Kainic Acid (Natural)

  • CAS:487-79-6
  • Formula:C10 H15 N O4
  • MW:213.23
  • Appearance:White to Off white powder
  • Purity:>99% by HPLC
Product Name Qty
Kainic Acid (Natural)
10 mg
Kainic Acid
5x10 mg
Kainic Acid (Natural)
50 mg


Kainic acid is a natural marine product originally isolated from the red marine alga D. Simplex. It is a potent central nervous system stimulant, acting through specific kainate receptors and has been developed as the prototype neuroexcitatory amino acid for the induction of seizures in experimental animals, at a typical dose of 10-30 mg/kg in mice.

Kainic acid is utilised in primary neuronal cell cultures and acute brain slice preparations to study the physiological effect of excitotoxicity and assess the neuroprotective capabilities of potential therapeutics.


Not for human therapeutic use or for medicinal purposes. For research applications only.

More Information
Alternate Name/Synonyms
(-)-a-Kainic Acid; Kainate; Digenic acid; Helminal; Digenin; Digensaeure; Kainsaeure
Chemical Name
(2S,3S,4S)-3-carboxy-4-(1-methylethenyl)-3-pyrrolidineacetic acid
Chemical Formula
C10 H15 N O4
Molecular Weight
White to Off white powder
>99% by HPLC
Soluble in water (10 mg/mL)
Storage Temp
Store desiccated at room temperature
Neurological disorders, Epilepsy
An excitatory and excitotoxic glutamate-mimic kainate receptor agonist used in epilepsy
Store in tightly-sealed vial. Protect from Moisture.
Certificate of Analysis 1
Certificate of Analysis 2
Certificate of Analysis 3
HandlingStore in tightly-sealed vial. Protect from Moisture.
CitationsPeripherally derived T regulatory and γδ T cells have opposing roles in the pathogenesis of intractable pediatric epilepsy
Altered mitochondrial acetylation profiles in a kainic acid model of temporal lobe epilepsy
Intranasal administration of the growth-compromised HSV-2 vector DeltaRR prevents kainate-induced seizures and neuronal loss in rats and mice
NAD(P)H fluorescence imaging of postsynaptic neuronal activation in murine hippocampal slices
Non-invasive PET imaging of brain inflammation at disease onset predicts spontaneous recurrent seizures and reflects comorbidities
Brain inflammation in a chronic epilepsy model: Evolving pattern of the translocator protein during epileptogenesis
Mitochondrial respiration deficits driven by reactive oxygen species in experimental temporal lobe epilepsy
P2X7 receptor antagonism reduces the severity of spontaneous seizures in a chronic model of temporal lobe epilepsy
Progressive ankylosis (Ank) protein is expressed by neurons and Ank immunohistochemical reactivity is increased by limbic seizures
Kainic Acid-Induced Post-Status Epilepticus Models of Temporal Lobe Epilepsy with Diverging Seizure Phenotype and Neuropathology
Susceptibility to seizure-induced excitotoxic cell death is regulated by an epistatic interaction between Chr 18 (Sicd1) and Chr 15 (Sicd2) loci in mice
Postnatal systemic inflammation exacerbates impairment of hippocampal synaptic plasticity in an animal seizure model
Confounding effect of EEG implantation surgery: Inadequacy of surgical control in a two hit model of temporal lobe epilepsy
Spatio‐temporal expression and inhibition of prolyl oligopeptidase contradict its involvement in key pathological mechanisms of kainic acid induced temporal lobe epilepsy in rats
TNF receptor I sensitizes neurons to erythropoietin- and VEGF-mediated neuroprotection after ischemic and excitotoxic injury
Postnatal inflammation increases seizure susceptibility in adult rats
Scavenging of highly reactive gamma-ketoaldehydes attenuates cognitive dysfunction associated with epileptogenesis
Mesenchymal stem cells protect CNS neurons against glutamate excitotoxicity by inhibiting glutamate receptor expression and function
Myelin-associated glycoprotein protects neurons from excitotoxicity
DeltaRR vaccination protects from KA-induced seizures and neuronal loss through ICP10PK-mediated modulation of the neuronal-microglial axis
Regulation of seizure spreading by neuroserpin and tissue-type plasminogen activator is plasminogen-independent
Strain-dependent differences in calcium signaling predict excitotoxicity in murine hippocampal neurons
TSPO PET upregulation predicts epileptic phenotype at disease onset independently from chronic TSPO expression in a rat model of temporal lobe epilepsy
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