The ProblemAlzheimer’s disease (AD) is a devastating neurological disorder that causes progressive loss of memory and decline in cognitive function in tens of millions of elderly people worldwide. Despite the emotional, social, and economic burden of AD and the large market opportunity it represents, pharmaceutical companies have had minimal success in developing effective treatments. Only five drugs, for example, are currently approved in the United States to treat AD, and none of them are addressing the mechanism behind Alzheimer’s or can claim any ability to slow disease progression or to offer lasting, long-term relief from the symptoms of AD. Despite the significant limitations of existing drugs, the global pharmaceutical market for AD treatment as of 2005 was still in excess of $3.9 billion.The market absence of disease-modifying drugs for treating AD relates to a myriad of factors. For starters, the medical research community’s understanding of all the factors that lead to the onset and progression of disease is incomplete. Second, no simple diagnostic test currently exists for AD, making early detection impossible. Third, AD diagnosis and the monitoring of AD progression currently rely on clinical signs and symptoms, which only manifest late in the pathologic course of the disease and the slow progression of AD makes clinical trials very lengthy. In this setting, it is unlikely for a disease-modifying drug to show as much of an impact on the disease course as it might when applied in the early disease stages, where pathological changes may be reversible before the onset of clinical manifestations. Fourth, no good screens currently exist in early-stage clinical development to predict which agents are most likely to demonstrate improvements in outcomes during pivotal registration trials. This inherently creates a suboptimal approach to rationale drug development, and markedly elevates the risk and cost of clinical research in the AD space.C2N’s Technology C2N Diagnostics is a company founded in 2007, for the purpose of exclusively commercializing a proprietary and novel metabolic labeling technology that seeks to bridge the gap between AD diagnosis and disease-modifying treatment. The approach uses in vivo stable isotope labeling to tag newly synthesized amyloid beta peptide (a believed key mediator of AD pathogenesis) in the cerebrospinal fluid, combined with mass spectrometry to detect the change in labeled amyloid over time. In this way, one can measure the rates of synthesis and degradation of beta amyloid, providing previously unavailable insights into the state of Alzheimer’s disease progression, and how therapeutics can potentially modify the course of the disease. Discovered at the Washington University School of Medicine by C2N’s scientific founders, Drs. Randy Bateman and David Holtzman, this technology was first presented as a major research breakthrough in the June 25, 2006 edition of Nature Medicine. It formed the basis of a 2006 Scientific American 50 award granted to Dr. Bateman, recognizing him as one of the top 50 scientific advancements of the year.Market ApplicationsC2N believes that its technology has immediate commercial application for biotechnology and pharmaceutical companies seeking to understand how their novel therapeutics alter the pathology of AD during the early stages of clinical drug development. Downstream potential applications are numerous, including: (i) the support of pre-clinical drug discovery work in AD; (ii) application of the same methodology to enhance clinical and pre-clinical drug discovery across a wide spectrum of other neurodegenerative disorders, where protein mishandling is implicated in the disease process (e.g. Parkinson’s Disease; Huntington’s chorea, Amyotrophic Lateral Sclerosis, schizophrenia, etc); (iii) the development of a serum-based biomarker assay that enables early AD (or other neurodegenerative disorder) diagnosis; and (iv) use of the assay to follow pre-clinical AD progression and to distinguish disease-modifying treatment responders from non-responders.