Arvanil - CAS:128007-31-8

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Arvanil (Synonyms:N-Vanillylarachidonamide)

目录号 : KCM10919 CAS No. : 128007-31-8 纯度 : ≥98%

Data Sheet 产品使用指南

Arvanil is a structural analog of capsaicin, which is the noxious active component of hot peppers of the Capsicum family. It is the amide of vanillylamine and arachidonic acid. Arvanil induces analgesia in rat and mouse models of pain. Arvanil has complex interactions with the cannabinoid system, in that it potentiates the agonist activity of endogenous cannabinoids by inhibiting the reuptake of arachidonoyl ethanolamide (AEA). It is an agonist at CB (K values of 0.25 to 0.52 μM), but not CB, receptors, and is resistant to hydrolysis by FAAH. The vasodilator, analgesic, and anti-inflammatory properties of arvanil are not clearly explained by its interactions with cannabinoid and vanilloid receptors, suggesting other possible sites of action.

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生物活性

Arvanil (N-Vanillylarachidonamide) is a mixed agonist of CB1 and TRPV1 receptors. Arvanil downregulates CD25, HLA-DR, CD134/OX40, blocks G1/S phase transition, and induces phosphorylation of Akt. Arvanil does not induce apoptosis in cells. Arvanil inhibits lymphocyte activation and ameliorates autoimmune encephalomyelitis. Arvanil can be used in research related to Huntington's disease, vomiting, and multiple sclerosis[1].

IC₅₀&Target

TRPV1 CB1

体外研究

Arvanil (10 μM; 48 h) strongly inhibits the proliferation of peripheral blood mononuclear cells (PBMCs) stimulated by OKT3, achieving an inhibition rate of 75.3% at a concentration of 10 μM, which is more effective than anandamide and capsaicin at the same concentration.
Arvanil (0.3-30 μM; 48 h) dose-dependently inhibited the proliferation of peripheral blood mononuclear cells (hPBMCs) stimulated by CD3CD28, achieving a 64.0% inhibition rate at 10 μM, while also reducing IFN-γ production but not affecting IL-5 levels at the same concentration.
Arvanil (3-10 μM; 48 h) inhibits the proliferation of IL-2-stimulated mouse CTLL-2 cells, with significant suppression observed at a concentration of 10 μM.
Arvanil (10 μM) inhibits the upregulation of activation markers CD25, HLA-DR, and CD134/OX40 on CD4+ T cells in peripheral blood mononuclear cells (hPBMCs) stimulated by OKT3[2].
Arvanil (10 μM; 48 h) does not induce apoptosis in CD4+ T cells derived from peripheral blood mononuclear cells (hPBMCs) stimulated with OKT3 [2].
Arvanil (10 μM; 48 h) can block the G1/S phase transition of peripheral blood mononuclear cells (hPBMCs) stimulated by OKT3 [2].

Cell Proliferation Assay

Cell Line:

murine CTLL-2 cells stimulated with interleukin-2 (IL-2)

Concentration:

3-10 μM

Incubation Time:

48 hours

Result:

Inhibited IL-2-stimulated CTLL-2 proliferation, with statistically significant inhibition observed at 10 μM (p<0.05); the inhibitory effect at 3 μM was less pronounced.

Cell Cycle Analysis

Cell Line:

OKT3-stimulated hPBMCs

Concentration:

10 μM

Incubation Time:

48 hours

Result:

Increased G1-phase cells to 86% and reduced S-phase cells to 13%.

体内研究

Arvanil (2 mg/kg; intraperitoneal injection; A single dose can alleviate the symptoms of excessive movement (increased activity, decreased rest) in a Huntington's disease rat model, which is associated with an increase in glutamate levels in the globus pallidus, and can also reduce the autonomous activity ability of normal rats [1].
Arvanil (2 mg/kg; intraperitoneal injection; Single dose administration can reduce the autonomous activity and exploratory behavior of normal rats, which is associated with an increase in GABA content in the pallidum [1].
Arvanil (1-2 mg/kg; intraperitoneal injection; Single administration of M6G 15 minutes before treatment can dose dependently inhibit the nausea and vomiting induced by morphine 6-glucoside in ferrets by activating CB1 and TRPV1 receptors; The dose of 2 mg/kg can significantly reduce the frequency of nausea and vomiting attacks, and this effect can be reversed by selective antagonists of the two receptors mentioned above.
Arvanil (0.5 mg/kg; administered twice before and after 3 days of experimental autoimmune encephalomyelitis (EAE) induction) treatment significantly improved experimental autoimmune encephalomyelitis in female SJL/J mice, reducing cumulative disease index by 48.2%, peak clinical score by 56.7%, maximum weight loss rate by 66.8%, and central nervous system inflammatory lesions by 51.3% [2].

Animal Model:	Sprague-Dawley (male, 3-4 months old, 300-400 g, bilateral intrastriatal injection of 375 nmol 3-nitropropionic acid per striatum, used 14 days post-lesion)【1】
Dosage:	2 mg/kg
Administration:	i.p.; single acute dose
Result:	Significantly reduced increased ambulatory activity (F(1,21)=18.74, P < 0.0005). Increased time spent in inactivity (F(1,21)=40.10, P < 0.0001). Enhanced lesion-induced reductions in stereotypic activity (F(1,22)=21.91, P < 0.0001) and hole entries (F(1,22)=43.18, P < 0.0001). Increased glutamate contents in the globus pallidus (F(1,21)=5.89, P < 0.05). Did not reverse GABA, glutamate, or dopamine deficits in the caudate-putamen.

Animal Model:	Sprague-Dawley (male, 3-4 months old, 300-400 g, bilateral intrastriatal injection of saline vehicle, allowed 14 days to recover)
Dosage:	2 mg/kg
Administration:	i.p.; single acute dose
Result:	Significantly reduced ambulatory activity, stereotypic activity, and number of hole entries. Increased time spent in inactivity. Increased GABA contents in the globus pallidus (F(1,19)=3.89, P < 0.05). Tended to increase globus pallidus GAD activity. Showed no effects on dopamine, DOPAC, TH activity, GABA, GAD activity, or glutamate contents in the caudate-putamen.

Animal Model:	Mustela putorius furo (adult male, 900-1500 g)
Dosage:	1 mg/kg; 2 mg/kg
Administration:	i.p.; single dose 15 min pre-M6G
Result:	Reduced M6G-induced emetic episodes compared to M6G alone. Dose-dependently reduced M6G-induced emetic episodes to a greater extent than the 1 mg/kg dose; this anti-emetic effect was reversed by pre-treatment with 5 mg/kg AM251 or 0.1 mg/kg IRTX, with emetic episode counts returning to levels not significantly different from M6G alone. Reduced M6G-induced vomiting episodes from 1.8 to 0.8 (P < 0.05); this effect was reversed by 5 mg/kg AM251 (to 1.4 episodes, P < 0.05 vs arvanil alone) and completely abolished by 0.1 mg/kg IRTX (to 1.8 episodes, P < 0.05 vs arvanil alone). Reduced M6G-induced tongue licking movements from 6.6 licks/h to 2.3 licks/h (P < 0.01 vs M6G); this effect was reversed by CB₁ and TRPV₁ antagonists. Dose-dependently reduced voluntary activity minutes in a 1-hour observation period; this sedative effect was not reversed by AM251 or IRTX. Pre-treatment with 5 mg/kg AM630 did not reduce the anti-emetic effects of arvanil (3.5 emetic episodes vs 1.8 emetic episodes with arvanil alone, P > 0.05).

分子式

C₂₈H₄₁NO₃

分子量

439.6

CAS号

128007-31-8

中文名称

N-[(4-羟基-3-甲氧基苯基)甲基]-5Z,8Z,11Z,14Z-二十碳烷四氨基;壬醛

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

纯度： ≥98%

Data Sheet

产品使用指南

[1]. de Lago E, et al. Arvanil, a hybrid endocannabinoid and vanilloid compound, behaves as an antihyperkinetic agent in a rat model of Huntington's disease. Brain Res. 2005;1050(1-2):210-216.

[2]. Malfitano AM, et al. Arvanil inhibits T lymphocyte activation and ameliorates autoimmune encephalomyelitis. J Neuroimmunol. 2006;171(1-2):110-119.

The molarity calculator equation

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The dilution calculator equation

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

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DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，注：如该浓度超过该批次药物DMSO溶解度，请先联系客服）；

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2. 一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。

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The molarity calculator equation

The dilution calculator equation

动物实验计算换算器