ADGEN, as part of its multiple research programs, has been using its patented technologies as an umbrella under which it has been developing a  series of chemical analogs based on the structures of our lead lipid mobilising protein, as well as novel phospho-tau inhibitor compounds. The lead  optimization process resulted in the production of new chemical entities (NCEs) for pre-clinical research programs. The final candidates which are  bound to be very similar in structure to our key lead compounds were designed to improve on their current regenerative or inhibiting properties,  brain penetration and cardiovascular safety profile. The production of potent apoliproteins modulators that stimulates brain reinnervation will be  used to slow down or, possibly stop disease progression, but more importantly, to delay the onset of the disease in people who are not  symptomatic but carry defective “at-risk” genes. We have been also working on modulators of the isoprenoid cascade to identify potent, brain  penetrating, FDPS and GGPPs inhibitors. These endeavours represent clear practical and achievable mid-term goals. It has been determined  that a five years delay in the onset of AD could translate into a reduction of the prevalence of Alzheimer's disease by 50% in occidental countries  over one generation and in a reduction of caring cost (direct and indirect) in excess of $1000 billions worldwide. The worldwide market for such a  drug in Alzheimer's disease alone is estimated to be in the order of $16-23 billion per year. ADGEN has identified several novel genetic and proteomic markers for age of onset, disease progression and response to standard therapies in  neurodegenerative diseases and stroke, all linked to the neuronal remodeling pathways. The ADGEN team has also discovered protective genetic  variants that attenuate risk and affect age at onset while providing interesting new therapeutic targets. These include CNTN5, HMGCR, IGFBP2,  APOB, OPN and ADAM23. Dr. Poirier’s research team has carried out extensive pharmacogenomic programs the past three decades with  international pharmas, including Warner-Lambert, Pfizer, ELi Llly, Novartis, Avantis, Servier, Astrazeneca and Bayer, principallly on cognitive  enhancer drugs exhibiting different modes of action. These programs have been associated with compound drug development where a focus was  built around individual response to specific therapeutic agents. In recent years, the same pharmacogenomic approach has been used with anti-  amyloid medications in both, prodromal and early Alzheimer cases with clear dichotomic drug responses and side effect profles. This approach has aided the interpretation of marginal drug effects and established a molecular basis for efficacy and safety in several experimental compounds in  randomised, double-blind, clinical trials. Dr. Poirier did worked with the genomic team at Motorola on experimental devices designed to perform  low-cost genetic profiles to be used in physician offices, an emerging market for both, the US and Europe. The initial research-business concept  holds true today, but in a broader sense. The ADGEN team has a well documented and proprietary knowledge of mechanisms for neuronal  remodeling through the study of neuronal degeneration caused by neurodegenerative diseases or trauma. 
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