Potent, active site-targeting kynurenine 3-monooxygenase (KMO; kynurenine 3-hydroxylase) inhibitor that protects against neurodegeneration in vivo.
UPF-648 is a potent, active site-targeting kynurenine 3-monooxygenase (KMO; kynurenine 3-hydroxylase) inhibitor (IC50 = 20 nM) that prevents productive binding of the substrate L-kynurenine by perturbing the local active-site structure. UPF-648 protects against neurodegeneration in a murine (30 mg/kg, i.p.) and a Drosophila (100 μM in maize media) model of Huntington′s disease by shifting kynurenine pathway metabolism towards enhanced neuroprotective kynurenic acid (KYNA) formation and away from the free radicals generator 3-hydroxykynurenine (3-HK) and the excitotoxic quinolinic acid (QUIN).
Current biology : CB, 21(11), 961-966 (2011-06-04)
Neuroactive metabolites of the kynurenine pathway (KP) of tryptophan degradation have been implicated in the pathophysiology of neurodegenerative disorders, including Huntington's disease (HD) [1]. A central hallmark of HD is neurodegeneration caused by a polyglutamine expansion in the huntingtin (htt)
Biochemistry and structural studies of kynurenine 3-monooxygenase reveal allosteric inhibition by Ro 61-8048
Triple-negative breast cancer (TNBC) is aggressive and has a poor prognosis. Kynurenine 3-monooxygenase (KMO), a crucial kynurenine metabolic enzyme, is involved in inflammation, immune response and tumorigenesis. We aimed to study the role of KMO in TNBC. KMO alteration and
Frontiers in pharmacology, 9, 724-724 (2018-07-28)
Neuropathic pain caused by a primary injury or dysfunction in the peripheral or central nervous system is a tremendous therapeutic challenge. Here, we have collected the first evidence from a single study on the potential contributions to neuropathic pain development
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