Kynurenine 3-monooxygenase

Kynurenine 3-monooxygenase (KMO, EC is a 56 kDa flavoenzyme that catalyzes the hydroxylation of L-kynurenine (L-Kyn) to 3-hydroxykynurenine (3-HK) in the kynurenine pathway, the major route for tryptophan metabolism.

Literature (7)

Kynurenine 3-monooxygenase Inhibitors

Cat. No. Product Name / Activity
3254 Ro 61-8048
Potent kynurenine 3-monooxygenase (KMO) inhibitor
4926 UPF 648
Potent kynurenine 3-monooxygenase (KMO) inhibitor

Kynurenine 3-monooxygenase (KMO, EC is a 56 kDa flavoenzyme that catalyzes the hydroxylation of L-kynurenine (L-Kyn) to 3-hydroxykynurenine (3-HK) in the kynurenine pathway, the major route for tryptophan metabolism.

KMO is found in the liver, kidney and some immune cells and is localized to the outer membrane of mitochondria where it is anchored via its hydrophobic C-terminus, which contains a putative targeting sequence for this location. Both the targeting sequence and a noncovalent flavin adenine dinucleotide (FAD) cofactor are required for proper enzyme function, which is dependent on FAD reduction.

Like IDO, KMO is induced in response to pro-inflammatory stimuli, and the conversion of L-Kyn to 3-HK forms the start of the "neurotoxic" fork in the kynurenine pathway, which results in the formation of toxic L-Trp metabolite, quinolinic acid (QUIN). The "neuroprotective" pathway that is regulated by kynurenine amino transferases (KATs) converts L-Kyn to kynurenic acid (KynA).

Inflammation can induce expression of KMO and drive the production of QUIN which is thought to exacerbate neurodegenerative disorders as well as anxiety, depression and epilepsy. Inhibitors of KMO have shown some success in inhibiting neuroinflammation or the progression of Parkinson's disease, Huntington's disease and Alzheimer's disease.

External sources of pharmacological information for Kynurenine 3-monooxygenase :

Literature for Kynurenine 3-monooxygenase

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