Singapore, Aug 31, 2010: Neurotech Pharmaceuticals, South Korea, has begun dosing in the phase I clinical testing of AAD-2004. The compound was developed as a dual function drug to remove free radicals and PGE2, the key mediators of nerve injury in Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). The phase I clinical trial was initiated to evaluate the safety, tolerability, and pharmacokinetics of AAD-2004 in healthy volunteers in April 2010. The first two cohorts of the clinical study is said to have been successfully completed without serious adverse events.

Free radicals and PGE2-mediated inflammation are expected to play a central role in the neurodegenerative process occurring in diseases including AD, PD, and ALS. According to the company, no drugs have been developed to prevent free radicals in the brain of AD, PD, and ALS due to poor blood-brain barrier permeability and adverse effects. Long-term use of conventional nonsteroidal anti-inflammatory drugs (NSAIDs) has been limited by the risk of cardiovascular infarction and thrombosis as well as gastrointestinal complications. Currently there are no FDA-approved drugs to protect nerve cells against toxic free radicals and inflammation evolving in the nervous system of patients with AD, PD, and ALS.

The scientific founders of Neurotech Pharmaceuticals discovered a novel chemical library on the premise that a single agent combining the anti-inflammatory attributes of aspirin with powerful anti-oxidant efficacy would constitute effective disease modifying therapeutics for nerve protection in neurodegenerative diseases, based on the additive/synergistic neuroprotective effects via compromising free radicals and inflammation.

With leading supports via 21C Frontier R&D Program in Neuroscience from Ministry of Education, Science, and Technology, a National Drug Discovery Program from Ministry of Health and Welfare, and Ajou University in South Korea, Neurotech Pharmaceuticals launched an Anti-Alzheimer's Drug discovery program. AAD-2004 was selected as a final drug candidate based upon safety and efficacy study in animal models of AD that improved cognitive function far better than antioxidants or NSAIDs as well as memantine, an FDA approved drug for the symptomatic treatment of AD. The therapeutic potential of AAD-2004 has been verified in animal models of ALS, PD, and major depression. Unlike conventional NSAIDs causing gastric damage, AAD-2004 did not produce gastric damage even at a dose 400-fold higher than maximally effective doses in animal models.

"While NASIDs cause gastric and cardiovascular risks by preventing production of prostaglandins PGI2 as well as PGE2 by inhibiting cyclooxygenases, AAD-2004 selectively prevents PGE2 production as an inhibitor of microsomal prostaglandin E synthase-1 (mPGES-1), the terminal isomerase catalyzing conversion of PGH2 to PGE2, at nanomolar concentrations, which explains why AAD-2004 is safer than NSAIDs. In addition, the potent spin trapping property of AAD-2004 provides additional efficacy and safety," said Dr Byoung J Gwag, CEO of Neurotech Pharmaceuticals and professor, Department of Pharmacology of Ajou University School of Medicine. "The marked safety and efficacy in preclinical studies make AAD-2004 a promising drug candidate to advance into clinical trials. We are so pleased to see safety profile of AAD-2004 in human healthy volunteers exposed to doses higher than maximally effective doses in preclinical studies."