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Details

Stereochemistry ACHIRAL
Molecular Formula C7H5NO4
Molecular Weight 167.1189
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of QUINOLINIC ACID

SMILES

OC(=O)C1=C(N=CC=C1)C(O)=O

InChI

InChIKey=GJAWHXHKYYXBSV-UHFFFAOYSA-N
InChI=1S/C7H5NO4/c9-6(10)4-2-1-3-8-5(4)7(11)12/h1-3H,(H,9,10)(H,11,12)

HIDE SMILES / InChI

Molecular Formula C7H5NO4
Molecular Weight 167.1189
Charge 0
Count
MOL RATIO 1 MOL RATIO (average)
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Description

Quinolinic acid is an endogenous N-methyl-D-aspartate receptor agonist synthesized from L-tryptophan via the kynurenine pathway and thereby has the potential of mediating N-methyl-D-aspartate neuronal damage and dysfunction. Elevated cerebrospinal fluid levels of quinolinic acid are correlated with the severity of neuropsychological deficits in patients who have AIDS. It can act as an endogenous brain excitotoxin when released by activated macrophages. Quinolinic acid is being used as a research tool to examine the role of excitotoxicity in neuronal degeneration associated with a number of neurological diseases (Alzheimer's disease, Huntington's disease, Parkinson's disease) which involve selective neurotransmitter deficits.

CNS Activity

Originator

Approval Year

Targets

Primary TargetPharmacologyConditionPotency
24.2 µM [Ki]
1.4 µM [IC50]
0.7 µM [IC50]

Conditions

ConditionModalityTargetsHighest PhaseProduct

PubMed

Sample Use Guides

In Vivo Use Guide
Unknown
Route of Administration: Unknown
In Vitro Use Guide
The effects of quinolinic acid (QUIN) on glutamate-induced excitotoxicity were examined in primary cultures of rat cerebellar granule neurons. Exposing these neurons to QUIN (< or =2.5 mM) in the presence of glucose and Mg2+ had no effect on their viability. Although pretreating neurons with QUIN (10 microM) for 6 h did not reduce necrotic death induced by glutamate exposure in the absence of glucose and Mg2+, QUIN pretreatment significantly suppressed glutamate-induced apoptosis by 68% (as indicated by DNA fragmentation) in cultures containing glucose and Mg2+. Furthermore, the N-methyl-D-aspartate (NMDA) receptor antagonist AP-5 reversed QUIN-induced neuroprotection, while the non-NMDA antagonist CNQX had no effect. This study demonstrates that pathophysiologically relevant concentrations of QUIN can protect neurons from apoptosis mediated via the NMDA receptor.
Substance Class Chemical
Record UNII
F6F0HK1URN
Record Status Validated (UNII)
Record Version