Compound: kainic acid
SMILES: O=C(O)[C@H]1NC[C@@H]([C@@H]1CC(=O)O)C(=C)C
InChIKey: VLSMHEGGTFMBBZ-OOZYFLPDSA-N
Synonyms: kainic acid, 487-79-6, Digenin, Digenic acid, Helminal, L-alpha-Kainic acid, alpha-Kainic acid, Acide kainique, Acido kainico, Acidum kainicum, NSC136038, SIV03811UC, DTXSID7040526, 2-Carboxy-4-isopropenyl-3-pyrrolidineacetic acid, NSC-759587, (2S,3S,4S)-3-(carboxymethyl)-4-prop-1-en-2-ylpyrrolidine-2-carboxylic acid, (3S,4R)-3-(carboxymethyl)-4-(prop-1-en-2-yl)-L-proline, DTXCID5020526, CHEBI:31746, (2S-(2alpha,3beta,4beta))-2-carboxy-4-(1-methylethenyl)-3-pyrrolidineacetic acid, 3-Pyrrolidineacetic acid, 2-carboxy-4-(1-methylethenyl)-, (2S-(2alpha,3beta,4beta))-, Acid, Digenic, Acid, Kainic, RefChem:915531, (2S,3S,4S)-3-(carboxymethyl)-4-prop-1-en-2-ylpyrrolidin-1-ium-2-carboxylate, Digensaeure, Kainsaeure, (2S,3S,4S)-3-(Carboxymethyl)-4-(prop-1-en-2-yl)pyrrolidine-2-carboxylic acid, alpha- Kainic acid, CHEMBL275040, 3-Pyrrolidineacetic acid, 2-carboxy-4-(1-methylethenyl)-, (2S,3S,4S)-, 3-Pyrrolidineacetic acid, 2-carboxy-4-isopropenyl-, 3-(Carboxymethyl)-4-isopropenylproline, NCGC00024504-05, 2-Carboxy-3-carboxymethyl-4-isopropenylpyrrolidine, NSC 136038, 3-Pyrrolidineacetic acid, 2-carboxy-4-(1-methylethenyl)-, (2S-(2-alpha,3-beta,4-beta))-, (-)-A-KAINIC ACID, Kainic acid [INN:JAN], (2S,3S,4S)-3-(carboxymethyl)-4-isopropenyl-pyrrolidine-2-carboxylic acid, 4071-38-9, CAS-487-79-6, Acide kainique [INN-French], Acido kainico [INN-Spanish], Acidum kainicum [INN-Latin], SR-01000075454, BRN 0086660, UNII-SIV03811UC, kainic-acid, DL-Kainic acid, NSC-136038, KAI, 1p1n, KAINIC ACID [MI], WRW5P6M3EM, Biomol-NT_000217, KAINIC ACID [INN], UPCMLD-DP146, Kainic acid, (+/-)-, Lopac0_000656, SCHEMBL15777, 4-22-00-01523 (Beilstein Handbook Reference), MLS001074661, KAINIC ACID [WHO-DD], BPBio1_001306, (-)-(.alpha.)-Kainic Acid, UPCMLD-DP146:001, UPCMLD-DP146:002, HMS2233K05, HMS3262C13, HMS3266C11, HMS3411A21, HMS3675A21, AAA48779, EX-A8001, HY-N2309, Tox21_110905, Tox21_500656, BDBM50002369, Kainic Acid - CAS 487-79-6, AKOS024456995, Tox21_110905_1, CCG-204742, EBC-618501, LP00656, SDCCGSBI-0050635.P002, NCGC00024504-02, NCGC00024504-03, NCGC00024504-04, NCGC00024504-06, NCGC00024504-07, NCGC00024504-08, NCGC00024504-09, NCGC00024504-15, NCGC00261341-01, DA-64702, SMR000471885, CS-0020451, EU-0100656, NS00075498, K 0250, M02036, Q390239, SR-01000597728, SR-01000075454-1, SR-01000075454-5, SR-01000075454-6, SR-01000075454-7, SR-01000597728-1, BRD-K52459018-001-09-1, rel-(3R,4R)-3-(carboxymethyl)-4-isopropenyl-D-proline, (3S,4S)-3-(Carboxymethyl)-4-(prop-1-en-2-yl)-L-proline, 2S-CARBOXY-4S-(1-METHYLETHENYL)-3S-PYRROLDINEACETIC ACID, L-proline, 3-(carboxymethyl)-4-(1-methylethenyl)-, (3S,4S)-, 3-Pyrrolidineacetic acid, 2-carboxy-4-(1-methylethenyl)-, (2R,3R,4R)-rel-, (2S-(2.ALPHA.,3.BETA.,4.BETA.))-2-CARBOXY-4-(1-METHYLETHENYL)-3-PYRROLIDINEACETIC ACID, InChI=1/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/s
Theoretical properties:
molecular_formula: C10H15NO4
molecular_weight: 213.23 g/mol
exact_mass: 213.10010796 g/mol
formal_charge: 0
hydrogen_bond_donor_count: 3
hydrogen_bond_acceptor_count: 5
rotatable_bond_count: 4
heavy_atom_count: 15
topological_polar_surface_area: 86.6 Å²
isotope_atom_count: 0
covalently_bonded_unit_count: 1
Physical properties:
Descriptions:
{"pubchem": "Kainic acid is a dicarboxylic acid, a pyrrolidinecarboxylic acid, a non-proteinogenic L-alpha-amino acid and a L-proline derivative. It has a role as an antinematodal drug and an excitatory amino acid agonist. It is a conjugate acid of a kainate(1-).", "chebi": null, "chembl": "KAINIC ACID is a small molecule listed in the ChEMBL database and has reached clinical trial phase 2.0.", "wikipedia": "Kainic acid, or kainate, is an acid that naturally occurs in some seaweed.  Kainic acid is a potent neuroexcitatory amino acid agonist that acts by activating receptors for glutamate, the principal excitatory neurotransmitter in the central nervous system. Glutamate is produced by the cell's metabolic processes and there are four major classifications of glutamate receptors: NMDA receptors, AMPA receptors, kainate receptors, and the metabotropic glutamate receptors. Kainic acid is an agonist for kainate receptors, a type of ionotropic glutamate receptor. Kainate receptors likely control a sodium channel that produces excitatory postsynaptic potentials (EPSPs) when glutamate binds.\nKainic 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. In fact, kainate seems to regulate serotonergic activity in the vertebrate retina.\nElectrical stimulation of designated areas of the brain are generally administered by passing an electric current through a wire that is inserted into the brain to lesion a particular area of the brain. Electrical stimulation indiscriminately destroys anything in the vicinity of the electrode tip, including neural bodies and axons of neurons passing through; therefore it is difficult to attribute the effects of the lesion to a single area. Chemical stimulation is typically administered through a cannula that is inserted into the brain via stereotactic surgery. Chemical stimulation, while more complicated than electrical stimulation, has the distinct advantage of activating cell bodies, but not nearby axons, because only cell bodies and subsequent dendrites contain glutamate receptors. Therefore, chemical stimulation by kainic acid is more localized than electrical stimulation. Both chemical and electrical lesions potentially cause additional damage to the brain due to the very nature of the inserted electrode or cannula. Therefore, the most effective ablation studies are performed in comparison to a sham lesion that duplicates all the steps of producing a brain lesion except the one that actually causes the brain damage, that is, injection of kainic acid or administration of an electrical shock."}