U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

Details

Stereochemistry ABSOLUTE
Molecular Formula C10H15NO4.H2O
Molecular Weight 231.2457
Optical Activity UNSPECIFIED
Defined Stereocenters 3 / 3
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of KAINIC ACID MONOHYDRATE

SMILES

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

InChI

InChIKey=FZNZRJRSYLQHLT-SLGZUKMRSA-N
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

HIDE SMILES / InChI

Molecular Formula C10H15NO4
Molecular Weight 213.2304
Charge 0
Count
Stereochemistry ABSOLUTE
Additional Stereochemistry No
Defined Stereocenters 3 / 3
E/Z Centers 0
Optical Activity UNSPECIFIED

Molecular Formula H2O
Molecular Weight 18.0153
Charge 0
Count
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Description
Curator's Comment: description was created based on several sources, including https://www.ncbi.nlm.nih.gov/pubmed/10821708 | https://www.ncbi.nlm.nih.gov/pubmed/28229936 | https://www.ncbi.nlm.nih.gov/pubmed/28222432 | https://www.ncbi.nlm.nih.gov/pubmed/28293167 | https://www.ncbi.nlm.nih.gov/pubmed/28303499

Kainic acid (kainate) is a natural marine acid present in some seaweed. Kainic acid is a potent neuroexcitatory amino acid that acts by activating receptors for glutamate, the principal excitatory neurotransmitter in the central nervous system. Kainic acid is commonly injected into laboratory animal models to study the effects of experimental ablation. Kainic acid is a direct agonist of the glutamic kainate receptors and large doses of concentrated solutions produce immediate neuronal death by overstimulating neurons to death. Such damage and death of neurons is referred to as an excitotoxic lesion. Thus, in large, concentrated doses kainic acid can be considered a neurotoxin, and in small doses of dilute solution kainic acid will chemically stimulate neurons. Kainic acid is utilised in primary neuronal cell cultures and acute brain slice preparations [5] to study of the physiological effect of excitotoxicity and assess the neuroprotective capabilities of potential therapeutics. Kainic acid is a potent central nervous system excitant that is used in epilepsy research to induce seizures in experimental animals, at a typical dose of 10–30 mg/kg in mice. In addition to inducing seizures, kainic acid is excitotoxic and epileptogenic. Kainic acid induces seizures via activation of kainate receptors containing the GluK2 subunit and also through activation of AMPA receptors, for which it serves as a partial agonist.

CNS Activity

Curator's Comment: KAINIC ACID cannot penetrate blood brain barrier, but active in brain of experimental animals

Originator

Sources: Proceedings of the Japan Academy, Volume 31, Pages 372-5, Journal,1955

Approval Year

TargetsConditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
PubMed

PubMed

TitleDatePubMed
Involvement of adrenal medulla grafts in the open field behavior.
2001-06
Expression of GluR6/7 subunits of kainate receptors in rat adenohypophysis.
2001-05
Blockade of AMPA/kainate receptors can either decrease or increase the survival of cultured neocortical cells depending on the stage of maturation.
2001-05
Kainate-induced genes in the hippocampus: lessons from expression patterns.
2001-05
Effects of dextromethorphan on the seizures induced by kainate and the calcium channel agonist BAY k-8644: comparison with the effects of dextrorphan.
2001-05
Comparative study of glutamate mediated gamma-aminobutyric acid release from nitric oxide synthase and tyrosine hydroxylase immunoreactive cells of the Cebus apella retina.
2001-04-13
Induction of Fos-like immunoreactivity in the ventral thalamus after electrical or chemical stimulation of various subcortical centres of rats.
2001-04-06
Differential in vitro degradation of particular Fos family members expressed by kainic acid in nuclear and cytosolic fractions of murine hippocampus.
2001-04-01
The influence of glutamate receptor 2 expression on excitotoxicity in Glur2 null mutant mice.
2001-04-01
Methods for inducing neuronal loss in preweanling rats using intracerebroventricular infusion of kainic acid.
2001-04
Expression of neuropsin in oligodendrocytes after injury to the CNS.
2001-04
The link between excitotoxic oligodendroglial death and demyelinating diseases.
2001-04
Intrathecal magnesium sulfate attenuates algogenic behavior and spinal amino acids release after kainic acid receptor activation in rats.
2001-03-30
Expression and regulation of Na pump isoforms in cultured cerebellar granule cells.
2001-03-26
Decreased epileptic susceptibility correlates with neuropeptide Y overexpression in a model of tolerance to excitotoxicity.
2001-03-16
Domain interactions regulating ampa receptor desensitization.
2001-03-15
Mitochondria control ampa/kainate receptor-induced cytoplasmic calcium deregulation in rat cerebellar granule cells.
2001-03-15
Identification of the amino acids on a neuronal glutamate receptor recognized by an autoantibody from a patient with paraneoplastic syndrome.
2001-03-15
Presynaptic kainate receptor mediation of frequency facilitation at hippocampal mossy fiber synapses.
2001-03-09
Rapid kindling of the hippocampus protects against neural damage resulting from status epilepticus.
2001-03-05
Neostriatal stimulation activates tongue-protruder muscle, but not tongue-retractor or facial muscles: an electrical and chemical microstimulation study in rats.
2001-03-02
Effects of glial glutamate transporter inhibitors on intracellular Na+ in mouse astrocytes.
2001-03-02
Tissue plasminogen activator protects hippocampal neurons from oxygen-glucose deprivation injury.
2001-03-01
N-methyl-D-aspartate receptor-mediated mitochondrial Ca(2+) overload in acute excitotoxic motor neuron death: a mechanism distinct from chronic neurotoxicity after Ca(2+) influx.
2001-03-01
Pharmacology and neuroprotective actions of mGlu receptor ligands.
2001-03
Effects of glutathione depletion by 2-cyclohexen-1-one on excitatory amino acids-induced enhancement of activator protein-1 DNA binding in murine hippocampus.
2001-03
Excitatory synaptic input to granule cells increases with time after kainate treatment.
2001-03
Kainate receptors keep the excitement high.
2001-03
Cortical and striatal neuronal cultures of the same embryonic origin show intrinsic differences in glutamate receptor expression and vulnerability to excitotoxicity.
2001-03
Kainate-activated cobalt uptake in the primary gustatory nucleus in goldfish: visualization of the morphology and distribution of cells expressing AMPA/kainate receptors in the vagal lobe.
2001-02-26
A spontaneous recurrent seizure-related Rattus NSF gene identified by linker capture subtraction.
2001-02-19
Changes in striatal electroencephalography and neurochemistry induced by kainic acid seizures are modified by dopamine receptor antagonists.
2001-02-16
Radioligand binding assays in the drug discovery process: potential pitfalls of high throughput screenings.
2001-02
Presynaptic kainate receptors that enhance the release of GABA on CA1 hippocampal interneurons.
2001-02
Glutamatergic and GABAergic inputs to the RVL mediate cardiovascular adjustments to noxious stimulation.
2001-02
Role of non-NMDA receptors in vasopressin and oxytocin release from rat hypothalamo-neurohypophysial explants.
2001-02
Regulation of X-chromosome-linked inhibitor of apoptosis protein in kainic acid-induced neuronal death in the rat hippocampus.
2001-02
Kainate-induced K+ efflux and plasma membrane depolarization in cultured cerebellar granule cells.
2001-01-22
Calcium inhibits willardiine-induced responses in kainate receptor GluR6(Q)/KA-2.
2001-01-22
Involvement of NMDA and AMPA/kainate receptors in the effects of endogenous glutamate on extracellular concentrations of dopamine and GABA in the nucleus accumbens of the awake rat.
2001-01-15
Interneurons unbound.
2001-01
Kainate acid lesions of the pedunculopontine region in the normal behaving primate.
2001-01
Brain-derived neurotrophic factor mediates an excitoprotective effect of dietary restriction in mice.
2001-01
Changes in nitric oxide synthesis and epileptic activity in the contralateral hippocampus of rats following intrahippocampal kainate injection.
2001-01
Metabotropic glutamate receptors modify ionotropic glutamate responses in neocortical pyramidal cells and interneurons.
2001-01
The role of RNA editing of kainate receptors in synaptic plasticity and seizures.
2001-01
Kainate receptors are involved in short- and long-term plasticity at mossy fiber synapses in the hippocampus.
2001-01
Stimulation of metabotropic but not ionotropic glutamatergic receptors in the nucleus accumbens is required for the D-amphetamine-induced release of functional dopamine.
2001
Kainate-induced seizures alter protein composition and N-methyl-D-aspartate receptor function of rat forebrain postsynaptic densities.
2001
Interleukin-6 deficiency reduces the brain inflammatory response and increases oxidative stress and neurodegeneration after kainic acid-induced seizures.
2001
Patents

Sample Use Guides

The chronic epileptic models were induced by the microinjection of kainic acid (KA) into rats’ hippocampus. The rat anesthetized with 10% chloralhydrate (0.35 ml/g) by intraperitoneal injection (i.p.) were fixed on the stereotactic apparatus. A hole was drilled in the skull with dental reamers. Using a micro-injector, seizure was induced with stereotactic-injection 3 μL KA (0.5 mg/ml) into the CA3 region of the left hippocampus, 5.0 mm posterior to the bregma, 5.0 mm left lateral from the mid-line, and 5.0 mm deep from the dura.
Route of Administration: Other
N2a cells viability were assayed by MTT after treatment with 0, 25, 50, 100 mM Kainic acid (KA). To observe the changes in the mitochondrial morphology in N2a cells, the KA and/or melatonin-treated N2a cells were incubated with the MitoTracker Red CMXRos probe (250 nM) (Invitrogen, Carlsbad, CA, USA) for 30 min at 37OC. After being washed three times in cold PBS, the cells were visualized under a Nikon C2 confocal laser scanning microscope (Nikon, Tokyo, Japan) with excitation of 579 nm and emission greater than 599 nm. For morphological quantification in neurites, z-sections were merged (using maximal projection) and the entire length (from tip to tip) of MitoTracker Red labeled mitochondria of neurites was measured. In cell bodies, mitochondria length was measured in each z-section of the entire soma. Quantification of mitochondria length was performed by using ImageJ software as previously described . The number of mitochondria was counted in control N2a cells (n = 50) and experimental groups (n = 40).
Substance Class Chemical
Created
by admin
on Mon Mar 31 21:35:16 GMT 2025
Edited
by admin
on Mon Mar 31 21:35:16 GMT 2025
Record UNII
I519JC63XY
Record Status Validated (UNII)
Record Version
  • Download
Name Type Language
KAINIC ACID HYDRATE
JAN  
Preferred Name English
KAINIC ACID MONOHYDRATE
Common Name English
3-PYRROLIDINEACETIC ACID, 2-CARBOXY-4-(1-METHYLETHENYL)-, MONOHYDRATE, (2S-(2.ALPHA.,3.BETA.,4.BETA.))-
Common Name English
KAINIC ACID HYDRATE [JAN]
Common Name English
3-PYRROLIDINEACETIC ACID, 2-CARBOXY-4-(1-METHYLETHENYL)-, HYDRATE (1:1), (2S,3S,4S)-
Common Name English
(-)-KAINIC ACID HYDRATE
Common Name English
Code System Code Type Description
FDA UNII
I519JC63XY
Created by admin on Mon Mar 31 21:35:16 GMT 2025 , Edited by admin on Mon Mar 31 21:35:16 GMT 2025
PRIMARY
EPA CompTox
DTXSID50206732
Created by admin on Mon Mar 31 21:35:16 GMT 2025 , Edited by admin on Mon Mar 31 21:35:16 GMT 2025
PRIMARY
CAS
58002-62-3
Created by admin on Mon Mar 31 21:35:16 GMT 2025 , Edited by admin on Mon Mar 31 21:35:16 GMT 2025
PRIMARY
PUBCHEM
11954253
Created by admin on Mon Mar 31 21:35:16 GMT 2025 , Edited by admin on Mon Mar 31 21:35:16 GMT 2025
PRIMARY
Related Record Type Details
ANHYDROUS->SOLVATE
PARENT -> SALT/SOLVATE
Related Record Type Details
ACTIVE MOIETY