Kynurenate is product of the metabolism of L-Tryptophan and appears in urine in Vitamin B6 deficiencies. Your body needs vitamin B6 (pyridoxine) to utilize amino acids derived from dietary protein. Inadequate vitamin B6 is one factor that leads to increased concentrations of kynurenate and xanthurenate in urine. These products of amino acid breakdown cannot be further metabolized in the absence of vitamin B6.

Kynurenic Acid is product of the metabolism of L-Tryptophan and appears in urine in Vitamin B6 deficiencies. Your body needs vitamin B6 (pyridoxine) to utilize amino acids derived from dietary protein.

Kynurenic Acid is product of the metabolism of L-Tryptophan and appears in urine in Vitamin B6 deficiencies. Your body needs vitamin B6 (pyridoxine) to utilize amino acids derived from dietary protein.

Kynurenic Acid is product of the metabolism of L-Tryptophan and appears in urine in Vitamin B6 deficiencies. Your body needs vitamin B6 (pyridoxine) to utilize amino acids derived from dietary protein.

Kynurenic acid, which is derived from the processing of tryptophan, is converted to quinolinic acid in the presence of B6 or P5P. While kynurenic is calming, quinolinic is an excitotoxin that can over stimulate nerves. 

Because of the specific inflammatory component of quinolinic acid, as well as the potentially protective role of kynurenic acid peripherally, laboratories measure the ratio of kynurenic acid to quinolinic acid. This ratio can act as a measure of disturbed kynurenine pathway metabolism. It suggests that tryptophan is catabolized via the kynurenine pathway, rather than the serotonin pathway.

Kynurenic acid and Quinolinic acid are tryptophan metabolites formed through the kynurenine pathway. Tryptophan is the amino acid precursor to serotonin; its major route for catabolism is the kynurenine pathway. Important products of the kynurenine pathway include xanthurenic acid and kynurenic acid, which can further metabolize into quinolinic acid. The historical importance of this pathway has mainly been as a source of the coenzyme NAD+, which is important for all redox reactions in the mitochondria.

However, it is now understood that kynurenic and quinolinic acid have physiologic implications. This alternate pathway is upregulated in response to inflammation and stress, which can lead to deficient serotonin production. Kynurenic acid has shown some neuroprotective properties in the brain, since it can stimulate NMDA receptors. However, its importance on the periphery is still not fully elucidated. Some studies outline antiinflammatory, analgesic, antiatherogenic, antioxidative, and hepatoprotective properties to peripheral kynurenic acid.

The correlation to levels of urinary excretion needs further study. Quinolinic acid, in and of itself, can be inflammatory and neurotoxic.

Kynurenic Acid is product of the metabolism of L-Tryptophan and appears in urine in Vitamin B6 deficiencies. Your body needs vitamin B6 (pyridoxine) to utilize amino acids derived from dietary protein.

Kynurenic acid and Quinolinic acid are tryptophan metabolites formed through the kynurenine pathway. Tryptophan is the amino acid precursor to serotonin; its major route for catabolism is the kynurenine pathway. Important products of the kynurenine pathway include xanthurenic acid and kynurenic acid, which can further metabolize into quinolinic acid. The historical importance of this pathway has mainly been as a source of the coenzyme NAD+, which is important for all redox reactions in the mitochondria.

However, it is now understood that kynurenic and quinolinic acid have physiologic implications. This alternate pathway is upregulated in response to inflammation and stress, which can lead to deficient serotonin production. Kynurenic acid has shown some neuroprotective properties in the brain, since it can stimulate NMDA receptors. However, its importance on the periphery is still not fully elucidated. Some studies outline antiinflammatory, analgesic, antiatherogenic, antioxidative, and hepatoprotective properties to peripheral kynurenic acid.

The correlation to levels of urinary excretion needs further study. Quinolinic acid, in and of itself, can be inflammatory and neurotoxic.

Kynurenic Acid is product of the metabolism of L-Tryptophan and appears in urine in Vitamin B6 deficiencies. Your body needs vitamin B6 (pyridoxine) to utilize amino acids derived from dietary protein.

Kynurenic Acid is product of the metabolism of L-Tryptophan and appears in urine in Vitamin B6 deficiencies. Your body needs vitamin B6 (pyridoxine) to utilize amino acids derived from dietary protein.

Kynurenic acid, a neuroactive metabolite produced from kynurenine, is regarded to be neuroprotective unless in excess amounts.

Kynurenine is a central metabolite of the amino acid tryptophan with vasodilatory properties.

Kynurenine is a central metabolite in the tryptophan degradation pathway, known as the kynurenine pathway, which plays a vital role in neurotransmitter balance, immune regulation, mitochondrial energy production, and oxidative stress control. It sits at a critical metabolic crossroads—linking the amino acid tryptophan with the synthesis of nicotinamide adenine dinucleotide (NAD+), a molecule essential for cellular energy and redox balance.

On the Neurotransmitter XL panel, kynurenine helps reveal whether tryptophan is being converted primarily into serotonin and melatonin (supporting mood and sleep) or diverted into stress- and inflammation-related pathways that generate neuroactive metabolites like quinolinic acid and kynurenic acid. Imbalances in kynurenine metabolism are often associated with chronic stress, immune activation, depression, fatigue, and mitochondrial dysfunction.

Kynurenine is the primary breakdown product of tryptophan.

- Kynurenine blood levels have been found higher in type 2 diabetes, obesity, CVD, ADHD in children, HOMA-IR.

- Higher kynurenine increases Treg cell differentiation via the AhR (aryl hydrocarbon receptor) pathway.

- Blood levels were lower in acute ischemic stroke patients, older age, adults with ADHD.

- Upregulation of other tryptophan breakdown enzymes KMO (Kynurenine monooxygenase) and KYNU (Kynureninase) may decrease kynurenine.

Kynurenine is the primary breakdown product of tryptophan.

- Kynurenine blood levels have been found higher in type 2 diabetes, obesity, CVD, ADHD in children, HOMA-IR.

- Higher kynurenine increases Treg cell differentiation via the AhR (aryl hydrocarbon receptor) pathway.

- Blood levels were lower in acute ischemic stroke patients, older age, adults with ADHD.

- Upregulation of other tryptophan breakdown enzymes KMO (Kynurenine monooxygenase) and KYNU (Kynureninase) may decrease kynurenine.