18186-43-1

Basic information

• Product Name: Serotonin β-D-Glucuronide
• Synonyms: Serotonin β-D-Glucuronide;3-(2-AMinoethyl)-1H-indol-5-yl β-D-Glucopyranosiduronic acid;5-HydroxytryptaMine Glucuronide;5-HydroxytryptaMine O-Glucuronide
• CAS NO: 18186-43-1
• Molecular Formula: C16H19N2O7
• Molecular Weight: 351.33126
• Product Categories: Aromatics;Glucuronides;Heterocycles;Intermediates & Fine Chemicals;Metabolites & Impurities;Pharmaceuticals
• Mol File: 18186-43-1.mol
• Article Data: 2

Chemical Properties

• Appearance: /
• Storage Temp.: Refrigerator, Under Inert Atmosphere
• Solubility: DMSO (Slightly), Methanol (Slightly, Sonicated), Water (Slightly)
• CAS DataBase Reference: Serotonin β-D-Glucuronide(CAS DataBase Reference)
• NIST Chemistry Reference: Serotonin β-D-Glucuronide(18186-43-1)
• EPA Substance Registry System: Serotonin β-D-Glucuronide(18186-43-1)

Safety Data

• Hazardous Substances Data: 18186-43-1(Hazardous Substances Data)

Usage

Chemical Properties

Pale Orange Solid

Uses

A metabolite of 5-Hydroxytryptamine, also known as Serotonin (S274990).

Upstream product

• 50-67-9 3-(2-aminoethyl)-1H-indol-5-ol 
• 63700-19-6 uridine-5'-diphospho-α-D-glucuronic acid trisodium salt 

Relevant articles and documents

Species and tissue differences in serotonin glucuronidation

1. Serotonin is a UGT1A6 substrate that is mainly found in the extrahepatic tissues where some UGT1As are expressed. The aim of the present study was to characterize serotonin glucuronidation in various tissues of humans and rodents.2. Serotonin glucuronidation in the human liver and kidney fitted to the Michaelis-Menten model, and the Km values were similar to that of recombinant UGT1A6. However, serotonin glucuronidation in the human intestine fitted to the Hill equation, indicating that it is likely catalyzed not only by UGT1A6, but also by another UGT1A isoform. Serotonin glucuronidation in the rat liver, intestine and kidney fitted well to the Michaelis-Menten model and exhibited monophasic kinetics in the kidney, but biphasic kinetics in the liver and intestine. Furthermore, serotonin glucuronidation in the rat brain fitted best to the Hill equation. Serotonin glucuronidation in the mouse tissues fitted to the Michaelis-Menten model and exhibited monophasic kinetics in the liver and intestine microsomes, but biphasic kinetics in the kidney and brain microsomes.3. In conclusion, we clarified that tissue and species differences exist in serotonin glucuronidation. It is necessary to take these potential differences into account when considering the pharmacodynamics and pharmacokinetics of serotonin.