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Purity: ≥98%
Kainic acid is a novel and potent excitatory amino acid and an agonist at excitatory amino acid receptor subtypes in the CNS. Kainate agonist; excitant and neurotoxin
| Targets |
Kainic acid is a cyclic analog of L-glutamate and an agonist of ionotropic kainate receptors (KARs).
Specific subunits include KA1 (GluK4), KA2 (GluK5), GluR5 (GluK1), and GluR6 (GluK2). KARs are highly expressed in the hippocampus (especially CA3 pyramidal cells), amygdala, entorhinal cortex, basal ganglia, and cerebellum. [3] |
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| ln Vitro |
Kainic acid induces robust depolarizations and eventually cell death in neurons, a central phenomenon in temporal lobe epilepsy. [3]
Bath application of KA can induce high-amplitude gamma oscillations (30-80 Hz) in the CA3 region of hippocampal brain slices from non-epileptic animals. [3] In brain slices from chronic epileptic mice (after unilateral hippocampal KA injection), gamma activity occurs in the CA3 region, and the discharge frequency of dendrite-inhibiting OLM interneurons shifts from the theta to the gamma frequency band. [3] In vitro, synchronized network-driven activities in the dentate gyrus of epileptic animals can be inhibited by pharmacological blockade of kainate receptors. [3] |
| ln Vivo |
Program plan implementation status for alginic acid (5 mg/kg; intraperitoneal injection; at least once for at least three hours, formula regimen continuous status) [1].
Systemic, intrahippocampal, or intra-amygdaloid administration of kainic acid induces acute status epilepticus (SE) characterized by behavioral seizures (e.g., facial clonus, wet-dog shakes, forelimb clonus, rearing and falling). [3] Following the initial SE, a latent period (5-40 days depending on species and administration route) occurs before the onset of spontaneous recurrent seizures, mimicking human temporal lobe epilepsy. [3] KA administration leads to neuropathological changes similar to hippocampal sclerosis in human TLE, including selective neuronal loss in CA1/CA3/hilus, granule cell dispersion, and aberrant mossy fiber sprouting in the dentate gyrus. [3] The hippocampus is often the seizure onset zone, even when KA is administered at distant sites (e.g., amygdala), suggesting a central role in seizure generation and propagation. [3] EEG features include interictal spikes, gamma oscillations (30-80 Hz), and ictal discharges originating from the hippocampus or amygdala. [3] Age affects susceptibility: very young (up to P15) and old rats (P60 and older) are more sensitive to KA-induced seizures and have shorter latency to SE compared to young adults (P20-P60). Seizures in immature brains cause less neuronal damage but may lead to long-term alterations in GABAergic signaling. [3] |
| Animal Protocol |
Animal/Disease Models: 8 weeks, 200-250 g male adult Wistar rats[1]: 5 mg/kg
Route of Administration: intraperitoneal (ip) injection; at least 3 hrs (hrs (hours)) every hour until status epilepticus occurs. Experimental Results: Induced epileptic seizures in rats. Systemic Administration (intraperitoneal, i.p.): In rats, a single dose of 6-15 mg/kg can induce status epilepticus (SE). Alternatively, multiple lower doses (e.g., 5 mg/kg/h) can be administered until SE occurs to reduce mortality. SE typically occurs about 1 hour after injection. Diazepam (20 mg/kg) and ketamine (50 mg/kg) can be used to terminate SE. Mortality rates range from 5% to 30%. [3] Intrahippocampal Administration: In rats, doses ranging from 0.4 to 2.0 µg (in a small volume, e.g., 0.2 µL) are injected directly into the hippocampus. This induces convulsive SE within 5-60 minutes. Similar protocols are used in mice and guinea pigs. [3] Intra-amygdaloid Administration: In rats, doses of 0.4–2 µg are injected into the amygdala, inducing acute seizures with symptoms similar to intrahippocampal injection, sometimes with additional signs like salivation and exophthalmos. In monkeys, doses of 0.5–10 µg/µl of saline are used, producing focal seizures with oral automatisms. [3] Post-SE Monitoring: Following SE induction, animals enter a latent period. The development of chronic epilepsy is assessed via long-term video-EEG monitoring to detect spontaneous recurrent seizures. Neuropathological examination is performed at various time points after SE to assess neuronal damage. [3] |
| ADME/Pharmacokinetics |
The provided text does not contain detailed pharmacokinetic data (e.g., absorption, distribution, metabolism, excretion, half-life, oral bioavailability) for kainic acid. [3]
Notably, systemic administration does not control the bioavailability of kainic acid in the brain. [3] Kainic acid enhances the permeability of the blood-brain barrier, an effect that can be observed within 1 hour of administration and before the onset of status epilepticus (SE). This increased permeability may lead to increased glutamate release in the hippocampus, thereby promoting seizures. [3] |
| Toxicity/Toxicokinetics |
Mortality rates in rats following systemic injection of kaempferol (KA) ranged from 5% to 30%. [3] KA is an excitotoxic agent. Its administration induces neuronal death, particularly in the CA3 and CA1 regions of the hippocampus, the amygdala, and other limbic system structures. The extent of damage is correlated with the severity and spread of seizures, rather than solely with the direct effects of the toxin. [3] Age-specific toxicity was observed: young rats (P15) and older rats were more susceptible, exhibiting shorter latency periods and more severe seizures compared to young adult rats (P20–P60). Interestingly, in very young animals (less than 3 weeks old), KA induced severe seizures with minimal brain damage, attributed to immature neural connections. [3] Distal neuropathological changes (beyond the injection site) were attributed to the spread of epileptiform activity during status epilepticus, rather than the direct neurotoxic effects of KA itself. Pre-administration of diazepam prevented hippocampal damage induced by intraamycinal injection of KA without affecting local amygdala damage. [3]
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| References |
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| Additional Infomation |
Kainic acid is a dicarboxylic acid, pyrrolidinecarboxylic acid, L-proline derivative, and non-protein L-α-amino acid. It has anti-nematode and excitatory amino acid agonist effects. It is the conjugate acid of kainic acid (1-). Kainic acid has been reported to be found in Digenea simplex, Apis cerana, and other organisms with relevant data. (2S-(2α,3β,4β))-2-carboxy-4-(1-methylvinyl)-3-pyrrolidineacetic acid is an anthelmintic extracted from Digenea simplex. It is a potent excitatory amino acid agonist acting on certain types of excitatory amino acid receptors and has been used to differentiate between different receptor types. Like many excitatory amino acid agonists, kainic acid can cause neurotoxicity and has been used in related experimental studies.
Kaloside was originally isolated from the red algae Digenea simplex and was initially used as an antiparasitic agent. [3] It has become an important tool in neuroscience for studying glutamate receptors, excitotoxicity, and constructing animal models of temporal lobe epilepsy (TLE). [3] The Kaloside model can reproduce key features of human temporal lobe epilepsy: latency after initial injury (status epilepticus), spontaneous recurrent seizures, and hippocampal sclerosis. [3] This model is often compared with other temporal lobe epilepsy models, such as the pilocarpine model and the electro-ignition model. The pilocarpine model is known for its high reliability in inducing seizures, while the electro-ignition model, although capable of precise targeting of specific neural networks, rarely induces spontaneous seizures or hippocampal sclerosis. [3] The choice between intracerebral injection and systemic injection of KA depends on the research question: intracerebral injection is used for focal network studies, while systemic injection is used for studies of broad susceptibility and disease. [3] This model helps to understand epilepsy occurrence, seizure occurrence, and to test potential therapies. [3] |
| Molecular Formula |
C10H15NO4.H2O
|
|---|---|
| Molecular Weight |
231.24568
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| Exact Mass |
213.1
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| CAS # |
487-79-6
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| Related CAS # |
Kainic acid hydrate;58002-62-3
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| PubChem CID |
10255
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| Appearance |
White to off-white solid powder
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
439.9±45.0 °C at 760 mmHg
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| Melting Point |
253-254ºC
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| Flash Point |
219.8±28.7 °C
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| Vapour Pressure |
0.0±2.3 mmHg at 25°C
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| Index of Refraction |
1.509
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| LogP |
0.5
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
5
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
15
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| Complexity |
300
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| Defined Atom Stereocenter Count |
3
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| SMILES |
CC(=C)[C@H]1CN[C@@H]([C@H]1CC(=O)O)C(=O)O
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| InChi Key |
VLSMHEGGTFMBBZ-OOZYFLPDSA-N
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| InChi Code |
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
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| Chemical Name |
(2S,3S,4S)-3-(carboxymethyl)-4-prop-1-en-2-ylpyrrolidine-2-carboxylic acid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~50 mg/mL (~234.49 mM)
H2O : ~25 mg/mL (~117.24 mM) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 5 mg/mL (23.45 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 50.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 5 mg/mL (23.45 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 50.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 5 mg/mL (23.45 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 4.3243 mL | 21.6216 mL | 43.2432 mL | |
| 5 mM | 0.8649 mL | 4.3243 mL | 8.6486 mL | |
| 10 mM | 0.4324 mL | 2.1622 mL | 4.3243 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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