1. Metabolic Enzyme/Protease
    Protein Tyrosine Kinase/RTK
    Neuronal Signaling
  2. Endogenous Metabolite
    Trk Receptor
  3. N-Acetyl-5-hydroxytryptamine

N-Acetyl-5-hydroxytryptamine (Synonyms: N-Acetylserotonin; Normelatonin; O-Demethylmelatonin)

Cat. No.: HY-107854 Purity: 99.86%
Handling Instructions

N-Acetyl-5-hydroxytryptamine is a Melatonin precursor, and that it can potently activate TrkB receptor.

For research use only. We do not sell to patients.

N-Acetyl-5-hydroxytryptamine Chemical Structure

N-Acetyl-5-hydroxytryptamine Chemical Structure

CAS No. : 1210-83-9

Size Price Stock Quantity
10 mM * 1 mL in DMSO USD 88 In-stock
Estimated Time of Arrival: December 31
50 mg USD 80 In-stock
Estimated Time of Arrival: December 31
100 mg   Get quote  
200 mg   Get quote  

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Based on 1 publication(s) in Google Scholar

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N-Acetyl-5-hydroxytryptamine is a Melatonin precursor, and that it can potently activate TrkB receptor.

IC50 & Target[1]

Human Endogenous Metabolite




In Vitro

N-Acetyl-5-hydroxytryptamine (NAS), a precursor of Melatonin, is acetylated from serotonin by AANAT (arylalkylamine N-acetyltransferase). N-acetylserotonin activates TrkB receptor in a circadian rhythm. N-Acetyl-5-hydroxytryptamine swiftly activates TrkB in a circadian manner and exhibits antidepressant effect in a TrkB-dependent manner. N-Acetyl-5-hydroxytryptamine rapidly activates TrkB, but not TrkA or TrkC, in a neurotrophin- and MT3 receptor-independent manner[1].

In Vivo

To explore whether N-Acetyl-5-hydroxytryptamine, can trigger TrkB activation in vivo, TrkB F616A knockin mice are employed, where it has been shown that TrkB F616A activation can be selectively blocked by 1NMPP1, a derivative of kinase inhibitor PP1, leading to TrkB-null phenotypes. To assess whether N-Acetyl-5-hydroxytryptamine can mimic BDNF, cortical neurons from TrkB F616A knockin mice are prepared. In alignment with a previous report, BDNF- and NAS-mediated TrkB phosphorylation are selectively reduced by 1NMPP1 but not by K252a, whereas serotonin or Melatonin had no effect . These findings suggest that NAS strongly provokes both wild-type TrkB and TrkB F616A tyrosine phosphorylation and activation[1].

Molecular Weight









Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 250 mg/mL (1145.48 mM; Need ultrasonic)

Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 4.5819 mL 22.9095 mL 45.8190 mL
5 mM 0.9164 mL 4.5819 mL 9.1638 mL
10 mM 0.4582 mL 2.2910 mL 4.5819 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.08 mg/mL (9.53 mM); Clear solution

  • 2.

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.08 mg/mL (9.53 mM); Clear solution

  • 3.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 2.08 mg/mL (9.53 mM); Clear solution

*All of the co-solvents are provided by MCE.
Animal Administration

Two-month-old TrkB F616A mice are pretreated with 1NMPP1 in drinking water (50 μM) 1 day before the experiment, followed by administration of N-Acetyl-5-hydroxytryptamine (20 mg/kg, i.p.) or Melatonin (1 mg/kg, i.p.). Mice are killed at 1 h. The brain homogenates are analyzed by immunoblotting with anti-p-TrkB. Two- to three-month-old BDNF forebrain conditional knockout mice are injected i.p. with N-Acetyl-5-hydroxytryptamine or Melatonin. Mice are killed at 0, 0.5, 1, or 2 h following drug administration. Brain lysates are prepared and analyzed by immunoblotting with anti-phospho-TrkB Y816[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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N-Acetyl-5-hydroxytryptamineN-Acetylserotonin Normelatonin O-DemethylmelatoninEndogenous MetaboliteTrk ReceptorTropomyosin related kinase receptorInhibitorinhibitorinhibit

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