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K0250

Sigma-Aldrich

Kainic acid monohydrate

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

Synonyme(s) :

Digenin, Kainate, 2-Carboxy-3-carboxymethyl-4-isopropenylpyrrolidine

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About This Item

Formule empirique (notation de Hill):
C10H15NO4 · H2O
Numéro CAS:
Poids moléculaire :
231.25
Numéro MDL:
Code UNSPSC :
12352106
ID de substance PubChem :
Nomenclature NACRES :
NA.77

product name

Kainic acid monohydrate, ≥99% (TLC)

Niveau de qualité

Pureté

≥99% (TLC)

Forme

powder

Impuretés

Glutamate, free

Solubilité

H2O: soluble

Température de stockage

2-8°C

Chaîne SMILES 

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

Clé InChI

FZNZRJRSYLQHLT-SLGZUKMRSA-N

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Description générale

Kainic acid monohydrate serves as an agonist for kainate-class ionotropic glutamate receptors, initiating seizures and neurodegeneration in live organisms. It is employed to induce experimental epilepsy in rodents and to explore the mechanisms underlying excitation-induced neuronal apoptosis.

Application

Kainic acid (KA) has been used:
  • tostudy mechanisms of excitation-induced apoptosis and epilepsy.
  • to hamper themitochondrial function ()
  • used to induce c-fosexpression in the mice′s brains, specifically targeting the dorsal hippocampus.()

Actions biochimiques/physiologiques

Kainic acid monohydrate disrupts mitochondrial function by inducing the release of lactate dehydrogenase (LDH) and reducing 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide (MTT). It also triggers the generation of lipid peroxides, which are key mediators in initiating and regulating inflammation and oxidative stress.
Kainic acid monohydrate is an agonist at the kainate class of ionotropic glutamate receptors, which induces seizures and neurodegeneration in vivo and is used to induce experimental epilepsy in rodents and study the mechanisms of excitation-induced neuronal apoptosis.

Caractéristiques et avantages

This compound is a featured product for Neuroscience research. Click here to discover more featured Neuroscience products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound is featured on the Excitatory Amino Acid Transporters and Glutamate Receptors (Ion Channel Family) pages of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

Notes préparatoires

Dissolve in 1-2 drops of 1N NaOH then bring to volume with water or aqueous buffer. Can be stored 1-2 days refrigerated.

Produit(s) apparenté(s)

Réf. du produit
Description
Tarif

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

Eyeshields, Gloves, type N95 (US)


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

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
Fudong Liu et al.
Stroke, 40(5), 1842-1848 (2009-03-07)
Over the past 5 years, experimental data have emerged that ischemia-induced cell death pathways may differ in males and females. Cell death in males is triggered by poly(ADP-ribose) polymerase activation and nuclear translocation of apoptosis-inducing factor. We have previously shown
Lily M Y Yu et al.
eNeuro, 3(1) (2016-03-30)
Epilepsy is a neurological disorder defined by the presence of seizure activity, manifest both behaviorally and as abnormal activity in neuronal networks. An established model to study the disorder in rodents is the systemic injection of kainic acid, an excitatory

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