Omeros Corporation (Nasdaq: OMER) today announced that the first report describing the effects of lectin-pathway inhibition by narsoplimab on urinary complement levels in kidney disease was presented yesterday at the Annual Meeting of the American Society of Nephrology (ASN). The work, conducted by a consortium from Denmark and the United Kingdom and led by Peter Garred, MD, DMSc, Chair and Professor of Clinical Molecular Medicine at the University of Copenhagen, was detailed at the ASN Annual Meeting in a poster entitled “Reduction of Urinary Levels of Lectin Pathway Complement Components in an IgA Vasculitis Patient after MASP-2 Inhibition with Narsoplimab”.
The patient, a 21-year-old woman, presented with a rapidly progressive glomerulonephritis. The objective was to stabilize her rapidly deteriorating kidney function to allow for renal transplantation. Her clinical course and response to the MASP-2 inhibitor narsoplimab are detailed in a publication by Selvaskandan et al.1 In brief, kidney biopsy revealed marked vascular damage with significant interstitial fibrosis, tubular atrophy and evidence of complement involvement. Diagnosed with IgA vasculitis, she developed rapidly worsening kidney function with highly elevated creatinine levels, hypertension, proteinuria, and hematuria despite treatment with systemic corticosteroids. She began treatment with narsoplimab. After one course of 12 weekly doses of narsoplimab, her kidney function stabilized and she was able to undergo successful renal transplantation without the need for dialysis.
As reported in yesterday’s ASN Annual Meeting presentation, complement levels assessed in urinary samples collected during the patient’s clinical course demonstrated substantial reduction in local complement activation associated with narsoplimab treatment-related lectin-pathway inhibition and stabilization of kidney function. Specifically, C4c/creatinine ratio, ficolin-3/creatinine ratio and C3bc/creatinine ratio levels were decreased 75%, 58% and 29%, respectively, from baseline to the end of the treatment. Levels of MBL and CL-11 remained stable during treatment. Further studies are ongoing to evaluate the use of urine as a non-invasive and readily accessible resource to monitor responses to narsoplimab treatment.
A second presentation directed to narsoplimab in IgA-related disease – Long-Term Phase 2 Efficacy of the MASP-2 Inhibitor Narsoplimab for Treatment of Severe IgA Nephropathy – was also included in yesterday’s program at the ASN Annual Meeting.
1Selvaskandan H, Kay Cheung C, Dormer J, Wimbury D, Martinez M, Xu G, Barratt J. Inhibition of the lectin pathway of the complement system as a novel approach in the management of IgA vasculitis-associated nephritis. Nephron. 2020;144(9):453-458. doi: 10.1159/000508841.
Narsoplimab, also known as “OMS721,” is an investigational human monoclonal antibody targeting mannan-binding lectin-associated serine protease-2 (MASP-2), a novel pro-inflammatory protein target and the effector enzyme of the lectin pathway of complement. 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. Omeros controls the worldwide rights to MASP-2 and all therapeutics targeting MASP-2.
A biologics license application (BLA) is pending before the U.S. FDA for use of narsoplimab in the treatment of HSCT-TMA, and the drug is in Phase 3 clinical programs for immunoglobulin A (IgA) nephropathy and atypical hemolytic uremic syndrome (aHUS). Narsoplimab is also being evaluated for the treatment of COVID-19 as part of the I-SPY-COVID-19 platform trial sponsored by Quantum Leap Healthcare Collaborative. FDA has granted narsoplimab breakthrough therapy designations for HSCT-TMA and for IgA nephropathy; orphan drug status for the prevention (inhibition) of complement-mediated thrombotic microangiopathies, for the treatment of HSCT-TMA and for the treatment of IgA nephropathy; and fast track designation for the treatment of patients with aHUS. The European Medicines Agency has granted orphan drug designation to narsoplimab for treatment in HSCT and for treatment of primary IgA nephropathy.
About Omeros Corporation
Omeros is a commercial-stage biopharmaceutical company committed to discovering, developing and commercializing small-molecule and protein therapeutics for large-market and orphan indications targeting inflammation, immunologic diseases (e.g., complement-mediated diseases and cancers) and central nervous system disorders. Its commercial product OMIDRIA® (phenylephrine and ketorolac intraocular solution) 1%/0.3% continues to gain market share in cataract surgery. Omeros’ lead MASP-2 inhibitor narsoplimab targets the lectin pathway of complement and is the subject of a biologics license application pending before FDA for the treatment of hematopoietic stem cell transplant-associated thrombotic microangiopathy. Narsoplimab is also in multiple late-stage clinical development programs focused on other complement-mediated disorders, including IgA nephropathy, atypical hemolytic uremic syndrome and COVID-19. OMS906, Omeros’ inhibitor of MASP-3, the key activator of the alternative pathway of complement, is in a Phase 1 clinical trial, and the company’s PDE7 inhibitor program OMS527, targeting addiction and movement disorders, has successfully completed a Phase 1 trial. Omeros’ pipeline holds a diverse group of preclinical programs including a proprietary-asset-enabled antibody-generating technology and a proprietary GPCR platform through which it controls 54 GPCR drug targets and their corresponding compounds. One of these novel targets, GPR174, modulates a new cancer immunity axis recently discovered by Omeros, and the company is advancing GPR174-targeting antibodies and small-molecule inhibitors. For more information about Omeros and its programs, visit www.omeros.com.
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,” “likely,” “look forward to,” “may,” “objective,” “plan,” “potential,” “predict,” “project,” “should,” “slate,” “target,” “will,” “would” and similar expressions and variations thereof. Forward-looking statements, including statements regarding Omeros’ research and development programs and the therapeutic application of research findings, 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, the impact of COVID-19 on our business, regulatory processes and oversight, challenges associated with manufacture or supply of our investigational or commercial products, delays in completion of ongoing or planned clinical trials, 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 (SEC) on March 1, 2021. 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, whether as a result of new information, future events or otherwise, except as required by applicable law.
Cook Williams Communications, Inc.
Investor and Media Relations