NECA
(Synonyms: 5'-N-乙基酰胺基腺苷,NECA) 目录号 : GC15304
NECA (NECA) 是一种非选择性腺苷受体激动剂。
Cas No.:35920-39-9
Sample solution is provided at 25 µL, 10mM.
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Animal experiment: | Male Wistar rats are used in this experiment. These animals range in weight between 350 and 425 g. They are housed individually in hanging wire cages under a 12-h light/dark cycle. The effects of 5'-N-Ethylcarboxamidoadenosine (NECA) are tested in four rats. In the experiment, either 5'-N-Ethylcarboxamidoadenosine (NECA) (5, 7.5, 10, 20 μg/kg) or vehicle (saline) is administered intraperitoneally 15 min prior to the start of test sessions. 5'-N-Ethylcarboxamidoadenosine (NECA) is administered following a random order crossover design. In most cases, animals are tested twice with the same dose[1]. |
References: [1]. Knapp CM, et al. Adenosine agonists CGS 21680 and NECA inhibit the initiation of cocaine self-administration. Pharmacol Biochem Behav. 2001 Apr;68(4):797-803. | |
NECA is a non-selective agnonist of adenosine receptor with the concentration of 10 μM [1].
Adenosine is an important endogenous signaling molecule and plays a pivotal role in regulating a wide range of physiological functions, such as immune system response and inflammation, via cooperated with its receptor. It has been shown that adenosine receptor agonists can be either anti-inflammatory or proinflammatory, and the dual role of the adenosine receptor agonists causing these opposing effects should provide a better guide for therapeutic intervention used for different diseases in clinic [2].
When tested with primary murine microglia cells, NECA treatment significantly inhibited the productions of CXCL10 and TNF-αinduced by LPS [1, 3].
In CD73(-/-) mice model infected with T. gondii cysts, administration of NECA protected CD73(-/-) mice against T. gondii-induced immunopathology via agonist adenosine receptor, which suggested that CD73-generated adenosine was critical for immune regulation during T.gondii infection [1]. In a mouse model with human uveitis, injection of NECA at an early stage after immunization with peptides 1-20 inhibited effect on both Th1 and Th17 responses [1, 4]. When tested with adult male Wistar rats of amygdala-kindled seizures, intravenous infusion of NECA after administration of PHT increased the PHT level in brain compared with control group by antognisting adenosine receptor thus strengthened the anticonvulsant properties of PHT against amygdala kindled seizures [5].
NECA是腺苷受体的非选择性激动剂，浓度为10 μM [1]。
腺苷是一种重要的内源性信号分子，通过与其受体协同作用，发挥调节多种生理功能的关键作用，如免疫系统反应和炎症等。已经证明，腺苷受体激动剂既可以是抗炎性的，也可以是促炎性的，腺苷受体激动剂引起这些相反效应的双重作用应该为临床上不同疾病的治疗干预提供更好的指导 [2]。
在小鼠原代小胶质细胞中进行实验，NECA处理显著抑制了LPS诱导的CXCL10和TNF-α产生[1，3]。在感染T. gondii囊泡的CD73（-/-）小鼠模型中，NECA的给药通过激动腺苷受体保护CD73（-/-）小鼠免受T. gondii诱导的免疫病理损伤，这表明CD73产生的腺苷在T.gondii感染期间的免疫调节中至关重要 [1]。在一个人类葡萄膜炎小鼠模型中，NECA注射可以在免疫肽1-20免疫后的早期阶段抑制Th1和Th17反应的作用[1，4]。在Wistar大鼠的杏仁核痉挛模型中，PHT给药后静脉注射NECA可以通过拮抗腺苷受体增强PHT的抗癫痫性质，从而增加脑内PHT水平[5]。
References:
[1]. Mahamed, D.A., L.E. Toussaint, and M.S. Bynoe, CD73-Generated Adenosine Is Critical for Immune Regulation during Toxoplasma gondii Infection. Infect Immun, 2015. 83(2): p. 721-9.
[2]. Solomou, S. and M. Korbonits, The role of ghrelin in weight-regulation disorders: Implications in clinical practice. Hormones (Athens), 2014. 13(4): p. 458-475.
[3]. Newell, E.A., et al., 2',3'-cAMP, 3'-AMP, 2'-AMP and adenosine inhibit TNF-alpha and CXCL10 production from activated primary murine microglia via A2A receptors. Brain Res, 2015. 1594: p. 27-35.
[4]. Liang, D., et al., Anti-inflammatory or proinflammatory effect of an adenosine receptor agonist on the Th17 autoimmune response is inflammatory environment-dependent. J Immunol, 2014. 193(11): p. 5498-505.
[5]. Sun, Z., et al., Activation of Adenosine Receptor Potentiates the Anticonvulsant Effect of Phenytoin Against Amygdala Kindled Seizures. CNS Neurol Disord Drug Targets, 2014.
| Cas No. | 35920-39-9 | SDF | |
| 别名 | 5'-N-乙基酰胺基腺苷,NECA | ||
| 化学名 | (2S,3S,4R,5S)-5-(6-amino-9H-purin-9-yl)-N-ethyl-3,4-dihydroxytetrahydrofuran-2-carboxamide | ||
| Canonical SMILES | O[C@H]1[C@@H](N2C3=NC=NC(N)=C3N=C2)O[C@H](C(NCC)=O)[C@H]1O | ||
| 分子式 | C12H16N6O4 | 分子量 | 308.3 |
| 溶解度 | ≥ 15.35mg/mL in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.2436 mL | 16.218 mL | 32.4359 mL |
| 5 mM | 0.6487 mL | 3.2436 mL | 6.4872 mL |
| 10 mM | 0.3244 mL | 1.6218 mL | 3.2436 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 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 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
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计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
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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