SEATTLE--(BUSINESS WIRE)--Nov. 6, 2017--
Omeros Corporation (NASDAQ: OMER) today announced that extended
follow-up data from patients with immunoglobulin A (IgA) nephropathy
treated with OMS721 were presented on November 4, 2017 at the American
Society of Nephrology (ASN) Meeting in New Orleans. These data describe
up to one-year follow-up of patients treated with OMS721 in the
glomerulonephropathy Phase 2 clinical trial. OMS721 is Omeros’ lead
human monoclonal antibody targeting mannan-binding lectin-associated
serine protease-2 (MASP-2), the effector enzyme of the lectin pathway of
the complement system.
During the Phase 2 clinical trial, which consisted of 12 weeks of
treatment and 6 weeks of follow-up, all patients with IgA nephropathy
demonstrated clinically meaningful improvement in proteinuria. The data
were statistically significant. These data, which are limited to the
duration of the clinical trial, were previously presented at the
54th European Renal Association-European Dialysis and Transplant
Association (ERA-EDTA) Congress in June 2017. The additional data
presented at the ASN meeting over the weekend describe the course of
these Phase 2 patients after the trial and while under usual care for up
to approximately one year after completion of OMS721 treatment.
As previously reported, all four IgA nephropathy patients demonstrated a
substantial reduction in proteinuria during the clinical trial,
including 24-hour urine protein levels and albumin/creatinine ratios
(uACRs). In the extended follow-up after completion of the Phase 2
trial, urine protein/creatinine ratios (uPCR) were measured according to
investigator practice standard. For purposes of post-hoc comparisons of
proteinuria during and after the clinical trial, each post-trial uPCR
value was converted to uACR (Zhao, Clin J Am Soc Nephrol 2016;11:947-55).
Proteinuria reduction was maintained in three of the four patients. In
these three patients, uACRs during extended follow-up remained
decreased. Specifically, those three patients maintained partial
remission relative to baseline during available follow-up (75.8%, 85.9%,
and 76.8% uACR decreases at 12, 11, and 3 months after cessation of
OMS721 dosing, respectively). Following a substantial drop in uACR
during dosing and trial follow-up, the fourth patient’s uACR returned to
approximately 88 percent of baseline at four months after the end of
treatment with OMS721.
Numerical improvement in estimated glomerular filtration rate (eGFR), a
measure of renal function, was observed in 3 of the 4 patients after the
trial. Post-treatment eGFR increases ranged from 7 to 17 mL/min/1.73 m2
relative to screening values. The patient with the most severe reduction
in kidney function demonstrated eGFR improvement from 30 mL/min/1.73 m2
to 47 mL/min/1.73 m2, an improvement of 57 percent. The
fourth patient demonstrated stable eGFR relative to screening.
OMS721 was well-tolerated in the clinical trial with fatigue and anemia
the most commonly reported adverse events. All adverse events were mild
to moderate; some were considered possibly related but most were
considered unrelated to OMS721. Following the clinical trial, all
patients have remained well.
A Phase 3 clinical program for OMS721 in IgA nephropathy has been
initiated and Omeros is finalizing a Phase 3 protocol with FDA. FDA has
granted OMS721 both breakthrough and orphan designations in IgA
nephropathy.
There is no approved treatment for IgA nephropathy, the most common
primary glomerulopathy globally. The disease is responsible for up to 10
percent of all dialysis patients. In the U.S. alone, an estimated
120,000 to 180,000 patients have this disease. Up to 40 percent of IgA
nephropathy patients develop end-stage renal disease, a life-threatening
condition, within 20 years following diagnosis.
About Omeros’ MASP Programs
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 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 clinical program for OMS721 in atypical hemolytic
uremic syndrome (aHUS) is in progress. A second Phase 3 clinical program
for OMS721 has been initiated in immunoglobulin A (IgA) nephropathy.
Also, two Phase 2 trials are ongoing. One is continuing to enroll OMS721
in IgA nephropathy following an earlier Phase 2 trial that generated
positive data in patients with IgA nephropathy and with lupus nephritis;
the other is enrolling and has reported positive data both in patients
with hematopoietic stem cell transplant-associated thrombotic
microangiopathy (TMA). A third Phase 3 program could begin later this
year in stem cell transplant-associated TMA. OMS721 can be administered
both intravenously and subcutaneously, and Omeros expects to
commercialize each formulation of OMS721 for different therapeutic
indications. In parallel, Omeros is 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 breakthrough
therapy designation for IgA nephropathy, orphan drug status for the
prevention (inhibition) of complement-mediated TMAs and for the
treatment of IgA nephropathy, and fast track designation for the
treatment of patients with aHUS.
Omeros also has identified MASP-3 as responsible for the conversion of
pro-factor D to factor D and as a critical activator of the human
complement system’s alternative pathway. The alternative pathway 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. Omeros is preparing to initiate
manufacturing scale-up of its MASP-3 antibodies in advance of clinical
trials.
About Omeros Corporation
Omeros is a commercial-stage
biopharmaceutical company committed to discovering, developing and
commercializing small-molecule and protein therapeutics for large-market
as well as orphan indications targeting inflammation,
complement-mediated diseases and disorders of the central nervous
system. The company’s drug product OMIDRIA® (phenylephrine
and ketorolac injection) 1% / 0.3% is marketed 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 other
IOL replacement procedures to maintain mydriasis (pupil dilation),
prevent miosis (pupil constriction), and to reduce postoperative eye
pain. Omeros has multiple Phase 3 and Phase 2 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 diverse group of preclinical programs and a
proprietary G protein-coupled receptor (GPCR) platform through which it
controls 54 new GPCR drug targets and corresponding compounds, a number
of which are in preclinical development. The company also exclusively
possesses a novel antibody-generating platform.
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 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 Quarterly Report on
Form 10-Q filed with the Securities and Exchange Commission on August 8,
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.
View source version on businesswire.com: http://www.businesswire.com/news/home/20171106005600/en/
Source: Omeros Corporation
Cook Williams Communications, Inc.
Jennifer Cook Williams
Investor
and Media Relations
360.668.3701
jennifer@cwcomm.org
