Purine
(Synonyms: 嘌呤; Purine (6CI,8CI); 3,5,7-Triazaindole; 3H-Imidazo[4,5-d]pyrimidine; 6H-Imidazo[4,5-d]pyrimidine; 7H-Purine; Isopurine; NSC 753; β-Purine) 目录号 : GC38275An aromatic heterocyclic organic compound
Cas No.:120-73-0
Sample solution is provided at 25 µL, 10mM.
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Purine is an aromatic heterocyclic organic compound. It is biosynthesized from amino acids and bicarbonate.1 Purine is the core structure of the nucleobases adenine and guanine, the nucleosides adenosine and guanosine , and the nucleotides, adenosine mono- , di- , and triphosphate , and guanosine mono- , di-, and triphosphate .
1.Berg, J.M., Tymoczko, J.L., and Stryer, L.Biochemistry(2002)
Cas No. | 120-73-0 | SDF | |
别名 | 嘌呤; Purine (6CI,8CI); 3,5,7-Triazaindole; 3H-Imidazo[4,5-d]pyrimidine; 6H-Imidazo[4,5-d]pyrimidine; 7H-Purine; Isopurine; NSC 753; β-Purine | ||
Canonical SMILES | C12=NC=NC=C1N=CN2 | ||
分子式 | C5H4N4 | 分子量 | 120.11 |
溶解度 | DMF: 20 mg/ml,DMSO: 30 mg/ml,PBS (pH 7.2): 10 mg/ml | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 8.3257 mL | 41.6285 mL | 83.257 mL |
5 mM | 1.6651 mL | 8.3257 mL | 16.6514 mL |
10 mM | 0.8326 mL | 4.1629 mL | 8.3257 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 | 只 | |||
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% DMSO % % Tween 80 % saline | ||||||||||
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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,
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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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Purine metabolites and complex diseases: role of genes and nutrients
Curr Opin Clin Nutr Metab Care 2021 Jul 1;24(4):296-302.PMID:33928921DOI:10.1097/MCO.0000000000000764.
Purpose of review: Purines have several important physiological functions as part of nucleic acids and as intracellular and extracellular signaling molecules. Purine metabolites, particularly uric acid, have been implicated in congenital and complex diseases. However, their role in complex diseases is not clear and they have both beneficial and detrimental effects on disease pathogenesis. In addition, the relationship between purines and complex diseases is affected by genetic and nutritional factors. This review presents latest findings about the relationship between purines and complex diseases and the effect of genes and nutrients on this relationship. Recent findings: Evidence from recent studies show strong role of purines in complex diseases. Although they are causal in only few diseases, our knowledge about their role in other diseases is still evolving. Of all the purines, uric acid is the most studied. Uric acid acts as an antioxidant as well as a prooxidant under different conditions, thus, its role in disease also varies. Other purines, adenosine and inosine have been less studied, but they have neuroprotective properties which are valuable in neurodegenerative diseases. Summary: Purines are molecules with great potential in disease pathogenesis as either metabolic markers or therapeutic targets. More studies need to be conducted to understand their relevance for complex diseases.
Yeast to Study Human Purine Metabolism Diseases
Cells 2019 Jan 17;8(1):67.PMID:30658520DOI:10.3390/cells8010067.
Purine nucleotides are involved in a multitude of cellular processes, and the dysfunction of Purine metabolism has drastic physiological and pathological consequences. Accordingly, several genetic disorders associated with defective Purine metabolism have been reported. The etiology of these diseases is poorly understood and simple model organisms, such as yeast, have proved valuable to provide a more comprehensive view of the metabolic consequences caused by the identified mutations. In this review, we present results obtained with the yeast Saccharomyces cerevisiae to exemplify how a eukaryotic unicellular organism can offer highly relevant information for identifying the molecular basis of complex human diseases. Overall, Purine metabolism illustrates a remarkable conservation of genes, functions and phenotypes between humans and yeast.
On the relevance of hydroxyl radical to Purine DNA damage
Free Radic Res 2021 Apr;55(4):384-404.PMID:33494618DOI:10.1080/10715762.2021.1876855.
Hydroxyl radical (HO•) is the most reactive toward DNA among the reactive oxygen species (ROS) generated in aerobic organisms by cellular metabolisms. HO• is generated also by exogenous sources such as ionizing radiations. In this review we focus on the Purine DNA damage by HO• radicals. In particular, emphasis is given on mechanistic aspects for the various lesion formation and their interconnections. Although the majority of the Purine DNA lesions like 8-oxo-purine (8-oxo-Pu) are generated by various ROS (including HO•), the formation of 5',8-cyclopurine (cPu) lesions in vitro and in vivo relies exclusively on the HO• attack. Methodologies generally utilized for the Purine lesions quantification in biological samples are reported and critically discussed. Recent results on cPu and 8-oxo-Pu lesions quantification in various types of biological specimens associated with the cellular repair efficiency as well as with distinct pathologies are presented, providing some insights on their biological significance.
The chemodiversity of Purine as a constituent of natural products
Chem Biodivers 2004 Mar;1(3):361-401.PMID:17191854DOI:10.1002/cbdv.200490033.
In this review, I describe various natural manifestations of Purine systems, i.e., methylated, higher-alkylated, and glycosylated forms. These comprise the Purine alkaloids, cytokines, as well as the Purine nucleoside antibiotics. In part, the compounds described herein were isolated from natural sources already long ago. However, some have been reported only during the last few years. The biological activities of most of the Purine derivatives are briefly described, and, in some cases, syntheses are formulated. In particular, this article introduces the main synthetic principles for the generation of the Purine ring system. The last chapter describes modern preparative routes for C-alkylation and C-arylation of purines.
Cytoprotective activities of kinetin Purine isosteres
Bioorg Med Chem 2021 Mar 1;33:115993.PMID:33497938DOI:10.1016/j.bmc.2021.115993.
Kinetin (N6-furfuryladenine), a plant growth substance of the cytokinin family, has been shown to modulate aging and various age-related conditions in animal models. Here we report the synthesis of kinetin isosteres with the Purine ring replaced by other bicyclic heterocycles, and the biological evaluation of their activity in several in vitro models related to neurodegenerative diseases. Our findings indicate that kinetin isosteres protect Friedreich́s ataxia patient-derived fibroblasts against glutathione depletion, protect neuron-like SH-SY5Y cells from glutamate-induced oxidative damage, and correct aberrant splicing of the ELP1 gene in fibroblasts derived from a familial dysautonomia patient. Although the mechanism of action of kinetin derivatives remains unclear, our data suggest that the cytoprotective activity of some Purine isosteres is mediated by their ability to reduce oxidative stress. Further, the studies of permeation across artificial membrane and model gut and blood-brain barriers indicate that the compounds are orally available and can reach central nervous system. Overall, our data demonstrate that isosteric replacement of the kinetin Purine scaffold is a fruitful strategy for improving known biological activities of kinetin and discovering novel therapeutic opportunities.