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SML0233

Sigma-Aldrich

Ro 61-8048

≥98% (HPLC)

Synonym(s):

3,4-Dimethoxy-N-[4-(3-nitrophenyl)-2-thiazolyl]-benzenesulfonamide, 3,4-Dimethoxy-N-[4-(3-nitrophenyl)thiazol-2-yl]benzenesulfonamide, Ro-61-8048

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About This Item

Empirical Formula (Hill Notation):
C17H15N3O6S2
CAS Number:
199666-03-0
Molecular Weight:
421.45
MDL number:
MFCD11040807
UNSPSC Code:
12352200
PubChem Substance ID:
329825246

Quality Level

100

Assay

≥98% (HPLC)

form

powder

color

faintly yellow to yellow

solubility

DMSO: ≥15 mg/mL

storage temp.

2-8°C

SMILES string

COc1ccc(cc1OC)S(=O)(=O)Nc2nc(cs2)-c3cccc(c3)[N+]([O-])=O

InChI

1S/C17H15N3O6S2/c1-25-15-7-6-13(9-16(15)26-2)28(23,24)19-17-18-14(10-27-17)11-4-3-5-12(8-11)20(21)22/h3-10H,1-2H3,(H,18,19)

InChI key

NDPBMCKQJOZAQX-UHFFFAOYSA-N

Application

Ro 61-8048 has been used as a kynurenine 3-monooxygenase (KMO) inhibitor to study its effects on nicotinamide adenine dinucleotide (NAD+) concentration in hepatocytes of mice.

Biochem/physiol Actions

Inhibition of kynurenine 3-hydroxylase by Ro 61-8048 reduces the episodes of dystonia and dyskinesias induced by decreased levels of kynurenic acid.
Ro 61-8048 is an inhibitor of kynurenine 3-monooxygenase (KMO) that increases kynurenic acid levels and reduces extracellular glutamate in the brain.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Certificates of Analysis (COA)

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Francesca M Notarangelo et al.
Developmental neuroscience, 41(1-2), 102-111 (2019-05-23)
Several lines of evidence support the hypothesis that abnormally elevated brain levels of kynurenic acid (KYNA), a metabolite of the kynurenine pathway (KP) of tryptophan degradation, play a pathophysiologically significant role in schizophrenia and other major neurodevelopmental disorders. Studies in
Paul B Larkin et al.
Biochimica et biophysica acta, 1860(11 Pt A), 2345-2354 (2016-07-10)
In mammals, the majority of the essential amino acid tryptophan is degraded via the kynurenine pathway (KP). Several KP metabolites play distinct physiological roles, often linked to immune system functions, and may also be causally involved in human diseases including
Melanie Hamann et al.
European journal of pharmacology, 586(1-3), 156-159 (2008-03-21)
Striatal dysfunctions seem to play a key role in the pathophysiology of dystonia in the dt(sz) mutant hamster, a model of paroxysmal non-kinesigenic dyskinesia, in which stress precipitates dystonic episodes. Previous examinations have shown changes in kynurenic acid levels and
Angelika Richter et al.
European journal of pharmacology, 478(1), 47-52 (2003-10-14)
The effects of the novel kynurenine 3-hydroxylase inhibitor 3,4-dimethoxy-N-[4-(3-nitrophenyl)thiazol-2-yl]benzenesulfonamide (Ro 61-8048) on severity of dystonia were examined in dt(sz) mutant hamsters, an animal model of paroxysmal dystonia, in which stress precipitates dystonic episodes. Ro 61-8048 (50, 100 and 150 mg/kg
Arghya Ray et al.
Leukemia, 34(2), 567-577 (2019-08-30)
Our prior studies showed that dysfunctional plasmacytoid dendritic cells (pDCs) contribute to multiple myeloma (MM) pathogenesis. Specifically, pDC interactions with tumor and T/NK effector cells in the bone marrow (BM) milieu induce immune suppression and MM cell proliferation. Delineation of
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