3031-95-6

中文名称 (2S)-2-[[5-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(phosphonooxymethyl)oxolan-2-yl]imidazole-4-carbonyl]amino]butanedioic acid

英文名称 (2S)-2-[[5-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(phosphonooxymethyl)oxolan-2-yl]imidazole-4-carbonyl]amino]butanedioic acid

CAS 3031-95-6

分子式 C13H19N4O12P

分子量 454.28

MOL 文件 3031-95-6.mol

3031-95-6 结构式

基本信息物理化学性质常见问题列表 (2S)-2-[[5-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(phosphonooxymethyl)oxolan-2-yl]imidazole-4-carbonyl]amino]butanedioic acid价格(试剂级)

基本信息

中文别名

化合物 T16837

英文别名

SAICAR
Succino-AICAR
5-Aminoimidazole-4-N-succinocarboxamide ribonucleotide
5'-Phosphoribosyl-4-(N-succinocarboxamide)-5-aminoimidazole
N-Succinyl-5-aMinoiMidazole-4-carboxaMide Ribose 5'-Phosphate
N-[[5-Amino-1-(5-O-phosphono-β-D-ribofuranosyl)-1H-imidazol-4-yl]carbonyl]-L-aspartic acid
N-[[5-Amino-1-(5-O-phosphono-b-D-ribofuranosyl)-1H-imidazoL-4-yl]carbonyl]-L-aspartic acid
L-Aspartic acid, N-[[5-amino-1-(5-O-phosphono-β-D-ribofuranosyl)-1H-imidazol-4-yl]carbonyl]-
2-[[1-(5-O-Phosphono-β-D-ribofuranosyl)-5-amino-1H-imidazol]-4-ylcarbonylamino]succinic acid
(2S)-2-[[5-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(phosphonooxymethyl)oxolan-2-yl]imidazole-4-carbonyl]amino]butanedioic acid

所属类别

化学试剂：多环化合物

物理化学性质

熔点>189°C (dec.)

密度2.18±0.1 g/cm3(Predicted)

储存条件Hygroscopic, -20°C Freezer, Under inert atmosphere

溶解度少许溶于甲醇和水

酸度系数(pKa)1.86±0.10(Predicted)

形态固体

颜色白色至灰白色

常见问题列表

用途

N-琥珀酰基-5-氨基咪唑-4-羧酰胺5'-磷酸核糖是嘌呤代谢产物。由于腺苷是神经元功能的有效抑制剂，可抑制几种兴奋递质的释放并引发神经元的直接过级化，因此腺苷琥珀酸裂合酶（ASase）缺乏症患者出现的症状可能反映了琥珀酰嘌呤对神经传递的干扰。

生物活性

SAICAR 是嘌呤核苷酸从头合成的中间体，以同工酶选择性性方式激活 PKM2，EC50 为 0.3 mM。SAICAR 刺激 PKM2 并促进癌细胞在葡萄糖限制条件下的存活。

靶点

Human Endogenous Metabolite

体外研究

SAICAR accumulation induces nuclear localization of PKM2. PKM2-SAICAR phosphorylates and activates Erk1/2, which in turn sensitizes PKM2 for SAICAR binding through phosphorylation. Additionally, PKM2-SAICAR was necessary to induce sustained Erk1/2 activation and mitogen-induced cell proliferation. SAICAR-PKM2 interaction is necessary and sufficient to induce H3 T11 and Erk1/2 phosphorylation.
Upon glucose starvation, cellular SAICAR concentration increases in an oscillatory manner and stimulates PKM2 activity in cancer cells. The SAICAR-PKM2 interaction also promotes cancer cell survival in glucose-limited conditions. In glucose-limited conditions, cells with higher SAICAR concentrations ( adsl-kd cells or cells overexpressing PAICS) survive better while paics-kd cells died earlier than control-kd cells. SAICAR promotes cancer cell survival in glucose-limited conditions.