Appearance:Solid powderPurity: > 98%
AAD-2004 is a microsomal prostaglandin E2 synthase-1 (mPGES-1) inhibitor potentially for the treatment of Alzheimer/'s type dementia, Parkinson/'s disease (PD), amyotrophic lateral sclerosis (ALS), Arthritis, Depression, Diabetes and Pancreatitis. AAD-2004 markedly suppressed neuronal loss and neuritic atrophy, and partially reversed depleted expression of calbindin in the brain of Tg-beta-CTF99/B6. AAD-2004 reduced autophagosome formation, axonopathy, and motor neuron degeneration, improving motor function and increasing life span.
1:Exp Neurobiol. 2013 Mar;22(1):31-7. doi: 10.5607/en.2013.22.1.31. Epub 2013 Mar 31. AAD-2004 Attenuates Progressive Neuronal Loss in the Brain of Tg-betaCTF99/B6 Mouse Model of Alzheimer Disease.Baek IS,Kim TK,Seo JS,Lee KW,Lee YA,Cho J,Gwag BJ,Han PL, PMID: 23585720 PMCID: PMC3620456 DOI: 10.5607/en.2013.22.1.31 Abstract: Alzheimer/'s disease (AD) is a neurodegenerative disease that proceeds with the age-dependent neuronal loss, an irreversible event which causes severe cognitive and psychiatric devastations. In the present study, we investigated whether the compound, AAD-2004 [2-hydroxy-5-[2-(4-trifluoromethylphenyl)-ethylaminobenzoic acid] which has anti-oxidant and anti-inflammatory properties, is beneficial for the brain of Tg-betaCTF99/B6 mice, a murine AD model that was recently developed to display age-dependent neuronal loss and neuritic atrophy in the brain. Administration of AAD-2004 in Tg-betaCTF99/B6 mice from 10 months to 18 months of age completely repressed the accumulation of lipid peroxidation in the brain. AAD-2004 markedly suppressed neuronal loss and neuritic atrophy, and partially reversed depleted expression of calbindin in the brain of Tg-beta-CTF99/B6. These results suggest that AAD-2004 affords neurodegeneration in the brain of AD mouse model.