-- Phase 3 Program Slated for This Year --
Omeros Corporation (NASDAQ: OMER) today announced additional
positive data from the company’s Phase 2 clinical trial of OMS721
for the treatment of serious kidney disorders, which frequently
lead to end-stage renal disease and dialysis. OMS721 is Omeros’
lead human monoclonal antibody targeting mannan-binding
lectin-associated serine protease-2 (MASP-2), the effector enzyme
of the complement system’s lectin pathway. The clinical trial data
include results from additional study patients treated with OMS721
as well as longer-term follow-up on earlier enrolled patients. The
new data corroborate and expand on trial results reported in the
fourth quarter of 2016. Based on the uniformly positive data in the
fully enrolled cohort of OMS721-treated patients with
immunoglobulin A nephropathy (IgAN), Omeros recently met with the
FDA to discuss the Phase 3 development program.
“The clinical responses in my IgA nephropathy patients treated
with OMS721 are truly impressive,” stated Geoffrey Block, M.D.,
Director of Clinical Research at Denver Nephrology. “These are
patients with significant renal impairment who had not responded to
steroid therapy. Each OMS721-treated patient substantially improved
while markedly reducing or stopping steroid use. Equally impressive
is that, after OMS721 treatment was completed, a legacy effect of
continued improvement was observed in each patient. I look forward
to participating in the Phase 3 clinical trial and to working with
Omeros to make this important drug broadly available to
patients.”
The Phase 2 open-label trial is evaluating OMS721 across four
different types of complement-associated kidney diseases: IgAN,
membranous nephropathy, lupus nephritis, and complement component 3
(C3) glomerulopathy. To meet enrollment criteria, patients must
have high levels of urinary protein (a marker used by nephrologists
to assess disease activity) despite well-controlled blood pressure
with stable dosing of renin-angiotensin system inhibitors and
ongoing treatment with a corticosteroid, thereby ensuring that
study patients are unlikely to improve spontaneously. Patients are
treated with OMS721 for a total of 12 weeks: four weeks maintaining
their entry corticosteroid dose; four weeks of corticosteroid
tapering, if tolerated; and four weeks of resultant corticosteroid
dose maintenance. Patients are then followed post-treatment for six
weeks.
The trial assesses the effect of OMS721 on urine protein
measures that are predictive of kidney failure, namely urine
albumin/creatinine ratio (uACR) and total 24-hour urine protein
excretion, and on the ability to reduce steroid dosing. Data were
analyzed for the pre-specified IgAN cohort of four patients (three
have completed treatment in the study and the fourth is finishing
treatment).
Treatment effects across all IgAN patients were highly
consistent, the magnitude of which are associated with improved
renal survival. Notably, uACR values continued to improve after
dosing was completed. In the three patients who completed
treatment, the mean baseline uACR was 1,400 mg/g and reached 671
mg/g at the end of treatment (52 percent decrease;
p = 0.02), continuing to decrease to 380 mg/g by the end
of the follow-up period. Measures of 24-hour urine protein
excretion tracked uACRs, with a mean reduction from 3,728 mg/day to
1,340 mg/day (64 percent decrease; p = 0.02). To date, after eight
weeks of treatment, the fourth patient’s uACR dropped from 1,628
mg/g to 733 mg/g, a decrease of 55 percent. Partial remission is
defined as greater than 50 percent reduction in 24-hour urine
protein excretion. In the patients who completed treatment, 24-hour
urine protein levels decreased by approximately 50 to 80 percent.
Concurrently, daily steroid doses for all patients were
substantially reduced or completely eliminated.
“The OMS721 data in IgAN patients demonstrate a strength and
rapidity of clinical response that I have not seen with other
agents in development,” said Jonathan Barratt, Ph.D., F.R.C.P.,
Professor of Renal Medicine in the Department of Infection,
Immunity & Inflammation at University of Leicester and
Honorary Consultant Nephrologist at Leicester General
Hospital. “There currently is no approved therapy for IgA
nephropathy. The mechanism of IgA nephropathy – and proteinuria in
general – has been closely linked to the lectin pathway of
complement, and OMS721 directly targets the pathway’s effector
enzyme MASP-2. This could uniquely position OMS721 not only for the
treatment of IgA nephropathy but for a host of other kidney
disorders as well.”
Encouraging results have also been observed in lupus nephritis.
Four of five patients showed a substantial (mean of 69 percent)
reduction in 24-hour urine protein excretion over the treatment
period. The fifth patient experienced a systemic disease flare and
showed a substantial increase. The majority of lupus responders
were able to taper their steroid doses. Three patients with
membranous nephropathy, a disease with inherent variability, have
completed treatment with mixed results. Additional analyses are
continuing in these patient groups.
Consistent with all other OMS721 clinical trials, no significant
safety concerns have been observed. The most commonly reported
adverse events in this trial are fatigue and anemia.
Omeros met with FDA recently to discuss these data and Phase 3
development. Following review of the data, FDA suggested that
Omeros apply for breakthrough therapy designation in IgAN. The
discussion included accelerated approval and an expedited approach
to full approval based on an endpoint of proteinuria, which could
be faster than accelerated approval. Omeros is preparing its
breakthrough application and a Phase 3 protocol for discussion with
FDA. The Phase 3 trial in IgAN is expected to begin this year.
“We’re pleased with the consistently positive data seen in IgAN
patients, further expanding the strong OMS721 clinical results
beyond those previously reported in aHUS and stem-cell transplant
patients,” stated Gregory A. Demopulos, M.D., chairman and chief
executive officer of Omeros. “We are submitting our breakthrough
therapy application to FDA and look forward to working closely with
U.S. and international regulators as we advance through our Phase 3
clinical programs across multiple indications for OMS721.”
No treatments are approved for IgAN, an orphan disease but the
most common primary glomerular disease globally. With an annual
incidence of approximately 1 per 100,000, it is estimated that 1 in
1,400 persons in the U.S. will develop IgAN in his or her lifetime.
As many as 40 percent of them will develop end-stage renal
disease.
About Omeros’ MASP ProgramsOmeros 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 is the effector enzyme of the lectin
pathway, one of the principal complement activation pathways.
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 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. OMS721 is Omeros’
lead human MASP-2 antibody. Following discussions with both the FDA
and the European Medicines Agency, a Phase 3 program for OMS721 in
atypical hemolytic uremic syndrome (aHUS) is in progress. Also, two
Phase 2 trials are ongoing. One is evaluating OMS721 in
glomerulonephropathies, which has generated positive data in
patients with immunoglobulin A (IgA) nephropathy and with lupus
nephritis; the other has reported positive data both in patients
with hematopoietic stem cell transplant-associated thrombotic
microangiopathy (TMA) and in those with aHUS. In addition to
potential intravenous administration, Omeros plans to commercialize
OMS721 for one or more therapeutic indications as a subcutaneous
injection and is also developing small-molecule inhibitors of
MASP-2. Based on requests from treating physicians, Omeros has
established a compassionate-use program for OMS721, which is active
in both the U.S. and Europe. The FDA has granted OMS721 both orphan
drug status for the prevention (inhibition) of complement-mediated
TMAs and fast track designation for the treatment of patients with
aHUS.
Omeros also has identified MASP-3 as the critical activator of
the human 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 its development
of antibodies and small-molecule inhibitors against MASP-3 to block
activation of the alternative pathway.
About Omeros CorporationOmeros 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. OMIDRIA is
the first and only FDA-approved drug (1) 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 and (2) that contains an NSAID
for intraocular use. 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-associated thrombotic microangiopathies;
complement-mediated glomerulonephropathies; Huntington’s disease
and cognitive impairment; and addictive and compulsive disorders.
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 StatementsThis 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 and commercial
operations, 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 Annual Report on Form 10-K filed with the Securities and
Exchange Commission on March 16, 2017. 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/20170330005487/en/
Cook Williams Communications, Inc.Jennifer Cook WilliamsInvestor
and Media Relations360.668.3701jennifer@cwcomm.org
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