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Merck
CN

K0250

红藻氨酸 一水合物

≥99% (TLC), powder, ionotropic glutamate receptor (kainate class) agonist

别名:

Digenin，卡英酸, 2-羧甲基-3-异丙烯基脯氨酸

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关于此项目

经验公式（希尔记法）:
C10H15NO4 · H2O
化学文摘社编号:
58002-62-3
分子量:
231.25
UNSPSC Code:
12352106
PubChem Substance ID:
24277985
NACRES:
NA.77
MDL number:
MFCD00150833
Assay:
≥99% (TLC)
Form:
powder
Quality level:
100

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产品名称

红藻氨酸 一水合物, ≥99% (TLC)

SMILES string

O.CC(=C)[C@H]1CN[C@@H]([C@H]1CC(O)=O)C(O)=O

InChI

1S/C10H15NO4.H2O/c1-5(2)7-4-11-9(10(14)15)6(7)3-8(12)13;/h6-7,9,11H,1,3-4H2,2H3,(H,12,13)(H,14,15);1H2/t6-,7+,9-;/m0./s1

InChI key

FZNZRJRSYLQHLT-SLGZUKMRSA-N

assay

≥99% (TLC)

form

powder

impurities

Glutamate, free

solubility

H2O: soluble

storage temp.

2-8°C

Quality Level

100

Gene Information

human ... GRIA1(2890), GRIA2(2891), GRIA4(2893), GRIK1(2897), GRIK2(2898), GRIK3(2899), GRIK4(2900), GRIK5(2901), SLC1A1(6505), SLC1A2(6506), SLC1A3(6507)
mouse ... Gria1(14799)
rat ... Gria1(50592), Grik1(29559), Grik4(24406), Grin2a(24409)

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相关类别

Application

红藻氨酸用于：
  • 研究兴奋性诱导细胞凋亡和癫痫的机制。
  • 破坏线粒体功能()
  • 诱导小鼠大脑的c-fos表达，特别针对背侧海马体。()

Biochem/physiol Actions

红藻氨酸-水合物是一种激动剂，属于红藻类离子性谷氨酸受体，在 体内 诱导癫痫发作和神经退行性变，被用于诱导啮齿类动物实验性癫痫，并研究兴奋性诱导神经元凋亡的机制。
红藻氨酸单水合物通过诱导乳酸脱氢酶(LDH)释放，还原3-(4,5-二甲基-2-噻唑基)-2,5-二苯基溴化四唑(MTT)来破坏线粒体功能。还可引发脂质过氧化物生成，它们是引起和调节炎症和氧化应激的关键因子。
红藻氨酸盐类离子性谷氨酸受体激动剂。

Features and Benefits

该化合物收录于 受体信号和信号转导手册的《兴奋性氨基酸转运体 和谷氨酸受体(离子通道家族)》 页面。想要浏览手册的其他页面， 请单击此处。
该化合物是神经科学研究的特色产品。点击这里 以发现更多的神经科学特色产品。在sigma.com/discover-bsm 上了解有关生物活性小分子在其他研究领域的更多信息。

General description

红藻氨酸单水合物可用作红藻氨酸类离子型谷氨酸受体的激动剂，引起活生物体的发作和神经退行病变。可用于诱发啮齿动物的实验性癫痫，探索兴奋诱发的神经元凋亡。

Preparation Note

溶解1-2滴的1N的氢氧化钠，然后用水或缓冲溶液定容。冷藏条件下可保存1-2天。

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)

历史批次信息供参考:

分析证书(COA)

Lot/Batch Number
MKCV7520
MKCR8874
MKCT1879
MKCR7601
MKCR2722

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Xing-Mei Zhang et al.
Current neuropharmacology, 9(2), 388-398 (2011-12-02)
Glutamate excitotoxicity contributes to a variety of disorders in the central nervous system, which is triggered primarily by excessive Ca(2+) influx arising from overstimulation of glutamate receptors, followed by disintegration of the endoplasmic reticulum (ER) membrane and ER stress, the
Xin Zhang et al.
Scientific reports, 9(1), 4518-4518 (2019-03-16)
Epilepsy is a multi-etiological brain dysfunction syndrome. Hippocampal neuronal damage induced by seizures may be one of the causes leading to cognitive impairment, but the underlying mechanism remains to be further elucidated. The kainic acid (KA) model of temporal lobe
A Kondratyev et al.
Brain research. Molecular brain research, 75(2), 216-224 (2000-02-25)
In the aftermath of prolonged continuous seizure activity (status epilepticus, SE), neuronal cell death occurs in the brain regions through which the seizure propagates. Recent studies have implicated apoptotic processes in this seizure-related injury. Because activation of caspase-3-like cysteine proteases
D Schmitz et al.
Proceedings of the National Academy of Sciences of the United States of America, 98(20), 11003-11008 (2001-09-27)
Hippocampal mossy fibers, which are the axons of dentate granule cells, form powerful excitatory synapses onto the proximal dendrites of CA3 pyramidal cells. It has long been known that high-affinity binding sites for kainate, a glutamate receptor agonist, are present
Qun Wang et al.
Molecular neurobiology, 31(1-3), 3-16 (2005-06-15)
Neuronal excitation involving the excitatory glutamate receptors is recognized as an important underlying mechanism in neurodegenerative disorders. Excitation resulting from stimulation of the ionotropic glutamate receptors is known to cause the increase in intracellular calcium and trigger calcium-dependent pathways that
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