| Stereochemistry | ABSOLUTE |
| Molecular Formula | C10H15NO4 |
| Molecular Weight | 213.2304 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 3 / 3 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CC(=C)[C@H]1CN[C@@H]([C@H]1CC(O)=O)C(O)=O
InChI
InChIKey=VLSMHEGGTFMBBZ-OOZYFLPDSA-N
InChI=1S/C10H15NO4/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)/t6-,7+,9-/m0/s1
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
Originator
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
| 8.0 nM [IC50] | |||
| 32.0 nM [Ki] | |||
| 10.0 nM [Ki] | |||
| 177.0 nM [Ki] |
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
PubMed
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).
ACTIVE MOIETY
SALT/SOLVATE (PARENT)
