Adenylosuccinic Acid
(Synonyms: 腺苷酸基琥珀酸,Aspartyl Adenylate) 目录号 : GC46083腺苷琥珀酸是一种嘌呤核苷酸，也是嘌呤核苷酸循环中的中间产物
Cas No.:19046-78-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Adenylosuccinic acid is a purine nucleotide and an intermediate in the purine nucleotide cycle.[1] It is converted into AMP and fumarate by adenylosuccinate lyase in the cytosol. Adenylosuccinic acid (10 µM) inhibits calcium-induced activation of non-selective cation channels in isolated rat brown adipocytes in a patch-clamp assay.[2] Adenylosuccinic acid (10 µM) increases glucose-induced insulin exocytosis in 832/13 INS-1 pancreatic β-cells.[3] It induces contractions in isolated guinea pig uterus strips when used at a concentration of 100 µM.[4]
腺苷琥珀酸是一种嘌呤核苷酸，也是嘌呤核苷酸循环中的中间产物。它在胞质中被腺苷琥珀酸裂解酶转化为AMP和富马酸。腺苷琥珀酸（10微米）通过贴片钳技术抑制离体大鼠棕色脂肪细胞中的非选择性阳离子通道的钙离子诱导活化。[2] 腺苷琥珀酸（10微米）增加了832/13 INS-1胰岛素分泌细胞中葡萄糖诱导的胰岛素外分泌。[3] 使用100 µM的浓度时，它会在离体豚鼠子宫带中引起收缩。[4]
Reference:
[1]. Waarde, A. Operation of the purine nucleotide cycle in animal tissues. Biol. Rev. Camb. Philos. Soc. 63(2), 259-298 (1988).
[2]. Halonen, J., and Nedergaard, J. Adenosine 5'-monophosphate is a selective inhibitor of the brown adipocyte nonselective cation channel. J. Membr. Biol. 188(1), 183-197 (2002).
[3]. Gooding, J.R., Jensen, M.W., Dai, X., et al. Adenylosuccinate is an insulin secretagogue derived from glucose-induced purine metabolism. Cell Rep. 13(1), 157-167 (2015).
[4]. Nishida, Y., and Miyamoto, T. Contractile effect of succinylpurines on guinea pig uterus. Gen. Pharmacol. 19(2), 277-279 (1988).
| Cas No. | 19046-78-7 | SDF | |
| 别名 | 腺苷酸基琥珀酸,Aspartyl Adenylate | ||
| 化学名 | N-[9-(5-O-phosphono-β-D-ribofuranosyl)-9H-purin-6-yl]-L-aspartic acid | ||
| Canonical SMILES | OP(OC[C@H]([C@@H](O)[C@H]1O)O[C@@]1([H])N2C=NC3=C(N[C@@H](CC(O)=O)C(O)=O)N=CN=C32)(O)=O | ||
| 分子式 | C14H14N5O11P • 4NH4 | 分子量 | 531.4 |
| 溶解度 | PBS (pH 7.2);10 mg/ml | 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 | 1.8818 mL | 9.4091 mL | 18.8182 mL |
| 5 mM | 0.3764 mL | 1.8818 mL | 3.7636 mL |
| 10 mM | 0.1882 mL | 0.9409 mL | 1.8818 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。
Adenylosuccinic Acid therapy ameliorates murine Duchenne Muscular Dystrophy
Sci Rep 2020 Jan 24;10(1):1125.PMID:31980663DOI:10.1038/s41598-020-57610-w.
Arising from the ablation of the cytoskeletal protein dystrophin, Duchenne Muscular Dystrophy (DMD) is a debilitating and fatal skeletal muscle wasting disease underpinned by metabolic insufficiency. The inability to facilitate adequate energy production may impede calcium (Ca2+) buffering within, and the regenerative capacity of, dystrophic muscle. Therefore, increasing the metabogenic potential could represent an effective treatment avenue. The aim of our study was to determine the efficacy of Adenylosuccinic Acid (ASA), a purine nucleotide cycle metabolite, to stimulate metabolism and buffer skeletal muscle damage in the mdx mouse model of DMD. Dystrophin-positive control (C57BL/10) and dystrophin-deficient mdx mice were treated with ASA (3000 µg.mL-1) in drinking water. Following the 8-week treatment period, metabolism, mitochondrial density, viability and superoxide (O2-) production, as well as skeletal muscle histopathology, were assessed. ASA treatment significantly improved the histopathological features of murine DMD by reducing damage area, the number of centronucleated fibres, lipid accumulation, connective tissue infiltration and Ca2+ content of mdx tibialis anterior. These effects were independent of upregulated utrophin expression in the tibialis anterior. ASA treatment also increased mitochondrial viability in mdx flexor digitorum brevis fibres and concomitantly reduced O2- production, an effect that was also observed in cultured immortalised human DMD myoblasts. Our data indicates that ASA has a protective effect on mdx skeletal muscles.
Adenylosuccinic Acid: a novel inducer of the cytoprotectant Nrf2 with efficacy in Duchenne muscular dystrophy
Curr Med Res Opin 2021 Mar;37(3):465-467.PMID:33331789DOI:10.1080/03007995.2020.1865699.
Adenylosuccinic Acid (ASA) modifies Duchenne muscular dystrophy (DMD) progression in dystrophic mdx mice and human DMD patients. Despite an established role for ASA in augmenting metabolism and cellular energy homeostasis, our previous data suggests an undiscovered ulterior mode of action capable of modifying DMD disease course. Here, we identify ASA as a novel inducer of nuclear factor erythroid 2-related factor-2 (Nrf2), master regulator of the antioxidant and cytoprotective response to cell stress.
Analogs of L-aspartic acid in chemotherapy for cancer
Cancer Treat Rep 1979 Jun;63(6):1095-108.PMID:38003doi
The interaction of analogs of L-aspartic acid with Adenylosuccinic Acid synthetase, L-asparagine synthetase, and L-aspartic acid transcarbamylase is discussed. Each of these enzymes is of critical importance in the economy of certain types of tumor cells. L-Alanosine, a new antitumor antibiotic, is shown to be accepted as a substrate by the enzymes of de novo purine biosynthesis which ordinarily use L-aspartic acid as a substrate; as a consequence of this interaction, an anabolite is thought to be produced which impairs the formation of adenine nucleotides by inhibiting adenylosuccinate synthetase, leading to an interruption in DNA synthesis. Homoserine-beta-adenylate, guanidinosuccinic acid, and PA2LA [3-(phosphonacetylamido)-L-alanine] are shown to be inhibitors of L-asparagine synthetase from murine lymphoblasts; each of these analogs of L-aspartic acid exhibits novel structural properties which can be used by synthetic chemists in the design of molecules with an even greater ability to block the biosynthesis of L-asparagine. Certain aspects of the mechanism of action of PALA (N-phosphonacetyl-L-aspartic acid) were examined. This agent, which is a potent inhibitor of mammalian L-aspartic acid transcarbamylase, is capable of stimulating the homologous enzyme from Escherichia coli under certain circumstances. In vivo the duration of inhibition produced by this agent is shown to be unusually protracted; for example, L-aspartic acid transcarbamylase in mouse liver remains at 30% of treatment levels for greater than or equal to 20 days after a single therapeutic dose of PALA. This long-lasting effect reflects either sluggish synthesis of new enzyme molecules in this organ or shuttling of the inhibitor from old to new molecules. It is suggested that new and still more potent analogs of L-aspartic acid be sought, and that they be screened, inter alia, against these target enzymes.
Biochemical genetics of Chinese hamster cell mutants with deviant purine metabolism. IV. Isolation of a mutant which accumulates Adenylosuccinic Acid and succinylaminoimidazole carboxamide ribotide
Somatic Cell Genet 1976 May;2(3):189-203.PMID:1028168DOI:10.1007/BF01538958.
The production, isolation, and characterization of a new complementation group (Ade-I) of adenine-requiring mutant of Chinese hamster cells (CHO-K1) is described. This mutant accumulates two intermediates of purine biosynthesis, both of which contain an aspartate moiety. One of these is shown to be Adenylosuccinic Acid (AMPS) by chromatographic analysis, while evidence is presented that strongly suggests the other intermediate is succinylaminoimidazole carboxamide ribotide (SAICAR). Thus, Ade-I is most likely lacking the activity of the enzyme adenylosuccinase (EC 4.3.2.2). The use of this and similar mutants for the analysis of regulation of purine biosynthesis in mammalian cells is discussed.
The dystrophin connection--ATP?
Med Hypotheses 1992 Jun;38(2):139-54.PMID:1326712DOI:10.1016/0306-9877(92)90087-s.
Clinical evidence is presented supporting the hypothesis that the metabolic abnormality in the dystrophin-defective muscular dystrophies (DMD and BMD) involves the ATP pathway. Objective laboratory data show corrective trends in the abnormal values of parameters relating to creatine and calcium metabolism (ATP) by use of glucagon-stimulated c-AMP and by use of synthetically produced Adenylosuccinic Acid (ASA). Disease accelerating mechanisms as suggested by analysis of the clinical features, and the therapeutic potential of ASA are discussed.