5-Hydroxyindole
(Synonyms: 5-羟基吲哚) 目录号 : GC61648
A neuroactive metabolite of L-tryptophan
Cas No.:1953-54-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
5-Hydroxyindole is a neuroactive metabolite of L-tryptophan .1 It is formed from L-tryptophan by gut microbiota expressing tryptophanase (TnaA) via 5-hydroxy-L-tyrptophan and indole intermediates.1,2 5-Hydroxyindole (0.03-30 mM) potentiates transient inward currents induced by acetylcholine in Xenopus oocytes expressing α7 nicotinic acetylcholine receptors (nAChRs).3 It also potentiates ion currents induced by serotonin in N1E-115 mouse neuroblastoma cells when used at a concentration of 1 mM.4 5-Hydroxyindole (30 mg/kg) decreases gastrointestinal transit time in rats.2 It induces convulsions in rats when administered at doses ranging from 50 to 100 mg/kg.5 Serum 5-hydroxyindole levels are positively correlated with working memory in patients with schizophrenia.1
1.Huang, J., Tong, J., Zhang, P., et al.Effects of neuroactive metabolites of the tryptophan pathway on working memory and cortical thickness in schizophreniaTransl. Psychiatry11(1)198(2021) 2.Waclawiková, B., Bullock, A., Schwalbe, M., et al.Gut bacteria-derived 5-hydroxyindole is a potent stimulant of intestinal motility via its action on L-type calcium channelsPLoS Biol.19(1)e3001070(2021) 3.Zwart, R., De Filippi, G., Broad, L.M., et al.5-Hydroxyindole potentiates human α7 nicotinic receptor-mediated responses and enhances acetylcholine-induced glutamate release in cerebellar slicesNeuropharmacology43(3)374-384(2002) 4.van Hooft, J.A., van der Haar, E., and Vijverberg, H.P.Allosteric potentiation of the 5-HT3 receptor-mediated ion current in N1E-115 neuroblastoma cells by 5-hydroxyindole and analoguesNeuropharmacology36(4-5)649-653(1997) 5.Mannaioni, G., Carpenedo, R., and Moroni, F.5-hydroxyindole causes convulsions and increases transmitter release in the CA1 region of the rat hippocampusBr. J. Pharmacol.138(1)245-253(2003)
| Cas No. | 1953-54-4 | SDF | |
| 别名 | 5-羟基吲哚 | ||
| Canonical SMILES | OC1=CC2=C(NC=C2)C=C1 | ||
| 分子式 | C8H7NO | 分子量 | 133.15 |
| 溶解度 | 储存条件 | Store at -20°C | |
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1 mg | 5 mg | 10 mg |
| 1 mM | 7.5103 mL | 37.5516 mL | 75.1033 mL |
| 5 mM | 1.5021 mL | 7.5103 mL | 15.0207 mL |
| 10 mM | 0.751 mL | 3.7552 mL | 7.5103 mL |
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5-Hydroxyindole-Based EZH2 Inhibitors Assembled via TCCA-Catalyzed Condensation and Nenitzescu Reactions
Molecules 2020 Apr 28;25(9):2059.PMID:32354194DOI:10.3390/molecules25092059.
5-Hydroxyindole derivatives have various demonstrated biological activities. Herein, we used 5-Hydroxyindole as a synthetic starting point for structural alterations in a combinatorial process to synthesize 22 different compounds with EZH2 inhibitor pharmacophores. A series of 5-hydroxyindole-derived compounds were screened inhibitory activities against K562 cells. According to molecular modeling and in vitro biological activity assays, the preliminary structure-activity relationship was summarized. Compound L-04 improved both the H3K27Me3 reduction and antiproliferation parameters (IC50 = 52.6 μM). These findings revealed that compound L-04 is worthy of consideration as a lead compound to design more potent EZH2 inhibitors. During the preparation of compounds, we discovered that trichloroisocyanuric acid (TCCA) is a novel catalyst which demonstrates condensation-promoting effects. To gain insight into the reaction, in situ React IR technology was used to confirm the reactivity. Different amines were condensed in high yields with β-diketones or β-ketoesters in the presence of TCCA to afford the corresponding products in a short time (10~20 min), which displayed some advantages and provided an alternative condensation strategy.
Gut bacteria-derived 5-Hydroxyindole is a potent stimulant of intestinal motility via its action on L-type calcium channels
PLoS Biol 2021 Jan 22;19(1):e3001070.PMID:33481771DOI:10.1371/journal.pbio.3001070.
Microbial conversion of dietary or drug substrates into small bioactive molecules represents a regulatory mechanism by which the gut microbiota alters intestinal physiology. Here, we show that a wide variety of gut bacteria can metabolize the dietary supplement and antidepressant 5-hydroxytryptophan (5-HTP) to 5-Hydroxyindole (5-HI) via the tryptophanase (TnaA) enzyme. Oral administration of 5-HTP results in detection of 5-HI in fecal samples of healthy volunteers with interindividual variation. The production of 5-HI is inhibited upon pH reduction in in vitro studies. When administered orally in rats, 5-HI significantly accelerates the total gut transit time (TGTT). Deciphering the underlying mechanisms of action reveals that 5-HI accelerates gut contractility via activation of L-type calcium channels located on the colonic smooth muscle cells. Moreover, 5-HI stimulation of a cell line model of intestinal enterochromaffin cells results in significant increase in serotonin production. Together, our findings support a role for bacterial metabolism in altering gut motility and lay the foundation for microbiota-targeted interventions.
Measurement of 5-Hydroxyindole compounds during L-5-HTP treatment in depressed patients
Folia Psychiatr Neurol Jpn 1976;30(4):463-73.PMID:1088138DOI:10.1111/j.1440-1819.1976.tb02669.x.
L-5-hydroxytryptophan (L-5-HTP), and immediate serotonin precursor, was given to the hospitalized depressed patients in an open clinical trial of the Phase 2 study for antidepressive effects of the agent. A relatively small dose, 150 mg orally for seven days, was employed, and seven of 14 patients responded to the treatment with mild or moderate amelioration of their depressive symptoms. Urinary excretion levels and plasma concentrations of three 5-Hydroxyindole compounds, 5-HTP, 5-HT and 5-HIAA, were measured during the drug treatment. Approximately 70% of the orally administered dose of L-5-HTP was recovered from the urine of depressed patients. Major part of urinary indoleamine metabolites was free and conjugate 5-HIAA. Excretion levels of these compounds in urine were not consistently altered in the depressed patients as compared to those in normal subjects. Clinical response to L-5-HTP treatment appeared to have some correlation with the biochemical measures in the depressed patients, that is, non-responders exhibited significantly lower excretion levels of 5-HT and 5-HIAA in urine, and lower plasma levels of 5-HT than responders. Administered L-5-HTP may not be fully utilized in the depressed patients who did not react to the agent.
Effect of 5-Hydroxyindole on ethanol potentiation of 5-hydroxytryptamine (5-HT)3 receptor-activated ion current in NCB-20 neuroblastoma cells
Neurosci Lett 2003 Feb 20;338(1):72-6.PMID:12565143DOI:10.1016/s0304-3940(02)01336-8.
We examined the effect of 5-Hydroxyindole (5-HI) on the potentiation of 5-hydroytryptamine (5-HT)(3) receptor function by ethanol (EtOH) so as to study whether EtOH potentiates channel function through increasing activation or blocking desensitization. We measured 5-HT(3) receptor current using a whole-cell voltage clamp technique with a method of rapid drug application in NCB-20 neuroblastoma cells. The 5-HI, an agent that block receptor desensitization, increased the decay time constant (tau), not the peak of 5-HT(3) receptor-mediated currents induced by 10 microM 5-HT. EtOH did not change the peak amplitude and tau of the current induced by 10 microM 5-HT. Coapplication of EtOH and 5-HI with 5-HT caused no increase in the peak currents, but tau was further increased. Therefore, a further block in desensitization could be induced by 5-HI, despite the presence of EtOH. These results indicate that EtOH potentiates 5-HT(3) receptor function, with these effects due at least in part by increasing channel activation rather than by blocking desensitization.
5-Hydroxyindole causes convulsions and increases transmitter release in the CA1 region of the rat hippocampus
Br J Pharmacol 2003 Jan;138(1):245-53.PMID:12522096DOI:10.1038/sj.bjp.0705007.
1 5-Hydroxyindole (5-OHi) is a proposed tryptophan metabolite able to cause convulsions when systemically injected into rodents. We studied its effects using microdialysis in vivo and electrophysiological approaches in vitro. 2 Local administration of 5-OHi into the CA1 region of the rat hippocampus, via a microdialysis probe, significantly increased glutamate concentrations in the dialysates. 3 In rat hippocampal slices, using extracellular recordings in the CA1 region, 5-OHi (30-300 microM) increased the amplitude of population spikes and fEPSPs. 4 In the same preparation, using intracellular recordings in CA1 pyramidal neurons, 5-OHi reduced the latency of firing induced by direct depolarization and increased both evoked excitatory and slow inhibitory postsynaptic potential amplitudes, without affecting the resting membrane potential, the after-hyperpolarization or the neuronal input resistance. It also altered GABA(A)-mediated neurotransmission by increasing the frequency and the amplitude of pharmacologically isolated spontaneous inhibitory postsynaptic currents (sIPSC). 5 In separate experiments, performed by measuring AMPA or NMDA-induced depolarization in cortical wedges, 5-OHi did not modify glutamate receptor agonist responses. 6 Our results show that 5-OHi causes convulsions, modifies the properties and the function of the hippocampal circuitry, and facilitates the output of both excitatory and inhibitory transmitters.