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  7. 2,3-Pyridinedicarboxylic acid
2,3-Pyridinedicarboxylic acid
2,3-Pyridinedicarboxylic acid Chemical Structure

2,3-Pyridinedicarboxylic acid

Catalog NO.: 89-00-9 CAS NO.: 89-00-9 Brand: BOC Sciences

Category
Inhibitor
Tag/Targets
NMDA Receptor
Molecular Formula
C7H5NO4
Molecular Weight
167.12

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WARNING: Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

cGMP Capacity

  • kg to MT scale
  • GMP batches production
  • Over 20 years of experience
  • HPAPI production with OEL < 1 μg/m³
  • Cleanroom Class 100 to Class 100,000
  • Special type of reactions in cGMP workshop
  • Cleaning level: Class A B C
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Product Description

Quinolinic acid is an endogenous NMDA agonist and transmitter candidate. It may distinguish between NMDA receptor subtypes. By overactivating NMDA receptors, quinolinic acid produces neurotoxicity, which has been implicated in certain neurodegenerative disorders.

Boiling Point
425 °C at 760 mmHg
Melting Point
188 °C
Density
1.551 g/cm3
InChI Key
GJAWHXHKYYXBSV-UHFFFAOYSA-N
InChI
InChI=1S/C7H5NO4/c9-6(10)4-2-1-3-8-5(4)7(11)12/h1-3H,(H,9,10)(H,11,12)
SMILES
C1=CC(=C(N=C1)C(=O)O)C(=O)O
Refractive Index
1.62
NCT NumberTitleCondition Or DiseasePhaseStart DateSponsorStatus
NCT04005781Effect of Bitter in Overweight Female Volunteers (PLAQOW)ObesityPhase 4October 1, 2019Universitaire Ziekenhuizen LeuvenNotyetrecruiting
NCT04005768Effect of Hydroxychloroquine Sulphate in Healthy Lean Females (PLAQHV)ObesityPhase 4August 1, 2019Universitaire Ziekenhuizen Leuven,Universitaire Ziekenhuizen LeuvenNotyetrecruiting
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1.Tryptophan-2,3-dioxygenase (TDO) inhibition ameliorates neurodegeneration by modulation of kynurenine pathway metabolites.
Breda C1, Sathyasaikumar KV2, Sograte Idrissi S1, Notarangelo FM2, Estranero JG1, Moore GG1, Green EW1, Kyriacou CP1, Schwarcz R2, Giorgini F3. Proc Natl Acad Sci U S A. 2016 Apr 25. pii: 201604453. [Epub ahead of print]
Metabolites of the kynurenine pathway (KP) of tryptophan (TRP) degradation have been closely linked to the pathogenesis of several neurodegenerative disorders. Recent work has highlighted the therapeutic potential of inhibiting two critical regulatory enzymes in this pathway-kynurenine-3-monooxygenase (KMO) and tryptophan-2,3-dioxygenase (TDO). Much evidence indicates that the efficacy of KMO inhibition arises from normalizing an imbalance between neurotoxic [3-hydroxykynurenine (3-HK); quinolinic acid (QUIN)] and neuroprotective [kynurenic acid (KYNA)] KP metabolites. However, it is not clear if TDO inhibition is protective via a similar mechanism or if this is instead due to increased levels of TRP-the substrate of TDO. Here, we find that increased levels of KYNA relative to 3-HK are likely central to the protection conferred by TDO inhibition in a fruit fly model of Huntington's disease and that TRP treatment strongly reduces neurodegeneration by shifting KP flux toward KYNA synthesis.
2.Atorvastatin Prevents Glutamate Uptake Reduction Induced by Quinolinic Acid Via MAPKs Signaling.
Vandresen-Filho S1,2, Martins WC3, Bertoldo DB3, Rieger DK3, Maestri M3, Leal RB3, Tasca CI3. Neurochem Res. 2016 Apr 15. [Epub ahead of print]
Statins have been shown to promote neuroprotection in a wide range of neurological disorders. However, the mechanisms involved in such effects of statins are not fully understood. Quinolinic acid (QA) is a neurotoxin that induces seizures when infused in vivo and promotes glutamatergic excitotoxicity in the central nervous system. The aim of this study was to evaluate the putative glutamatergic mechanisms and the intracellular signaling pathways involved in the atorvastatin neuroprotective effects against QA toxicity. Atorvastatin (10 mg/kg) treatment for 7 days prevented the QA-induced decrease in glutamate uptake, but had no effect on increased glutamate release induced by QA. Moreover, atorvastatin treatment increased the phosphorylation of ERK1 and prevented the decrease in Akt phosphorylation induced by QA. Neither atorvastatin treatment nor QA infusion altered glutamine synthetase activity or the levels of phosphorylation of p38MAPK or JNK1/2 during the evaluation.
Preparing Stock Solutions
ConcentrationVolumeMass1 mg5 mg10 mg
1 mM5.9837 mL29.9186 mL59.8372 mL
5 mM1.1967 mL5.9837 mL11.9674 mL
10 mM0.5984 mL2.9919 mL5.9837 mL
50 mM0.1197 mL0.5984 mL1.1967 mL
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BOC Sciences is a trusted global supplier of research chemicals, biochemicals, and pharmaceutical ingredients, serving the life sciences, biotech, and pharmaceutical industries. Headquartered in New York, we offer a comprehensive product portfolio that includes inhibitors, building blocks, carbohydrates, nucleosides, nucleotides, GMP products, impurities and metabolites, APIs, natural compounds, ADC-related chemicals, and stem cell molecules.

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