SOURCE: Pipex Pharmaceuticals, Inc.

February 15, 2007 08:54 ET

Pipex Pharmaceuticals' COPREXA™ Awarded $306,172 NIH Grant for Preclinical Testing in Alzheimer's Disease

ANN ARBOR, MI -- (MARKET WIRE) -- February 15, 2007 -- Pipex Pharmaceuticals, Inc. (OTCBB: PPXP), a specialty pharmaceutical company developing innovative late-stage drug candidates for the treatment of neurologic and fibrotic diseases, announced that its lead anti-copper drug candidate, COPREXA™ (oral tetrathiomolybdate) received a grant from the National Institutes of Health (NIH) to support to test its utility for the treatment for Alzheimer's Disease (AD), a life threatening neurodegenerative disease in which copper dyshomeostasis is implicated. This grant was awarded in the amount of $306,172 to Dr. Joseph F. Quinn, Associate Director, Clinical Core, NIA-Layton Aging and Alzheimer's Disease Center Co-Director at Oregon Health Sciences University as principal investigator with, Dr. George J. Brewer, Chairman of Pipex's Scientific Advisory Board and inventor of COPREXA™ as a collaborator for the grant.

Correlation of Free-Copper and Alzheimer's Disease

Over the last several years, an increasing body of evidence points to dysfunctional copper homeostasis in the pathogenesis of AD. Recently, a published prospective clinical study conducted in 3718 patients in the U.S. over 6 years, which included subjects that consumed a vitamin containing copper supplement (1.6mg of copper a day,) when taken together with a high saturated and trans fat diet resulted in an equivalent of 19 years of mental decline (p < 0.001).

A separate European clinical study conducted in 53 patients correlated the levels of the highly reactive "free copper" (also known as copper not bound to proteins) pool in serum to disease severity in AD patients versus aged-matched control patients. These results demonstrated that the "free copper" serum pool (p < 0.0001) was highly increased in AD patients.

These clinical studies are complemented by preclinical studies that show that AD amyloid-â plaques when treated with copper chelating agents in-vitro loosen and reverse fibril formation as determined by spectroscopy. Other investigations have shown that reduction in intracellular neuronal copper levels downregulates the expression of amyloid precursor protein (APP), a hallmark AD protein.

COPREXA's specificity and unique mechanism of action for rapidly lowering toxic free copper levels, combined with its history of success in completed pivotal clinical trials of neurologically presenting Wilson's disease, may position COPREXA™ as the first available therapeutic agent capable of correcting the serum and CNS free copper dyshomeostasis that might represent an important fundamental cause of AD. COPREXA's ability to specifically bind only toxic free copper, differentiates it from other non-specific metal chelating compounds previously investigated for neurodegenerative diseases.

Dr. George J. Brewer, Emeritus Professor of Human Genetics at the University of Michigan, inventor of COPREXA™ and grant collaborator commented, "The peer review process and receipt of this NIH grant provides us with additional confidence in the science of our approach of using an COPREXA™, an agent which is capable of selectively lowering the levels of free copper in the brains of patients with copper-implicated neurodegenerative diseases, such as neurologically presenting Wilson's disease and possibly Alzheimer's disease."

About the NIH Grant

The $306,172 grant was awarded by the NIH's National Institute on Aging (NIA). Under the grant, entitled, "Copper Complexing with Tetrahiomolybdate in a Murine Model of Alzheimers Disease," the well established Tg2576 mouse model of Alzheimer's disease is being used. One cohort of mice will be studied in an Alzheimer pathology prevention experiment, with COPREXA™ therapy initiated at 8 months (prior to the appearance of plaque pathology) and continued until the age of 14 months (when plaque pathology is typically well established in untreated animals). A second cohort of mice will be studied in an Alzheimer pathology treatment experiment, with treatment initiated at 14 months and continued until the age of 16 months. In each case, both Tg2576 and wild-type mice will randomized to COPREXA™ or vehicle only. Wild-type will be included to serve as a reference population for behavioral and biochemical outcome measures. The efficacy and safety of the dose will be monitored during the treatment period by plasma ceruloplasmin levels, with the COPREXA™ dose adjusted if necessary to optimize the degree of copper complexing. Safety will also be monitored by following the weights of the mice and by performing routine motor testing (rotorod, open field testing) on a monthly basis. At the end of the treatment period in each experiment, the spatial memory of the mice will be tested in the Morris Water Maze, as an index of amyloid-associated neurologic function. Mice will then be euthanized and brain tissue harvested for determination of metal levels (copper, zinc, and molybdenum), beta amyloid, neuritic dystrophy, synaptic density, and oxidative and nitrosative damage to brain proteins. This strategy will achieve the specific aims of 1) determining if COPREXA™ prevents amyloid pathology 2) determining if COPREXA™ prevents amyloid-associated neuronal damage 3) determining if COPREXA™ attenuates established beta amyloid pathology and 4) determining if COPREXA™ attenuates established amyloid-associated neuronal damage.

Market Opportunity for COPREXA™ in Alzheimer's Disease

It is estimated that more than 4.5 million Americans and 12 million people worldwide suffer from AD. Risk factors for the disease include age and family history. Age is the most important risk factor for AD; the number of people with the disease doubles every five years beyond age 65. According to the Alzheimer's Association, the disease affects one in 10 persons over the age of 65, and 50% of those over 85 years old.

There is an urgent need for an effective treatment for the illness, caused in part by the rising health care, institutional, and social costs for the treatment and care of Alzheimer's sufferers. In May 2002, the National Institute on Aging (NIA) reported that the cost of care to family, caregivers and society in general was estimated to exceed $100 billion per year, up from $18 billion in 1996, ranking AD as the disease with the greatest economic cost to society. These costs are expected to rise sharply as the baby-boom generation ages and more people become at risk for the disease. As people live longer, their risk of developing AD increases.

The market for treatment of AD is equally large, accounting for $3 billion in worldwide sales in 2004. This market is expected to grow to $5 billion by 2009. Aricept®, an FDA-approved acetylcholinesterase inhibitor, is the top-selling treatment, accounting for 40% of the Alzheimer's-drug market in 2004 with $1.35 billion in sales and year-over-year revenues growing by 17% per annum.

About COPREXA™

COPREXA™, is an oral, small-molecule, anti-copper agent that is highly specific for the reduction of free copper in serum, the most toxic form of copper in the body, and is thus ideally suited for the treatment of central nervous system (CNS) diseases in which abnormal serum and CNS copper homeostasis are implicated. We are also developing COPREXA™ for fibrotic disorders based upon the rationale that the fibrotic disease process is dependent upon the availability of free copper in the body. COPREXA™ has demonstrated the ability to inhibit fibrosis in a number of well established animal models through the sequestration of available copper and inhibition of key fibrotric cytokines, including secreted protein acid rich in cysteine (SPARC), NF(KAPPA)B, TGF-(BETA), FGF-2, IL-1, IL-6, IL-8, and connective tissue growth factor (CTGF).

COPREXA™ has also completed a one-year open label phase II clinical trial for the treatment of Idiopathic Pulmonary Fibrosis (IPF), a deadly lung disease and is also in a phase II clinical trial for the treatment of primary biliary cirrhosis (PBC), a fibrotic disease of the hepatic system. This phase II clinical trial is being supported by a $850,000 grant from the FDA's Orphan Drug Group.

About Pipex Pharmaceuticals, Inc.

Pipex Pharmaceuticals, Inc. ("Pipex") is a specialty pharmaceutical company that is developing proprietary, late-stage drug candidates for the treatment of neurologic and fibrotic diseases. Pipex's strategy is to exclusively in-license proprietary, clinical-stage drug candidates and complete the further clinical testing, manufacturing and regulatory requirements sufficient to seek marketing authorizations via the filing of New Drug Applications (NDAs) with the FDA in the U.S. and Marketing Application Authorizations (MAAs) with the European Medicines Evaluation Agency (EMEA). For further information, please visit, www.pipexpharma.com.

This press release contains forward-looking statements, within the meaning of Section 21E of the Securities Exchange Act of 1934, that reflect Pipex Pharmaceuticals, Inc. and Pipex Therapeutics, Inc. ("we" or "our") current expectations about its future results, performance, prospects and opportunities, including statements regarding the potential use of COPREXA™ for the treatment of Alzheimer's disease, inflammatory and fibrotic diseases, as well as its the prospects for regulatory filings in the treatment of neurologic Wilson's disease. Where possible, the Company has tried to identify these forward-looking statements by using words such as "anticipates," "believes," "intends," or similar expressions. These statements are subject to a number of risks, uncertainties and other factors that could cause actual events or results in future periods to differ materially from what is expressed in, or implied by, these statements. We cannot assure you that we will be able to successfully develop or commercialize products based on our technologies, including COPREXA™, TRIMESTA™, SOLOVAX™, EFFIRMA™ or Anti-CD4 802-2, particularly in light of the significant uncertainty inherent in developing, manufacturing and conducting preclinical and clinical trials of new pharmaceuticals, and obtaining regulatory approvals, that our technologies will prove to be safe and effective, that our cash expenditures will not exceed projected levels, that we will be able to obtain future financing or funds when needed, that product development and commercialization efforts will not be reduced or discontinued due to difficulties or delays in clinical trials or due to lack of progress or positive results from research and development efforts, that we will be able to successfully obtain any further grants and awards, maintain our existing grants which are subject to performance, that we will be able to patent, register or protect our technology from challenge and products from competition or maintain or expand our license agreements with our current licensors, or that our business strategy will be successful. All forward-looking statements made in this press release are made as of the date hereof, and the Company assumes no obligation to update the forward-looking statements included in this news release whether as a result of new information, future events, or otherwise. The forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially from those set forth or implied by any forward-looking statements.

Contact Information

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