AM630

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AM630

本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。

CAS NO:

164178-33-0

包装与价格：

包装	价格(元)
5mg	电议
10mg	电议
50mg	电议
100mg	电议

产品介绍

化学性质

Physical Appearance	A solid
Storage	Store at -20°C
M.Wt	504.36
Cas No.	164178-33-0
Formula	C₂₃H₂₅IN₂O₃
Synonyms	AM 630;AM-630
Solubility	≥25.2 mg/mL in DMSO; insoluble in H2O; ≥2.53 mg/mL in EtOH with gentle warming and ultrasonic
Chemical Name	[6-iodo-2-methyl-1-(2-morpholin-4-ylethyl)indol-3-yl]-(4-methoxyphenyl)methanone
Canonical SMILES	CC1=C(C2=C(N1CCN3CCOCC3)C=C(C=C2)I)C(=O)C4=CC=C(C=C4)OC
运输条件	蓝冰运输或根据您的需求运输。
一般建议	为了使其更好的溶解，请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异，仅做参考。若实验所需浓度过大至产品溶解极限，请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存，请尽快用完。

资料参考

AM630是一种选择性的和竞争性的大麻素受体拮抗剂，作用于CB1受体和CB2受体，Ki值分别为5 μM和31.2 nM[1]。

在转染CB1的CHO细胞中，AM630显著抑制毛喉素刺激的cAMP的产生。在转染CB2的细胞中，AM630促进毛喉素刺激的cAMP的产生，EC50值为230.4 nM。AM630也抑制GTPγS与转染CB2细胞的细胞膜的结合。此外，在TG感觉神经元中，AM630可激活TRPA1通道，随后使TRPA1和TRPV1通道脱敏。而且，在WT小鼠中，AM630显著减弱辣椒素（CAP）诱导的热痛觉过敏[1，2]。

参考文献：
1. Ross R A, Brockie H C, Stevenson L A, et al. Agonist-inverse agonist characterization at CB1 and CB2 cannabinoid receptors of L759633, L759656 and AM630. British journal of pharmacology, 1999, 126(3): 665-672.
2. Patil M, Patwardhan A, Salas M M, et al. Cannabinoid receptor antagonists AM251 and AM630 activate TRPA1 in sensory neurons. Neuropharmacology, 2011, 61(4): 778-788.

试验操作

Cell experiment:[1]
Cell lines	Trigeminal ganglia (TG) sensory neurons
Reaction Conditions	10 μM AM630 for 3 min incubation
Applications	The application of cannabinoid receptor antagonist AM630 (10 μM) activated a robust Ca²⁺accumulation in a subset (35 ~ 40%) of TG neurons. The AM630-evoked Ca²⁺influxes into TG sensory neurons were concentration-dependent, with an EC50 value being 15.6 μM.
Animal experiment:[2]
Animal models	Swiss ICR mice
Dosage form	1, 2 or 3 mg/kg Administered intraperitoneally twice a day for 7 days
Applications	Chronic AM630 treatment alleviated anxiety-like behaviors in the light-dark box and elevated plus maze tests. Meanwhile, chronic AM630 treatment increased gene and reduced protein expression of CB2 receptors, GABA_Aα2and GABA_Aγ2in cortex and amygdala.
Note	The technical data provided above is for reference only.
	References: 1. Patil M, Patwardhan A, Salas MM, et al. Cannabinoid receptor antagonists AM251 and AM630 activate TRPA1 in sensory neurons. Neuropharmacology, 2011, 61(4): 778-788. 2. García-Gutiérrez MS, García-Bueno B, Zoppi S, et al. Chronic blockade of cannabinoid CB2 receptors induces anxiolytic-like actions associated with alterations in GABA(A) receptors. British Journal of Pharmacology, 2012, 165(4): 951-964.