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Arecaidine Sale

(Synonyms: 槟榔次碱) 目录号 : GC60596


Arecaidine Chemical Structure

Cas No.:499-04-7

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Arecaidine, a pyridine alkaloid, is a potent GABA uptake inhibitor. Arecaidine is a substrate of H+-coupled amino acid transporter 1 (PAT1, SLC36A1) and competitively inhibits L-proline uptake[1][2].

[1]. D Lodge, et al. Effects of the Areca nut constituents arecaidine and guvacine on the action of GABA in the cat central nervous system. Brain Res. 1977 Nov 18;136(3):513-22. [2]. Valerie Voigt, et al. Transport of the areca nut alkaloid arecaidine by the human proton-coupled amino acid transporter 1 (hPAT1). J Pharm Pharmacol. 2013 Apr;65(4):582-90.

Chemical Properties

Cas No. 499-04-7 SDF
别名 槟榔次碱
Canonical SMILES O=C(C1=CCCN(C)C1)O
分子式 C7H11NO2 分子量 141.17
溶解度 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 7.0837 mL 35.4183 mL 70.8366 mL
5 mM 1.4167 mL 7.0837 mL 14.1673 mL
10 mM 0.7084 mL 3.5418 mL 7.0837 mL
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给药剂量 mg/kg 动物平均体重 g 每只动物给药体积 ul 动物数量
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Research Update

Minimal Arecaidine concentrations showing a promotion effect during DMBA-induced hamster cheek pouch carcinogenesis

J Oral Pathol Med 1996 Feb;25(2):65-8.PMID:8667258DOI:10.1111/j.1600-0714.1996.tb00194.x.

The purpose of the present study was to determine the minimal Arecaidine concentrations showing a synergistic effect on DMBA-induced hamster cheek pouch carcinogenesis. One hundred and twelve male adult Syrian golden hamsters were divided into 16 groups, each containing seven animals. After eight weeks of DMBA initiation and then four weeks of Arecaidine promotion, 100% tumor incidence was found with Arecaidine concentrations of 400 micrograms/ml and 500 micrograms/ml; average tumor numbers were 1.86 +/- 0.63 and 1.86 +/- 0.93 respectively (P < 0.05). After four weeks of DMBA and a subsequent eight weeks of Arecaidine painting, all hamsters developed visible tumors with Arecaidine concentrations of 900 micrograms/ml and 1000 micrograms/ml; average tumor numbers were 1.86 +/- 0.82 and 2.14 +/- 1.09 respectively (P < 0.05). The tumor dimensions varied little and differences were not statistically significant. Without DMBA pretreatment, regardless of the high Arecaidine concentrations (1000 micrograms/ml, 2000 micrograms/ml and 3000 micrograms/ml) applied, no visible tumor growth was observed; only hyperkeratosis and inflammation could be discerned histologically. Thus, the minimal concentrations of Arecaidine displaying a synergistic effect in the DMBA-induced hamster cheek pouch of carcinogenesis were found to be 400 micrograms/ ml applied for four weeks after eight weeks of DMBA application, and 900 micrograms/ml applied for eight weeks after four weeks of DMBA painting. These findings may be useful for other studies concerning the tumorgenicity of Arecaidine.

Synthesis, Biological Evaluation, and Docking Studies of Antagonistic Hydroxylated Arecaidine Esters Targeting mAChRs

Molecules 2022 May 16;27(10):3173.PMID:35630651DOI:10.3390/molecules27103173.

The muscarinic acetylcholine receptor family is a highly sought-after target in drug and molecular imaging discovery efforts aimed at neurological disorders. Hampered by the structural similarity of the five subtypes' orthosteric binding pockets, these efforts largely failed to deliver subtype-selective ligands. Building on our recent successes with arecaidine-derived ligands targeting M1, herein we report the synthesis of a related series of 11 hydroxylated Arecaidine esters. Their physicochemical property profiles, expressed in terms of their computationally calculated CNS MPO scores and HPLC-logD values, point towards blood-brain barrier permeability. By means of a competitive radioligand binding assay, the binding affinity values towards each of the individual human mAChR subtypes hM1-hM5 were determined. The most promising compound of this series 17b was shown to have a binding constant towards hM1 in the single-digit nanomolar region (5.5 nM). Similar to our previously reported arecaidine-derived esters, the entire series was shown to act as hM1R antagonists in a calcium flux assay. Overall, this study greatly expanded our understanding of this recurring scaffolds' structure-activity relationship and will guide the development towards highly selective mAChRs ligands.

Transport of the areca nut alkaloid Arecaidine by the human proton-coupled amino acid transporter 1 (hPAT1)

J Pharm Pharmacol 2013 Apr;65(4):582-90.PMID:23488788DOI:10.1111/jphp.12006.

Objectives: The pyridine alkaloid Arecaidine is an ingredient of areca nut preparations. It is responsible for many physiological effects observed during areca nut chewing. However, the mechanism underlying its oral bioavailability has not yet been studied. We investigated whether the H⁺-coupled amino acid transporter 1 (PAT1, SLC36A1), which is expressed in the intestinal epithelium, accepts Arecaidine, arecoline, isoguvacine and other derivatives as substrates. Methods: Inhibition of L-[³H]proline uptake by Arecaidine and derivatives was determined in Caco-2 cells expressing hPAT1 constitutively and in HeLa cells transiently transfected with hPAT1-cDNA. Transmembrane transport of Arecaidine and derivatives was measured electrophysiologically in Xenopus laevis oocytes. Key findings: Arecaidine, guvacine and isoguvacine but not arecoline strongly inhibited the uptake of L-[³H]proline into Caco-2 cells. Kinetic analyses revealed the competitive manner of L-proline uptake inhibition by Arecaidine. In HeLa cells transfected with hPAT1-cDNA an affinity constant of 3.8 mm was obtained for Arecaidine. Electrophysiological measurements at hPAT1-expressing X. laevis oocytes demonstrated that Arecaidine, guvacine and isoguvacine are transported by hPAT1 in an electrogenic manner. Conclusion: We conclude that hPAT1 transports Arecaidine, guvacine and isoguvacine across the apical membrane of enterocytes and that hPAT1 might be responsible for the intestinal absorption of these drug candidates.

Quantification of Salivary Arecoline, Arecaidine and N-Methylnipecotic Acid Levels in Volunteers by Liquid Chromatography-Tandem Mass Spectrometry

J Anal Toxicol 2015 Nov-Dec;39(9):714-9.PMID:26232451DOI:10.1093/jat/bkv077.

Relatively little is known about the metabolism of areca nut in human saliva. We here describe the simultaneous quantification of areca nut metabolites: arecoline, Arecaidine and N-methylnipecotic acid in saliva samples after chewing one 5 g areca nut by using liquid chromatography-tandem mass spectrometry (LC-MS-MS). Time courses of salivary areca nut metabolites in five adult male areca nut chewer volunteers were investigated. The limits of quantification were all 1.25 ng/mL for arecoline, Arecaidine and N-methylnipecotic acid. Intra- and interday imprecisions were <4.2 and 13.6%, respectively. The within-day accuracy ranged from 82.2 to 116.7%, and the between-day accuracy ranged from 78.3 to 115.6%. Through areca nut chewing time course study, we found that salivary arecoline, Arecaidine and N-methylnipecotic acid concentrations varied greatly over time between experiment individuals. Our findings suggest that arecoline might be metabolized slightly to Arecaidine at 30 min after areca nut chewing and arecoline might be metabolized slightly to N-methylnipecotic acid at 25 min after areca nut chewing in the mouth. We first provide simultaneous quantification of human salivary arecoline, Arecaidine and N-methylnipecotic acid levels using LC-MS-MS. This method may facilitate future research design in the pathogenic effects of areca nut exposure.

A metabolomic approach to the metabolism of the areca nut alkaloids arecoline and Arecaidine in the mouse

Chem Res Toxicol 2006 Jun;19(6):818-27.PMID:16780361DOI:10.1021/tx0600402.

The areca alkaloids comprise arecoline, Arecaidine, guvacoline, and guvacine. Approximately 600 million users of areca nut products, for example, betel quid chewers, are exposed to these alkaloids, principally arecoline and Arecaidine. Metabolism of arecoline (20 mg/kg p.o. and i.p.) and Arecaidine (20 mg/kg p.o. and i.p.) was investigated in the mouse using a metabolomic approach employing ultra-performance liquid chromatography-time-of-flight mass spectrometric analysis of urines. Eleven metabolites of arecoline were identified, including Arecaidine, arecoline N-oxide, Arecaidine N-oxide, N-methylnipecotic acid, N-methylnipecotylglycine, arecaidinylglycine, arecaidinylglycerol, Arecaidine mercapturic acid, arecoline mercapturic acid, and arecoline N-oxide mercapturic acid, together with nine unidentified metabolites. Arecaidine shared six of these metabolites with arecoline. Unchanged arecoline comprised 0.3-0.4%, Arecaidine 7.1-13.1%, arecoline N-oxide 7.4-19.0%, and N-methylnipecotic acid 13.5-30.3% of the dose excreted in 0-12 h urine after arecoline administration. Unchanged Arecaidine comprised 15.1-23.0%, and N-methylnipecotic acid 14.8%-37.7% of the dose excreted in 0-12 h urine after Arecaidine administration. The major metabolite of both arecoline and Arecaidine, N-methylnipecotic acid, is a novel metabolite arising from carbon-carbon double-bond reduction. Another unusual metabolite found was the monoacylglyceride of Arecaidine. What role, if any, that is played by these uncommon metabolites in the toxicology of arecoline and Arecaidine is not known. However, the enhanced understanding of the metabolic transformation of arecoline and Arecaidine should contribute to further research into the clinical toxicology of the areca alkaloids.