108535-01-9

Basic information

• Product Name: 5,5'-dihydroxy-4,4'-bitryptamine
• Synonyms: 5,5'-dihydroxy-4,4'-bitryptamine;3,3'-Bis(2-aminoethyl)-4,4'-bi[1H-indole-5-ol];5,5'-Dihydroxy-4,4'-bi(1H-indole-3-ethanamine)
• CAS NO: 108535-01-9
• Molecular Formula: C₂₀H₂₂N₄O₂
• Molecular Weight: 350.41
• Mol File: 108535-01-9.mol
• Article Data: 3

Chemical Properties

• Boiling Point: 689.7°Cat760mmHg
• Flash Point: 370.9°C
• Appearance: /
• Density: 1.404g/cm³
• CAS DataBase Reference: 5,5'-dihydroxy-4,4'-bitryptamine(CAS DataBase Reference)
• NIST Chemistry Reference: 5,5'-dihydroxy-4,4'-bitryptamine(108535-01-9)
• EPA Substance Registry System: 5,5'-dihydroxy-4,4'-bitryptamine(108535-01-9)

Safety Data

• Hazardous Substances Data: 108535-01-9(Hazardous Substances Data)

Upstream product

• 52-90-4 L-Cysteine 
• 153-98-0 serotonin hydrochloride 
• 50-67-9 3-(2-aminoethyl)-1H-indol-5-ol 
• 69-89-6 xanthine 

Relevant articles and documents

Oxidation of serotonin by superoxide radical: Implications to neurodegenerative brain disorders

Many new lines of evidence implicate both superoxide anion radical (O2.-) and biogenic amine neurotransmitters in the pathological mechanisms that underlie neuronal damage caused by methamphetamine (MA), glutamate- mediated oxidative toxicity, ischemia-reperfusion, and other neurodegenerative brain disorders. In this investigation the oxidation of 5- hydroxytryptamine (5-HT, serotonin) by an O2.- -generating system (xanthine/xanthine oxidase) in buffered aqueous solution at pH 7.4 has been studied. The major product of the O2.- -mediated oxidation of 5-HT is tryptamine-4,5-dione (T-4,5-D). However, O2.- and H2O2, cogenerated by the xanthine oxidase-mediated oxidation of xanthine to uric acid, together react with trace levels of iron that contaminate buffer constituents to give a chemically ill-defined oxo-iron species. This species mediates the oxidation of 5-HT to a C(4)-centered carbocation intermediate that reacts with 5-HT to give 5,5'-dihydroxy-4,4'-bitryptamine (4,4'-D) and with uric acid to give 9-[3-(2-aminoethyl)-5-hydroxy-1H-indol-4-yl]-2,6,8-triketo- 1H,3H,7H-purine (7) as the major products. These products differ from those formed in the HO.-mediated oxidation of 5-HT under similar conditions. When the reaction is carried out in the presence of the intraneuronal nucleophile glutathione (GSH), T-4,5-D is scavenged to give 7-(S-glutathionyl)tryptamine- 4,5-dione, whereas the putative carbocation intermediate is scavenged to give 4-(S-glutathionyl)-5-hydroxytryptamine. T-4,5-D also reacts with the sulfhydryl residues of a model protein, alcohol dehydrogenase, and inhibits its activity. Previous investigators have proposed that T-4,5-D is a serotonergic neurotoxin. This raises the possibility that T-4,5-D and perhaps other putative intraneuronal metabolites formed by the O2.-/H2O2/oxo- iron-mediated oxidations of 5-HT might be endotoxins that contribute to neurodegeneration in brain regions innervated by serotonergic neurons caused by MA, ischemia-reperfusion, and other neurodegenerative brain disorders.

Further insights into the oxidation chemistry of 5-hydroxytryptamine

An important product of electrochemical oxidation of 5-hydroxytryptamine (5-HT) in acid solution is the purple compound tryptamine-4,5-dione (6). However, any attempt to concentrate a solution containing 6 causes it to disappear. The most important reaction of 6 is dimerization to give another purple compound 7,7'-bi-(5-hydroxytryptamine-4-one). Dione 6 can also apparently react with 2,4'-bi-5-hydroxytryptamine to give the trimer 4-[7'-(tryptamine-4,5-dione)]-2,4'-bi-5-hydroxytryptamine. Finally, 6 and other oxidation products of 5-HT react during the concentration step to yield what appears to be a trimer or perhaps a higher oligomer. This oligomer has not been identified, but it has been shown to decompose to give, in part, the neurotoxin 5-hydroxytryptamine-4,7-dione.