AAD-2004

• CAT Number: I000348
• CAS Number: 927685-43-6
• Molecular Formula: C16H14F3NO3
• Molecular Weight: 325.28
• Purity: ≥95%
• Target: Microsomal Prostaglandin E2 Synthase-1 (mPGES-1) Inhibitor
• Solubility: Soluble in DMSO
• Storage: 0 - 4°Cfor short term (days to weeks), or -20 °C for long term (months).
• IUPAC Name: 2-hydroxy-5-[2-[4-(trifluoromethyl)phenyl]ethylamino]benzoic acid
• InChI: InChI=1S/C16H14F3NO3/c17-16(18,19)11-3-1-10(2-4-11)7-8-20-12-5-6-14(21)13(9-12)15(22)23/h1-6,9,20-21H,7-8H2,(H,22,23)
• InChIKey: UTMVACIBQLDZLP-UHFFFAOYSA-N
• SMILES: C1=CC(=CC=C1CCNC2=CC(=C(C=C2)O)C(=O)O)C(F)(F)F

AAD-2004 (Cat.No:I000348) 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.

Reference

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.