75523-11-4

Basic information

• Product Name: INDOMETHACIN ACYL-B-D-GLUCURONIDE
• Synonyms: Indometacin-acyl-beta-D-glucuronide;Indomethacin-acyl-beta-D-glucuronide min. 95%;INDOMETHACIN ACYL-B-D-GLUCURONIDE;Indomethacin Acyl--D-glucuronide;Indomethacin acyl-β-D-glucuronide ,98%;1-[1-(4-Chlorobenzoyl)-5-Methoxy-2-Methyl-1H-indole-3-acetate] β-D-Glucopyranuronic Acid;IndoMethacin Glucuronide
• CAS NO: 75523-11-4
• Molecular Formula: C₂₅H₂₄ClNO₁₀
• Molecular Weight: 533.915
• Product Categories: Glucuronides;Inhibitors;Intermediates & Fine Chemicals;Pharmaceuticals;Metabolites & Impurities
• Mol File: 75523-11-4.mol
• Article Data: 1

Chemical Properties

• Melting Point: 82-84°C
• Boiling Point: 708.474°C at 760 mmHg
• Flash Point: 382.271°C
• Appearance: /
• Density: 1.574g/cm³
• Vapor Pressure: 0mmHg at 25°C
• Refractive Index: 1.664
• Storage Temp.: Hygroscopic, -20°C Freezer, Under Inert Atmosphere
• CAS DataBase Reference: INDOMETHACIN ACYL-B-D-GLUCURONIDE(CAS DataBase Reference)
• NIST Chemistry Reference: INDOMETHACIN ACYL-B-D-GLUCURONIDE(75523-11-4)
• EPA Substance Registry System: INDOMETHACIN ACYL-B-D-GLUCURONIDE(75523-11-4)

Safety Data

• Hazardous Substances Data: 75523-11-4(Hazardous Substances Data)

Usage

Uses

Indomethacin Acyl-β-D-glucuronide is a metabolite of Indomethacin (I641000). Acyl glucuronides have been implicated in the toxicity of many xenobiotics and marketed drugs.

InChI:InChI=1/C25H24ClNO10/c1-11-15(10-18(28)36-25-21(31)19(29)20(30)22(37-25)24(33)34)16-9-14(35-2)7-8-17(16)27(11)23(32)12-3-5-13(26)6-4-12/h3-9,19-22,25,29-31H,10H2,1-2H3,(H,33,34)/t19-,20-,21-,22?,25+/m1/s1

Upstream product

• 1428774-23-5 [1-(4-chloro-benzoyl)-5-methoxy-2-methyl-1H-indol-3-yl]-acetic acid 4-[2-(diethoxy-phosphoryloxy)-ethyl]-phenyl ester 
• 1245697-26-0 UDP-glucuronic acid 
• 53-86-1 [1-(4-chlorobenzoyl)-5-methoxy-2-methylindol-3-yl]acetic acid 

Relevant articles and documents

Comparative in vitro metabolism of phospho-tyrosol-indomethacin by mice, rats and humans

Phospho-tyrosol-indomethacin (PTI; MPI 621), a novel anti-cancer agent, is more potent and safer than conventional indomethacin. Here, we show that PTI was extensively metabolized in vitro and in vivo. PTI was rapidly hydrolyzed by carboxylesterases to generate indomethacin as its major metabolite in the liver microsomes and rats. PTI additionally undergoes cytochromes P450 (CYP)-mediated hydroxylation at its tyrosol moiety and O-demethylation at its indomethacin moiety. Of the five major human CYPs, CYP3A4 and CYP2D6 catalyze the hydroxylation and O-demethylation reactions of PTI, respectively; whereas CYP1A2, 2C9 and 2C19 are inactive towards PTI. In contrast to PTI, indomethacin is primarily O-demethylated by CYP2C9, which prefers acidic substrates. The hydrolyzed and O-demethylated metabolites of PTI are further glucuronidated and sulfated, facilitating drug elimination and detoxification. We observed substantial inter-species differences in the metabolic rates of PTI. Among the liver microsomes from various species, PTI was the most rapidly hydrolyzed, hydroxylated and O-demethylated in mouse, human and rat liver microsomes, respectively. These results reflect the differential expression patterns of carboxylesterase and CYP isoforms among these species. Of the human microsomes from various tissues, PTI underwent more rapid carboxylesterase- and CYP-catalyzed reactions in liver and intestine microsomes than in kidney and lung microsomes. Together, our results establish the metabolic pathways of PTI, reveal significant inter-species differences in its metabolism, and provide insights into the underlying biochemical mechanisms.