.

Omeros also believes that it has identified the proteins that activate the
complement system's alternative pathway, which is linked to a wide range of
immune-related disorders. In addition to its lectin pathway inhibitors, the
Company is advancing the development of antibodies that would block activation
of the alternative pathway alone or in combination with the lectin pathway.

About Omeros Corporation

Omeros is a clinical-stage biopharmaceutical company committed to discovering,
developing and commercializing products targeting inflammation, coagulopathies
and disorders of the central nervous system. The Company's most clinically
advanced product candidates, OMS302 for lens replacement surgery and OMS103HP
for arthroscopy, are derived from its proprietary PharmacoSurgery™ platform
designed to improve clinical outcomes of patients undergoing a wide range of
surgical and medical procedures. Omeros has five clinical development
programs. Omeros may also have the near-term capability, through its GPCR
program, to add a large number of new drug targets and their corresponding
compounds to the market. Behind its clinical candidates and GPCR platform,
Omeros is building a diverse pipeline of protein and small-molecule
preclinical programs targeting inflammation, coagulopathies and central
nervous system disorders.

Forward-Looking Statements

This press release contains forward-looking statements as defined within the
Private Securities Litigation Reform Act of 1995, which are subject to the
"safe harbor" created by those sections. These statements include, but are not
limited to, Omeros' expectations regarding when it will submit a CTA for
OMS721 and begin clinical trials; the diseases that may be treated by OMS721;
the potential competitive advantages of OMS721; and that Omeros may have
capability, through its GPCR program, to add a large number of new drug
targets and their corresponding compounds to the market. 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,
the risks, uncertainties and other factors described under the heading "Risk
Factors" in the Company's Annual Report on Form 10-K filed with the Securities
and Exchange Commission on March 18, 2013. 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 publicly, even if new information becomes
available in the future.

SOURCE Omeros Corporation

Contact: Jennifer Cook Williams, Cook Williams Communications, Inc., Investor
and Media Relations, 360.668.3701,
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