Glycine-15N
(Synonyms: 甘氨酸 15N) 目录号 : GC64249
Glycine-15N 是一种 15N 标记的 Glycine。Glycine 是中枢神经系统的一种抑制性神经递质，同时也是 glutamate 的一种联合激动剂，有促进谷氨酸能 NMDA (N-methyl-D-aspartic acid ) 受体兴奋的潜能。
Cas No.:7299-33-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Glycine-15N is the 15N-labeled Glycine. Glycine is an inhibitory neurotransmitter in the CNS and also acts as a co-agonist along with glutamate, facilitating an excitatory potential at the glutaminergic N-methyl-D-aspartic acid (NMDA) receptors[1].
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [2]. Johnson JW, et al. Glycine potentiates the NMDA response in cultured mouse brain neurons. Nature. 1987 Feb 5-11;325(6104):529-31.
| Cas No. | 7299-33-4 | SDF | Download SDF |
| 别名 | 甘氨酸 15N | ||
| 分子式 | C2H515NO2 | 分子量 | 76.06 |
| 溶解度 | H2O : 25 mg/mL (328.69 mM; Need ultrasonic and warming); H2O : 25 mg/mL (328.69 mM; Need ultrasonic) | 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 | 13.1475 mL | 65.7376 mL | 131.4752 mL |
| 5 mM | 2.6295 mL | 13.1475 mL | 26.295 mL |
| 10 mM | 1.3148 mL | 6.5738 mL | 13.1475 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 | ||||||||||
| 计算重置 | ||||||||||
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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Synthesis of 15N-labeled heterocycles via the cleavage of C-N bonds of anilines and Glycine-15N
Chem Commun (Camb) 2021 Jun 1;57(44):5442-5445.PMID:33949517DOI:10.1039/d1cc01734a.
A nitrogen replacement process that directly incorporates the 15N atom of Glycine-15N into anilines was reported. The process involves a Csp2-N bond cleavage of anilines driven by dearomatization and a Csp3-N bond cleavage of Glycine-15N driven by aromatization. A variety of 15N-labeled aromatic heterocycles can be prepared via this process.
Suppression of Glycine-15N incorporation into urinary uric acid by adenine-8-13C in normal and gouty subjects
J Clin Invest 1968 May;47(5):1193-203.PMID:5645862DOI:10.1172/JCI105808.
Adenine inhibited the de novo synthesis of purines in both normal and gouty man as shown by inhibition of the incorporation of glycine-(15)N into urinary uric acid without altering the incorporation of glycine-(15)N into urinary creatinine. The diminished purine synthesis did not result in a diminution in the 24 hr excretion of uric acid. This observation was explainable in part by the prompt conversion of adenine to uric acid. In addition to this direct conversion, adenine-8-(13)C provided a slow and prolonged contribution to urinary uric acid.A feedback inhibition of purine synthesis by nucleotides derived from adenine provides the best interpretation of these results.
Renal urate excretion in five cases of hypouricemia with an isolated renal defect of urate transport
J Rheumatol 1977 Spring;4(1):86-94.PMID:886556doi
Renal urate excretion was studied in two familial, one suspected familial, and two isolated cases of hypouricemia due to a renal defect. All had very low plasma urate concentrations. In four cases, the urate clearances were approximately the same as the creatinine clearances, and in one case reduced to about one-third. In all cases the urate clearances were minimally diminished by both pyrazinamide and probenecid. This renal response to the drugs is probably due to and isolated tubular defect in the reabsorptive transport mechanism of urate. Following intravenous administration of uric acid, one patient excreted uric acid in the urine more rapidly than a normal subject. In this patient, uric acid secretion from renal tubules was clearly demonstrated during infusion of uric acid. In de novo synthesis of purine, no definite abnormalities were found by incorporation of Glycine-15N to uric acid.