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K0250

Sigma-Aldrich

Kainic acid monohydrate

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

Sinônimo(s):

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

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About This Item

Fórmula empírica (Notação de Hill):
C10H15NO4 · H2O
Número CAS:
Peso molecular:
231.25
Número MDL:
Código UNSPSC:
12352106
ID de substância PubChem:
NACRES:
NA.77

Nome do produto

Kainic acid monohydrate, ≥99% (TLC)

Nível de qualidade

Ensaio

≥99% (TLC)

Formulário

powder

Impurezas

Glutamate, free

solubilidade

H2O: soluble

temperatura de armazenamento

2-8°C

cadeia de caracteres 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

chave InChI

FZNZRJRSYLQHLT-SLGZUKMRSA-N

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Descrição geral

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.

Aplicação

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.()

Ações bioquímicas/fisiológicas

Agonist for kainate class of ionotropic glutamate receptors.
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.

Características e benefícios

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.

Nota de preparo

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

produto relacionado

Nº do produto
Descrição
Preços

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Equipamento de proteção individual

Eyeshields, Gloves, type N95 (US)


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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
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
M Nakai et al.
Journal of neurochemistry, 74(2), 647-658 (2000-01-26)
The present study evaluated whether nuclear factor-kappaB (NF-kappaB) activation contributes to the apoptotic-like death of striatal neurons induced by kainic acid (KA) receptor stimulation. Intrastriatally infused KA (1.25-5.0 nmol) produced substantial neuronal loss as indicated by an 8-73% decrease in
Seena S Mathew et al.
Neuropharmacology, 55(1), 106-116 (2008-05-30)
We examined the mechanisms of kainate (KA) induced modulation of GABA release in rat prefrontal cortex. Pharmacologically isolated IPSCs were recorded from visually identified layer II/III pyramidal cells using whole-cell patch clamp techniques. KA produced an increase in evoked IPSC
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

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