Press Releases

Promedior Announces Presentation of Preclinical Data at AASLD Demonstrating that Pentraxin-2 Suppresses Liver Fibrosis

Promedior’s First-in-Class Pentraxin-2 Therapeutic, PRM-151, Represents a Promising New Mechanism for Treating a Wide Range of Fibrotic Diseases

MALVERN, PA, November 2, 2011 —Promedior, Inc., a clinical stage biotechnology company developing novel therapies to treat fibrotic, inflammatory and neovascular diseases, today announced that data from preclinical studies of Serum Amyloid P (Pentraxin-2) will be presented at the Annual Meeting of the American Association for the Study of Liver Diseases (AASLD 2011), being held November 4-8, 2011, in San Francisco, CA.  The data to be presented highlight the efficacy and utility of Pentraxin-2 in suppressing fibrosis and providing a clear hepatoprotective effect in independent models of liver fibrosis.  In liver fibrosis, Pentraxin-2 inhibits the activation of monocytes, fibrocytes and hepatic stellate cells.  Promedior’s lead product, PRM-151, is a recombinant form of the naturally circulating human protein Pentraxin-2, which has been shown to regulate the cell populations that control fibrosis, inflammation and pathologic neovascularization. 

The schedule and details of the poster presentation about Pentraxin-2 at AASLD are as follows:

Abstract Title: Serum amyloid P attenuates hepatic fibrosis in mice by inhibiting the activation of fibrocytes and hepatic stellate cells
Session Title: Basic Fibrosis
Research and Stellate Cell Biology
Session Type: Poster
Location: Poster Hall
Start time: Sunday, November 6, 2011 at 8:00 AM

About PRM-151
Promedior is developing PRM-151 (rhPTX-2 for injection) for the treatment of Idiopathic Pulmonary Fibrosis (IPF) and other chronic systemic fibrosis indications. In a Phase 1 study in healthy volunteers and IPF patients, PRM-151 was safe and well-tolerated, and showed activity against efficacy biomarkers by reducing IPF-related peripheral blood fibrocyte and IL-6 levels. PRM-151 currently is being tested in a Phase 1b clinical study in IPF patients to evaluate the safety, tolerability and dose-responsive changes in validated cellular and soluble biomarkers of disease. PRM-151 is also being tested in a Phase 2a clinical study to evaluate the efficacy, safety, and tolerability of PRM-151 in preventing post-surgical scarring in glaucoma patients following glaucoma filtration surgery.

About Promedior
Promedior is a clinical-stage biotechnology company developing a novel biology platform for the treatment of fibrosis, inflammation, and neovascular retinal diseases. Promedior's platform of protein therapeutics is based upon Pentraxin-2, an endogenous human serum protein that regulates the body’s response to injury. Pentraxin-2 therapeutics treat fibrosis and neovascular diseases by naturally regulating monocyte-derived cells (macrophages and fibrocytes) that control the fibrotic process and drive pathologic neovascularization. Based upon a unique mechanism of action, Pentraxin-2 localizes to sites of tissue damage and stimulates monocytes to differentiate into regulatory macrophages rather than pro-fibrotic macrophages and fibrocytes, thereby reversing inflammatory, fibrotic, and neovascular processes and promoting normal healing. By acting upstream of these pathologic processes utilizing a natural regulatory pathway, Pentraxin-2 therapeutics provide a superior therapeutic approach and an inherently safer profile.

Using its novel approach, Promedior is initially developing a pipeline of drugs to address the most severe and difficult-to-treat fibrotic and inflammatory conditions of the eye, lung and kidney such as glaucoma, age-related macular degeneration and diabetic retinopathy (eye); pulmonary fibrosis, scleroderma and COPD (lung); and acute and chronic nephropathy (kidney). For additional information about Promedior, please visit

Media Contact:

Kathryn Morris
The Yates Network


Crystal structure of human Pentraxin-2, a naturally occurring protein that is the foundation of Promedior's proprietary platform. Learn More >