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(S)-nicotine + NADPH + O2
(S)-nicotine N1-oxide + NADP+ + H2O
-
(S)-nicotine N-1'-oxygenation
-
-
?
1,1-dimethylhydrazine + NADPH + O2
formaldehyde + CH3N2H3 + NADP+
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine + NADPH + H+ + O2
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine N-oxide + NADP+ + H2O
10-(N,N-dimethylaminopentyl)-2-(trifluoromethyl)phenothiazine + NADPH + O2
?
-
-
-
-
?
10-N-(n-octylamino)-2-(trifluoromethyl) phenothiazine + NADPH + O2
10-N-(n-octylamino)-2-(trifluoromethyl) phenothiazine N-oxide + NADP+ + H2O
-
-
-
-
?
3-hydroxy-nabumetone + NADPH + H+ + O2
? + NADP+ + H2O
activation reaction
-
-
?
4-aminobenzoic acid hydrazide + NADPH + O2
?
-
-
-
?
amphetamine + NADPH + O2
amphetamine N-oxide + NADP+ + H2O
-
-
-
-
?
benzydamine + NADPH + H+ + O2
benzydamine N-oxide + NADP+ + H2O
benzylamine + [reduced NADPH-hemoprotein reductase] + O2
benzylamine N-oxide + [oxidized NADPH-hemoprotein reductase] + H2O
-
-
-
-
?
chlorpromazine + NADPH + H+ + O2
chlorpromazine N-oxide + NADP+ + H2O
-
-
-
?
cimetidine + NADPH + O2
cimetidine S-oxide + NADP+ + H2O
-
-
-
-
?
clomiphene + NADPH + H+ + O2
clomiphene N-oxide + NADP+ + H2O
clomiphene is used in infertility medication
-
-
?
clomipramine + NADPH + H+ + O2
clomipramine N-oxide + NADP+ + H2O
-
-
-
?
clozapine + NADPH + H+ + O2
clozapine N-oxide + NADP+ + H2O
-
-
-
?
clozapine + NADPH + O2
?
-
-
-
-
?
cysteamine + NADPH + O2
cysteamine N-oxide + NADP+ + H2O
dapsone + NADPH + O2
?
bioactivation by isozyme FMO3, not FMO1, results in covalent adduct formation
-
-
?
dasatinib + NADPH + H+ + O2
dasatinib N-oxide + NADP+ + H2O
-
-
-
?
demeton-O + NADPH + O2
demeton-O sulfoxide + NADP+ + H2O
-
-
-
-
?
dihydrolipoic acid + NADPH + O2
?
-
-
-
-
?
ethiofencarb + NADPH + O2
ethiofencarb sulfoxide + NADP+ + H2O
-
-
-
-
?
ethionamide + NADPH + H+ + O2
ethionamide S-oxide + NADP+ + H2O
ethionamide + NADPH + O2 + H+
2-ethyl-N-hydroxypyridine-4-carbothioamide + NADP+ + H2O
fenthion + NADPH + O2
fenthion sulfoxide + NADP+ + H2O
-
-
-
-
?
GSK5182 + NADPH + H+ + O2
GSK5182 N-oxide + NADP+ + H2O
an antidiabetic lead molecule
-
-
?
hypotaurine + H2O + NAD+
taurine + NADH
-
metabolism of cysteine
-
?
hypotaurine + NADH + H+ + O2
taurine + NAD+ + H2O
hypotaurine + NADPH + H+ + O2
taurine + NADP+ + H2O
imipramine + NADPH + O2
?
-
-
-
-
?
indole + NADPH + H+ + O2
indole N-oxide + NADP+ + H2O
itopride + NADPH + H+ + O2
itopride N-oxide + NADP+ + H2O
itopride + NADPH + O2
?
-
-
-
-
?
L-methionine + NADPH + O2
L-methionine S-oxide + NADP+ + H2O
lipoic acid + NADPH + O2
?
loxapine + NADPH + H+ + O2
loxapine N-oxide + NADP+ + H2O
-
-
-
?
methimazole + NADPH + O2
?
methiocarb + NADPH + O2
methiocarb sulfoxide + NADP+ + H2O
-
-
-
-
?
methyl 4-tolyl sulfide + NADPH + O2
methyl 4-tolyl sulfoxide + NADP+ + H2O
-
-
-
-
?
methylthioalkyl glucosinolate + NADPH + H+ + O2
methylsulfinylalkyl glucosinolate S-oxide + NADP+ + H2O
-
-
-
-
?
N,N-dimethylamphetamine + NADPH + H+ + O2
N,N-dimethylamphetamine N-oxide + NADP+ + H2O
N-oxygenation mainly by isozyme FMO1, low activity with isozyme FMO3
-
-
?
N,N-dimethylaniline + NADH + H+ + O2
N,N-dimethylaniline N-oxide + NAD+ + H2O
-
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
N,N-dimethylaniline + NADPH + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
phenethylamine + NADPH + O2
phenethylamine N-oxide + NADP+ + H2O
-
isozyme FMO3
-
-
?
ranitidine + NADPH + O2
?
-
-
-
-
?
S-farnesylcysteine + NADPH + O2
S-farnesylcysteine S-oxide + NADP+ + H2O
-
-
-
-
?
S-farnesylcysteine methyl ester + NADPH + O2
?
-
-
-
-
?
selegiline + NADPH + O2
selegiline N-oxide + NADP+
-
-
-
-
?
sulfamethoxazole + NADPH + O2
?
bioactivation by isozyme FMO3, not FMO1, results in covalent adduct formation
-
-
?
sulindac sulfide + NADPH + O2
(S,R)-sulindac + NADP+ + H2O
-
-
-
-
?
tamoxifen + NADPH + H+ + O2
tamoxifen N-oxide + NADP+ + H2O
tamoxifen + NADPH + O2
tamoxifen N-oxide + NADP+ + H2O
thiacetazone + 2 NADPH + 2 H+ + 2 O2
thiacetazone carbodiimide + 2 NADP+ + 2 H2O
thiacetazone + 2 NADPH + 2 O2
(E)-{(2E)-[4-(acetylamino)benzylidene]hydrazinylidene}(amino)methanesulfinic acid + 2 NADP+ + H2O
-
bioactivation by EtaA
-
-
?
tigecycline + NADPH + O2
11a-hydroxytigecycline + NADP+ + H2O
-
detoxification, the organism is resistant against the antibiotic
-
-
?
tozasertib + NADPH + H+ + O2
tozasertib N-oxide + NADP+ + H2O
-
-
-
?
trimethylamine + NADPH + H+ + O2
trimethylamine N-oxide + NADP+ + H2O
trimethylamine + NADPH + O2
trimethylamine N-oxide + NADP+ + H2O
tyramine + NADPH + O2
tyramine N-oxide + NADP+ + H2O
-
-
-
-
?
voriconazole + NADPH + H+ + O2
?
-
liver microsomes, a potent second-generation triazole antifungal agent with broad-spectrum activity against clinically important fungi
-
-
?
xanomeline + NADPH + H+ + O2
xanomeline N-oxide + NADP+ + H2O
-
-
-
?
[7-(2,6-dichloro-phenyl)-5-methyl-benzo[1,2,4]triazin-3-yl]-[4-(2-pyrrolidin-1-yl-ethoxy)-phenyl]-amine + NADPH + H+ + O2
[7-(2,6-dichlorophenyl)-5-methyl-benzo[1,2,4]triazin-3-yl]-(4-[2-(1-oxy-pyrrolidin-1-yl)-ethoxy]-phenyl)-amine + NADP+ + H2O
-
i.e. TG100435, a multitargeted Src family kinase inhibitor with anticancer activity, FMO3 is the primary enzyme responsible for TG100855 formation, enzyme-mediated retroreduction of TG100855 back to TG100435 is observed catalyzed by a cytochrome P450 reductase, overview
i.e. TG100855, the N-oxide product is also a multitargeted Src family kinase inhibitor with anticancer activity
-
?
additional information
?
-
1,1-dimethylhydrazine + NADPH + O2
formaldehyde + CH3N2H3 + NADP+
-
possibly, and other 1,1-disubstituted hydrazines
-
?
1,1-dimethylhydrazine + NADPH + O2
formaldehyde + CH3N2H3 + NADP+
-
possibly, and other 1,1-disubstituted hydrazines
-
?
1,1-dimethylhydrazine + NADPH + O2
formaldehyde + CH3N2H3 + NADP+
-
possibly, and other 1,1-disubstituted hydrazines
-
?
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine + NADPH + H+ + O2
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine N-oxide + NADP+ + H2O
-
reaction in microsomal detoxification pathway of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, a neurotoxin to nigrostriatal dopaminergic neurons
-
-
?
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine + NADPH + H+ + O2
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine N-oxide + NADP+ + H2O
-
reaction in microsomal detoxification pathway of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, a neurotoxin to nigrostriatal dopaminergic neurons
-
-
?
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine + NADPH + H+ + O2
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine N-oxide + NADP+ + H2O
-
one of the predominant enzmyes responsible for the oxygenation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
-
-
?
benzydamine + NADPH + H+ + O2
benzydamine N-oxide + NADP+ + H2O
-
-
-
-
?
benzydamine + NADPH + H+ + O2
benzydamine N-oxide + NADP+ + H2O
-
-
-
?
benzydamine + NADPH + H+ + O2
benzydamine N-oxide + NADP+ + H2O
-
-
-
-
?
benzydamine + NADPH + H+ + O2
benzydamine N-oxide + NADP+ + H2O
-
-
-
-
?
benzydamine + NADPH + H+ + O2
benzydamine N-oxide + NADP+ + H2O
-
-
-
-
?
cysteamine + NADPH + O2
cysteamine N-oxide + NADP+ + H2O
-
-
-
-
?
cysteamine + NADPH + O2
cysteamine N-oxide + NADP+ + H2O
-
-
-
-
?
cysteamine + NADPH + O2
cysteamine N-oxide + NADP+ + H2O
-
-
-
-
?
cysteamine + NADPH + O2
cysteamine N-oxide + NADP+ + H2O
-
-
-
-
?
ethionamide + NADPH + H+ + O2
ethionamide S-oxide + NADP+ + H2O
ethionamide is a pro-drug requiring bioactivation to exert toxicity
-
-
?
ethionamide + NADPH + H+ + O2
ethionamide S-oxide + NADP+ + H2O
ethionamide is a pro-drug requiring bioactivation to exert toxicity
-
-
?
ethionamide + NADPH + O2 + H+
2-ethyl-N-hydroxypyridine-4-carbothioamide + NADP+ + H2O
-
bioactivation by isozymes FMO1 and FMO3
-
-
?
ethionamide + NADPH + O2 + H+
2-ethyl-N-hydroxypyridine-4-carbothioamide + NADP+ + H2O
-
bioactivation by EtaA
-
-
?
hypotaurine + NADH + H+ + O2
taurine + NAD+ + H2O
S-oxygenation
-
-
?
hypotaurine + NADH + H+ + O2
taurine + NAD+ + H2O
S-oxygenation
-
-
?
hypotaurine + NADPH + H+ + O2
taurine + NADP+ + H2O
S-oxygenation
-
-
?
hypotaurine + NADPH + H+ + O2
taurine + NADP+ + H2O
S-oxygenation
-
-
?
indole + NADPH + H+ + O2
indole N-oxide + NADP+ + H2O
-
-
-
-
?
indole + NADPH + H+ + O2
indole N-oxide + NADP+ + H2O
-
-
-
-
?
itopride + NADPH + H+ + O2
itopride N-oxide + NADP+ + H2O
-
-
-
?
itopride + NADPH + H+ + O2
itopride N-oxide + NADP+ + H2O
-
-
-
-
?
L-methionine + NADPH + O2
L-methionine S-oxide + NADP+ + H2O
-
-
-
-
?
L-methionine + NADPH + O2
L-methionine S-oxide + NADP+ + H2O
-
-
-
-
?
L-methionine + NADPH + O2
L-methionine S-oxide + NADP+ + H2O
-
-
-
-
?
L-methionine + NADPH + O2
L-methionine S-oxide + NADP+ + H2O
-
-
-
-
?
lipoic acid + NADPH + O2
?
-
-
-
-
?
lipoic acid + NADPH + O2
?
-
-
-
-
?
methimazole + NADPH + O2
?
-
-
-
-
?
methimazole + NADPH + O2
?
-
-
-
?
methimazole + NADPH + O2
?
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
-
?
N,N-dimethylaniline + NADPH + H+ + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
?
N,N-dimethylaniline + NADPH + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
-
?
N,N-dimethylaniline + NADPH + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
-
?
N,N-dimethylaniline + NADPH + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
-
?
N,N-dimethylaniline + NADPH + O2
N,N-dimethylaniline N-oxide + NADP+ + H2O
-
-
-
-
?
tamoxifen + NADPH + H+ + O2
tamoxifen N-oxide + NADP+ + H2O
-
-
-
?
tamoxifen + NADPH + H+ + O2
tamoxifen N-oxide + NADP+ + H2O
tamoxifen is used in breast cancer medication
-
-
?
tamoxifen + NADPH + O2
tamoxifen N-oxide + NADP+ + H2O
-
tamoxifen metabolism pathways involving FMOs and CYP450s, tamoxifen N-oxide is reconverted into tamoxifen by reduced hemoglobin and NADPH-P450 oxidoreductase, a metabolic cycle in vivo, overview
-
-
?
tamoxifen + NADPH + O2
tamoxifen N-oxide + NADP+ + H2O
-
tamoxifen N-oxygenation represents a detoxication pathway, low level of tamoxifen N-oxide production in human liver microsomes may be explained by the kinetics of FMO1 versus FMO3
-
-
?
tamoxifen + NADPH + O2
tamoxifen N-oxide + NADP+ + H2O
-
tamoxifen N-oxygenation represents a detoxication pathway, high activity by isozyme FMO1
-
-
?
tamoxifen + NADPH + O2
tamoxifen N-oxide + NADP+ + H2O
-
tamoxifen N-oxygenation represents a detoxication pathway
-
-
?
tamoxifen + NADPH + O2
tamoxifen N-oxide + NADP+ + H2O
-
tamoxifen N-oxygenation represents a detoxication pathway
-
-
?
thiacetazone + 2 NADPH + 2 H+ + 2 O2
thiacetazone carbodiimide + 2 NADP+ + 2 H2O
-
bioactivation by isozymes FMO1 and FMO3, two-step process
-
-
?
thiacetazone + 2 NADPH + 2 H+ + 2 O2
thiacetazone carbodiimide + 2 NADP+ + 2 H2O
-
bioactivation by EtaA
-
-
?
trimethylamine + NADPH + H+ + O2
trimethylamine N-oxide + NADP+ + H2O
-
-
-
-
?
trimethylamine + NADPH + H+ + O2
trimethylamine N-oxide + NADP+ + H2O
-
-
-
?
trimethylamine + NADPH + H+ + O2
trimethylamine N-oxide + NADP+ + H2O
-
-
-
-
?
trimethylamine + NADPH + H+ + O2
trimethylamine N-oxide + NADP+ + H2O
-
mutations of FMO3 are involved in trimethylaminuria, primary trimethylaminuria is multifactorial in origin in that enzyme dysfunction can result from kinetic incompetencies as well as impaired assembly of holoprotein, overview
-
-
?
trimethylamine + NADPH + O2
trimethylamine N-oxide + NADP+ + H2O
-
-
-
-
?
trimethylamine + NADPH + O2
trimethylamine N-oxide + NADP+ + H2O
-
preferred substrate of isozyme FMO3
-
-
?
trimethylamine + NADPH + O2
trimethylamine N-oxide + NADP+ + H2O
-
-
-
-
?
trimethylamine + NADPH + O2
trimethylamine N-oxide + NADP+ + H2O
-
-
-
-
?
additional information
?
-
enhanced disease susceptibility1, EDS1, controls defense activation and programmed cell death conditioned by intracellular Toll-related immune receptors that recognize specific pathogen effectors in Arabidopsis thaliana, EDS1 is also needed for basal resistance to invasive pathogens by restricting the progression of disease, EDS1 with phytoalexin-deficient 4, PAD4, regulates accumulation of the phenolic defense molecule salicylic acid, EDS1 is regulated by FMO and the Nudix hydrolase NUDT7
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-
?
additional information
?
-
-
enhanced disease susceptibility1, EDS1, controls defense activation and programmed cell death conditioned by intracellular Toll-related immune receptors that recognize specific pathogen effectors in Arabidopsis thaliana, EDS1 is also needed for basal resistance to invasive pathogens by restricting the progression of disease, EDS1 with phytoalexin-deficient 4, PAD4, regulates accumulation of the phenolic defense molecule salicylic acid, EDS1 is regulated by FMO and the Nudix hydrolase NUDT7
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-
?
additional information
?
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-
isozyme FMO1 is an essential component of biologically induced systemic acquired resistance, e.g. versus the bacterial pathogen Pseudomonas syringae pv maculicola, resistance is accompanied by accumulation of salicylic acid, overview
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-
?
additional information
?
-
-
the enzyme is important for pathogen defense and resistance participating in the detoxification of virulence factors produced by pathogens, overview
-
-
?
additional information
?
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-
tigecycline displays a broad spectrum of antibacterial activity and circumvents the efflux and ribosomal protection resistance mechanisms, Mg2+-complexing is required for ribosome binding, 11a-hydroxytigecycline forms a weaker complex with magnesium than tigecycline, structure, overview
-
-
?
additional information
?
-
-
benzydamine is a weak base and an indazole derivative with analgesic and antipyretic properties used in human and veterinary medicine, it is metabolized to a wide range of metabolites. One of the main metabolites, benzydamine N-oxide is produced in the liver and brain by flavin-containing monooxygenases
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?
additional information
?
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-
enzyme regulation, overview
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-
?
additional information
?
-
arylamine compounds, such as sulfamethoxazole and dapsone, are metabolized in epidermal keratinocytes to arylhydroxylamine metabolites that autooxidize to arylnitroso derivatives, which in turn bind to cellular proteins and can act as antigens/immunogens, methimazole and 4-aminobenzoic acid hydrazide attenuate the protein haptenation, overview
-
-
?
additional information
?
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-
effects of genetic variants of isozyme FMO3 on N- and S-oxygenation activities, FMO3 polymorphisms are responsible for the genetic disorder trimethylaminuria, or fish-like odor syndrome, overview
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-
?
additional information
?
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-
FMO oxygenates a number of drugs and xenobiotics containing a soft-nucleophile heteroatom, mostly sulfur- and nitrogen-containing xenobiotics, isozymes FMO1-FMO3 are involved in detoxication and drug metabolism, FMO3 deficiency causes the disease trimethylaminuria
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-
?
additional information
?
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-
FMOs are, together with cytochrome P450 monooxygenases, the major oxidative enzymes in phase I metabolism, extrahepatic metabolism of carbamate and organophosphate thioether compounds, isozyme FMO1 shows higher turnover numbers than isozyme FMO3 for all pesticides studies, overview
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-
?
additional information
?
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-
FMOs catalyze NADPH-dependent monooxygenation of soft-nucleophilic nitrogen, sulfur, and phosphorous atoms contained within various drugs, pesticides, and xenobiotics, isozyme FMO3 is responsible for the majority of FMO-mediated xenobiotic metabolism in the adult human liver, FMO3 mutations causing defects in trimethylamine N-oxygenation, result in the disorder known as trimethylaminuria, TMAU, or fish-odour syndrome, overview, interindividual variability in the expression of FMO3 affect drug and exogenous chemical metabolism in the liver and other tissues
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?
additional information
?
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nitrogen- and sulfur-containing endogenous substrates and physiologic functions, FMO is not induced by xenobiotics, isozyme FMO3 mutant alleles contribute to the disease known as trimethylaminuria, the enzyme is involved in detoxification and drug metabolism, overview, expression of FMO5 is markedly down-regulated in the liver of humans with type II diabetes, patients diagnosed with atrial fibrillation document a significant increase in the expression of FMO1, FMO may be associated with sideroblastic anemia, FMO3 mutations lead to trimethylaminuria, detailed overview
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?
additional information
?
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the enzyme catalyzes the NADPH-dependent N-and S-oxidation of a variety of therapeutics, environmental toxicants, carcinogens, and nutrients
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?
additional information
?
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drug metabolism, overview, enzyme mutations are involved in development of trimethylaminuria or fish-odor-syndrome, overview
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?
additional information
?
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drug metabolism, overview, enzyme mutations are involved in development of trimethylaminuria or fish-odor-syndrome, overview
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?
additional information
?
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drug metabolism, overview, enzyme mutations are involved in development of trimethylaminuria or fish-odor-syndrome, overview
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?
additional information
?
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drug metabolism, overview, enzyme mutations are involved in development of trimethylaminuria or fish-odor-syndrome, overview
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?
additional information
?
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drug metabolism, overview, most humans are homozygous for a nonsense mutation that inactivates FMO2. But a substantial proportion of sub-Saharan Africans express functional FMO2 and, thus, are predicted to respond differently to drugs and other foreign chemicals
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?
additional information
?
-
drug metabolism, overview, most humans are homozygous for a nonsense mutation that inactivates FMO2. But a substantial proportion of sub-Saharan Africans express functional FMO2 and, thus, are predicted to respond differently to drugs and other foreign chemicals
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?
additional information
?
-
drug metabolism, overview, most humans are homozygous for a nonsense mutation that inactivates FMO2. But a substantial proportion of sub-Saharan Africans express functional FMO2 and, thus, are predicted to respond differently to drugs and other foreign chemicals
-
-
?
additional information
?
-
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drug metabolism, overview, most humans are homozygous for a nonsense mutation that inactivates FMO2. But a substantial proportion of sub-Saharan Africans express functional FMO2 and, thus, are predicted to respond differently to drugs and other foreign chemicals
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?
additional information
?
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drug metabolism, overview, the FMO1 gene is downregulated in the spinal cord of patients with the neurodegenerative disease amyotrophic lateral sclerosis, but is upregulated in the myocardial tissue of patients with atrial fibrillation
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?
additional information
?
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drug metabolism, overview, the FMO1 gene is downregulated in the spinal cord of patients with the neurodegenerative disease amyotrophic lateral sclerosis, but is upregulated in the myocardial tissue of patients with atrial fibrillation
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?
additional information
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drug metabolism, overview, the FMO1 gene is downregulated in the spinal cord of patients with the neurodegenerative disease amyotrophic lateral sclerosis, but is upregulated in the myocardial tissue of patients with atrial fibrillation
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drug metabolism, overview, the FMO1 gene is downregulated in the spinal cord of patients with the neurodegenerative disease amyotrophic lateral sclerosis, but is upregulated in the myocardial tissue of patients with atrial fibrillation
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additional information
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FMO2 catalyzes the S-oxygenation of organophosphates representing a detoxification pathway
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additional information
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FMO2 catalyzes the S-oxygenation of organophosphates representing a detoxification pathway
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additional information
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FMO2 catalyzes the S-oxygenation of organophosphates representing a detoxification pathway
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additional information
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FMO2 catalyzes the S-oxygenation of organophosphates representing a detoxification pathway
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additional information
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FMO2 catalyzes the S-oxygenation of organophosphates representing a detoxification pathway
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additional information
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human FMO3 regulatory elements, overview
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human FMO3 regulatory elements, overview
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the enzyme is regulated by hormones, e.g. testosterone
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comparison of in vivo activity of FMO enzyme with P450 enzme in N-oxygenation of drugs at different pH values, overview
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comparison of in vivo activity of FMO enzyme with P450 enzme in N-oxygenation of drugs at different pH values, overview
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additional information
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FMO oxygenates a number of drugs and xenobiotics containing a soft-nucleophile heteroatom, mostly sulfur- and nitrogen-containing xenobiotics, and is involved in detoxication
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additional information
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nitrogen- and sulfur-containing endogenous substrates and physiologic functions, the enzyme is involved in detoxification and drug metabolism, overview, hepatic total FMO activity is enhanced in mouse models of type I and type II diabetes
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the enzyme is involved in fatty acid oxidation in the liver, as well as in drug detoxification
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additional information
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regulation of hepatic Fmo isozymes, overview
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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flavin-containing monooxygenases catalyze the addition of oxygen to many sulfur-, nitrogen-, phosphorus-, and selenium-containing compounds including pesticides, therapeutics, and dietary substances
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additional information
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regulation of the enzyme expression by hypersaline conditions and the osmoregulatory hormonecortisol, overview
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additional information
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regulation of the enzyme expression by hypersaline conditions and the osmoregulatory hormonecortisol, overview
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additional information
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nitrogen- and sulfur-containing endogenous substrates and physiologic functions, the enzyme is involved in detoxification and drug metabolism, overview
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additional information
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the enzyme is involved in oxidative metabolism of drugs and other chemicals
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additional information
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the enzyme is involved in oxidative metabolism of drugs and other chemicals
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additional information
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benzydamine is a weak base and an indazole derivative with analgesic and antipyretic properties used in human and veterinary medicine, it is metabolized to a wide range of metabolites. One of the main metabolites, benzydamine N-oxide is produced in the liver and brain by flavin-containing monooxygenases
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additional information
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the enzyme is involved in detoxification, generally, metabolites produced by FMO-catalysed reactions are more hydrophilic and less toxic, and are easily excreted from the body
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additional information
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FMO oxygenates a number of drugs and xenobiotics containing a soft-nucleophile heteroatom, mostly sulfur- and nitrogen-containing xenobiotics, and is involved in detoxication
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additional information
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the enzyme plays an important role in drug metabolism, insulin itself has no effect on FMO1 activity in non-diabetic animals, but hepatic isozyme FMO1 and intestinal CYP3A activity are correlated with average blood glucose concentration in untreated diabetic rats, and insulin reduces CYP3A activity, thus also regulates FMO1 indirectly
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additional information
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the substrate specificity of Saccharomyces cerevisiae FMO is more restricted than that of mammalian FMOs, reflecting its role in maintaining redox balance in the cell
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additional information
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FMO oxygenates a number of drugs and xenobiotics containing a soft-nucleophile heteroatom, mostly sulfur- and nitrogen-containing xenobiotics, and is involved in detoxication
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additional information
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nitrogen- and sulfur-containing endogenous substrates and physiologic functions, the enzyme is involved in detoxification and drug metabolism, overview
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additional information
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benzydamine is a weak base and an indazole derivative with analgesic and antipyretic properties used in human and veterinary medicine, it is metabolized to a wide range of metabolites. One of the main metabolites, benzydamine N-oxide is produced in the liver and brain by flavin-containing monooxygenases
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