1367074-64-3

Basic information

• Product Name: N-2-ethoxyethyl-(1-p-chlorobenzoyl-5-hydroxy-2-methylindole)-3-acetamide
• CAS NO: 1367074-64-3
• Molecular Weight: 414.889
• Mol File: 1367074-64-3.mol
• Article Data: 1

Chemical Properties

• CAS DataBase Reference: N-2-ethoxyethyl-(1-p-chlorobenzoyl-5-hydroxy-2-methylindole)-3-acetamide(CAS DataBase Reference)
• NIST Chemistry Reference: N-2-ethoxyethyl-(1-p-chlorobenzoyl-5-hydroxy-2-methylindole)-3-acetamide(1367074-64-3)
• EPA Substance Registry System: N-2-ethoxyethyl-(1-p-chlorobenzoyl-5-hydroxy-2-methylindole)-3-acetamide(1367074-64-3)

Safety Data

• Hazardous Substances Data: 1367074-64-3(Hazardous Substances Data)

Upstream product

• 110-76-9 2-ethoxy-1-ethanamine 
• 2504-32-7 O-Desmethyl-Indomethacin 
• 53-86-1 [1-(4-chlorobenzoyl)-5-methoxy-2-methylindol-3-yl]acetic acid 

Downstream Products

• 1367074-69-8 C₂₂⁽¹¹⁾CH₂₅ClN₂O₄ 

Relevant articles and documents

11C-labeled analogs of indomethacin esters and amides for brain cyclooxygenase-2 imaging: Radiosynthesis, in vitro evaluation and in vivo characteristics in mice

There is great potential in the use of positron emission tomography (PET) and suitable radiotracers for the study of cyclooxygenase type 2 (COX-2) enzyme in living subjects. In the present study, we prepared and evaluated five 11C-labeled ester and amide analogs derived from indomethacin as potential PET imaging agents for the in vivo visualization of the brain COX-2 enzyme. Five 11C-labeled COX-2 inhibitors, with different lipophilicities and moderate COX-2 inhibitory activity, were prepared by treatment of the corresponding O-desmethyl precursors with [11C] methyl triflate and purified by HPLC (radiochemical yields of 55-71%, radiochemical purity of >93%, and the specific activities of 22-331 GBq/μmmol). In mice, radioactivity in the brain for all radiotracers was low, with very low brain-to-blood ratios. A clear inverse relationship was observed between brain uptake at 1 min postinjection and the lipophilicity (experimental log P7.4) of the studied 11C-radiotracers. Pretreatment of mice with cyclosporine A to block P-glycoproteins caused a significant increase in brain uptake of radioactivity following injection of the 11C-radiotracer compared to control. HPLC analysis showed that each radiotracer was rapidly metabolized, and a few metabolites, which were more polar than the original radiotracers, were found in both plasma and brain. No specific binding of the tracers towards the COX-2 enzyme in the brain was clearly revealed by in vivo blocking study. Further structural refinement of the tracer agent is necessary for better enhancement of brain uptake and for sufficient metabolic stability.