Arachidonoyl Serotonin - CAS:187947-37-1

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Arachidonoyl Serotonin (Synonyms:N-Arachidonoylserotonin; AA-5-HT)

目录号 : KCM12214 CAS No. : 187947-37-1 纯度 : ≥98%

Data Sheet 产品使用指南

Arachidonoyl serotonin is an inhibitor of fatty acid amide hydrolase (FAAH), the enzyme responsible for inactivation of anandamide and other endogenous cannabinoids. It inhibits the FAAH activity isolated from mouse neuroblastoma cells with an IC value of 12 µM. Both the K and the V of the enzyme are affected, indicating the Arachidonoyl serotonin is a very tight binding, competitive inhibitor of FAAH. Arachidonoyl serotonin does not inhibit cPLA and is essentially devoid of cannabimimetic activity.

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生物活性

Arachidonoyl Serotonin is a dual FAAH inhibitor and TRPV1 antagonist. Arachidonoyl Serotonin blocks Anandamide hydrolysis, increases brain Anandamide levels, and promotes CB1 receptor signaling in the dorsal hippocampus. Arachidonoyl Serotonin normalizes HPA axis dysregulation, reduces plasma corticosterone levels, and induces anxiolytic-like effects in mice. Arachidonoyl Serotonin reverses behavioral despair, inhibits contextual fear memory retrieval, and produces dose-dependent antinociceptive effects in rodents. Arachidonoyl Serotonin inhibits intestinal motility. Arachidonoyl Serotonin can be used to study stress-related disorders, traumatic memory and related psychiatric disorders, pain, and intestinal motility disorders.

体外研究

Arachidonoyl Serotonin (30 min) inhibited FAAH in rat meninges with an IC50 of 8 μM.
Arachidonoyl Serotonin (2 h) is a potent antagonist of hTRPV1 in HEK293 cells, with an IC50 of 0.27 μM.
Arachidonoyl Serotonin (50 μM) does not inhibit MAGL even at concentrations up to 50 μM in cell-free homogenates.

体内研究

N-arachidonoylseletonin (2.5-5 mg/kg; intraperitoneal injection; Three doses were administered 24 hours, 5 hours, and 1 hour before FST testing or sacrifice to reverse stress-induced behavioral despair and restore HPA axis dysregulation to normal. The most significant behavioral effect was observed in rats at a dose of 5 mg/kg.
N-Arachidonoylseletonin (0.1-1 mg/kg; intraperitoneal injection; 30 minutes before the test, inhibit the retrieval of situational fear memory in mice.
N-Arachidonoylseletonin (1-20 mg/kg; intraperitoneal injection; Single time; 30 minutes before labeling, significant inhibitory effects were observed on intestinal motility in mice at doses of 10 mg/kg and above, with the effect partially mediated by CB1 receptors .
N-Arachidonoylseletonin (15 mg/kg; intraperitoneal injection; Single dose significantly inhibited intestinal peristalsis in CB1 receptor deficient mice, although this effect was partially dependent on the CB1 receptor (wild-type inhibited 42% vs. mutant mice inhibited 22%).

Animal Model:	Wistar rats (male, 220-240 g, 4 h restraint stress model)
Dosage:	2.5 mg/kg; 5 mg/kg
Administration:	i.p.; three times at 24 h, 5 h, and 1 h prior to FST test or sacrifice
Result:	Reversed behavioral despair at 5 mg/kg, significantly decreasing immobility time and increasing climbing time. Completely reversed stress-induced elevation of plasma corticosterone levels at 5 mg/kg. Significantly increased BDNF mRNA and protein levels in the hippocampus at 2.5 mg/kg. Increased BDNF mRNA levels and showed a trend for increase in protein levels at 5 mg/kg. Significantly elevated anandamide (AEA) levels in the medial PFC at 2.5 mg/kg. Did not significantly alter BDNF levels in non-stressed animals except for a decrease in mRNA expression at 5 mg/kg. Caused a significant elevation of corticosterone levels in non-stressed rats at 2.5 mg/kg.

Animal Model:	Swiss mice (male, 25-30 g)
Dosage:	0.1, 0.3, and 1.0 mg/kg (i.p.); 0.125, 0.25, and 0.5 nmol (intra-hippocampal)
Administration:	i.p. (30 min before test); intra-hippocampal (10 min before test)
Result:	Decreased freezing responses at all i.p. doses (0.1, 0.3, 1 mg/kg) during the expression of contextual fear memory. Did not affect freezing when administered before conditioning at 0.3 mg/kg. Decreased freezing at intra-hippocampal doses of 0.125 and 0.25 nmol, but the 0.5 nmol dose was ineffective. Did not interfere with basal motor activity in the open field test.

Animal Model:	ICR mice (Male, 20-22 g)
Dosage:	1, 2.5, 5, 10, 15, 20 mg/kg
Administration:	i.p.; single dose; 30 min before marker
Result:	Inhibited intestinal motility in a dose-dependent manner, with significant effects starting at 10 mg/kg. Was significantly reduced by rimonabant (0.1 mg/kg) when combined with a 15 mg/kg dose. Increased the inhibitory effect of anandamide and PEA at 5 mg/kg. Increased small intestine levels of anandamide (1.85 pmol/mg lipid at 10 mg/kg vs. control 1.08 pmol/mg lipid) and 2-AG (2.30 nmol/mg lipid at 10 mg/kg vs. control 1.23 nmol/mg lipid) starting from 10 mg/kg. Increased PEA levels at 15 mg/kg (9.36 pmol/mg lipid vs. control 6.60 pmol/mg lipid).

Animal Model:	CB1 receptor-deficient mice and wild-type littermates (Female, 19-22 g)
Dosage:	15 mg/kg
Administration:	i.p.; single dose; 30 min before marker
Result:	Significantly reduced intestinal motility in CB1 receptor-deficient mice. Induced a larger reduction in motility in wild-type mice (42% inhibition) compared to CB1 receptor-deficient mice (22% inhibition).

Animal Model:	FAAH-deficient mice (Female, 19-22 g)
Dosage:	15 mg/kg
Administration:	i.p.; single dose; 30 min before marker
Result:	Significantly reduced intestinal motility in FAAH-deficient mice.

分子式

C₃₀H₄₂N₂O₂

分子量

462.67

CAS号

187947-37-1

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

-80°C

纯度： ≥98%

Data Sheet

产品使用指南

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Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2

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