Pipex Pharmaceuticals, Inc. (AMEX: PP) (”Pipex”), a specialty pharmaceutical company developing innovative late-stage drug candidates for the treatment of neurologic and fibrotic diseases, announced the presentation of preliminary results using its lead anti-copper drug candidate, COPREXA (oral tetrathiomolybdate), in the most commonly utilized transgenic pre-clinical murine model of Alzheimer’s Disease (AD) at the 2007 Society for Neuroscience annual meeting on November 4th in San Diego, CA. These studies were funded by a grant from the National Institute on Aging (NIA) of the National Institutes of Health (NIH).

Joseph Quinn, M.D., Associate Professor of Neurology at Oregon Health & Science University (OHSU) and primary investigator of this study commented, “These preliminary results of a significant reduction in central nervous system copper (p < 0.05) and a 40% reduction in insoluble amyloid beta (p < 0.05) are encouraging from a standpoint of COPREXA’s ability to be a potentially disease modifying therapy for AD. These preliminary results need to be replicated and expanded before we proceed to clinical trials.”

Steve H. Kanzer, Chairman & Chief Executive Officer of Pipex, commented, “Since the serendipitous finding of Dr. Larry Sparks in 2003 that free copper in the drinking water of high cholesterol-fed animals plays an important role in the formation of Alzheimer’s-like disease, the last four years has witnessed a tremendous body of collaborating evidence implicating free copper in the pathogenesis of AD. These studies have taken the form of human dietary copper epidemiological studies in the elderly, post-mortem pathology studies of human amyloid plaques and their co-localization with copper, comparative human studies finding elevated levels of serum free copper in AD patients compared to age-matched controls, as well as many molecular studies establishing free copper’s high binding affinity and oxidizing effects on the majority of recognized AD-related proteins, including, amyloid beta, tau, amyloid precursor protein (APP), beta secretase, and apolipoprotein E (apoE) phenotypes 2/3/4. References (1-9). Taken together, this mounting body of evidence implicates elevated free copper levels in the central nervous system as a consistent and prominent cause of the characteristic copper-containing insoluable amyloid beta plaques, neurofibrillary tangles, cognitive impairment and neurodegeneration that defines AD. As a society in which 50% of our population over the age of 75 are already afflicted by AD and countless others at risk of developing AD, AD is the disease of our time, and it is high time that we pay attention to the risks that free copper poses to our susceptible elderly population (especially those at genetic risk for AD) and pursue with vigor potential therapeutic interventions such as those that our company is developing that specifically aim to lower the central nervous system copper burden of already affected patients. The experiments conducted and results presented by Dr. Joseph Quinn and colleagues at Oregon Health & Science University represent the first prospectively defined controlled therapeutic intervention study in mice or man that is specifically targeted to lower free copper levels in the central nervous system for the purpose of treating AD and the results demonstrate that lowering such free copper can lower insoluable amyloid beta levels by 40%.and thus a disease modifying effect in AD. OHSU’s efforts and results would not have been achieved without the support of the National Institute on Aging to whom Pipex would like to take the opportunity to thank. We look forward to the further results of Dr. Quinn’s group regarding their ongoing additional cohorts of transgenic Tg2576 animals currently being tested pursuant to a protocol in which COPREXA is being administered to animals after the typical apparent onset of disease at 10-12 months of age.”

Dr. George Brewer, Professor Emeritus at the University of Michigan and inventor of COPREXA, said, “The strength of the association between copper’s causative relationship and Alzheimer’s disease parallels my experience in treating neurologic Wilson’s disease, a disease of similar neurodegeneration. While a different form of disease, in COPREXA treated neurologic Wilson’s disease, we have seen a reversal or improvement in the neurologic scores of these patients. Currently, there are no adequate approved or disease modifying treatments for Alzheimer’s and these results represent an important step forward for the 4.5 million Americans suffering from Alzheimer’s.”