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Deethylation pathways

Ethotoin. Chemically, 3-ethyl-5-phenylhy-dantoin, ethotoin (Ic) undergoes two biotransformation pathways leading to inactive products p-hydroxylation [pathway (1)] and deethylation [pathway (2)]. This product has relatively low potency compared to that of phenytoin. Like phenytoin, ethotoin displays saturable metabolism with respect to the formation of the two metabolites (18). [Pg.273]

Other chlorotriazines (simazine, propazine, terbuthylazine) follow the same biotransformation pathway of atrazine therefore, urinary excretion of bi-dealkylated, deisopropylated, and deethylated metabolites is not compound specific. When simultaneous exposure to different chlorotriazines occurs, the unmodified compound measured in urine, even though it represents a minor portion of the absorbed dose, may be useful for a qualitative confirmation of exposure. [Pg.15]

Fig. 4.3. Hydrolysis pathways in the metabolism of epicainide (4.29). Pathway a direct hydrolysis of the secondary amide function. Pathway b hydrolysis of the primary amide (4.30) formed by oxidative (V-dealkylation. Pathway c hydrolysis of the intermediary metabolite (4.31) formed by (V-deethylation and subsequent oxidation of the pyrrolidine moiety [17]. Fig. 4.3. Hydrolysis pathways in the metabolism of epicainide (4.29). Pathway a direct hydrolysis of the secondary amide function. Pathway b hydrolysis of the primary amide (4.30) formed by oxidative (V-dealkylation. Pathway c hydrolysis of the intermediary metabolite (4.31) formed by (V-deethylation and subsequent oxidation of the pyrrolidine moiety [17].
A simple example in this class with which to begin is A,A-diethyl-m-to-luamide 0V,/V-dicthyl-3-mcthylbenzamidc, DEET, 4.82), an extensively used topical insect repellant. The hydrolysis product 3-methylbenzoic acid was detected in the urine of rats dosed intraperitoneally or topically with DEET. However, amide hydrolysis represented only a minor pathway, the major metabolites resulting from methyl oxidation and A-dealkylation [52], Treatment of rats with /V,/V-dicthylbcnzamidc (4.83), a contaminant in DEET, produced the same urinary metabolites as its secondary analogue, A-ethylbenzamide (see Sect. 4.3.1.2). This observation can be explained by invoking a metabolic pathway that involves initial oxidative mono-A-deethylation followed by enzymatic hydrolysis of the secondary amide to form ethylamine and benzoic acid [47], Since diethylamide was not detected in these experiments, it appears that A,A-diethylbenzamide cannot be hydrolyzed by amidases, perhaps due to the increased steric bulk of the tertiary amido group. [Pg.122]

Fig. 4.6. Metabolic pathways of 4- [(diethylamino)aeetyl]amino -N-(2,6-dimethylphenyl)benzamide (4.140) in mice [86]. The metabolites formed by consecutive IV-deethylation (4.141 and 4.142) as well as of the parent compound are hydrolyzed at the amido bond to produce ameltolide (4.143). Fig. 4.6. Metabolic pathways of 4- [(diethylamino)aeetyl]amino -N-(2,6-dimethylphenyl)benzamide (4.140) in mice [86]. The metabolites formed by consecutive IV-deethylation (4.141 and 4.142) as well as of the parent compound are hydrolyzed at the amido bond to produce ameltolide (4.143).
Enrofloxacin is mainly eliminated by hepatic metabolism, and systemic clearance of the drug varies between species. In sheep, horses, dogs and pigs the average clearance of enrofloxacin is in the range 5.75-8.56 mL/min kg, while enrofloxacin clearance (mL/min kg) differs more widely between other species rabbits (17.9), llamas (12.0), chickens (3.3), turkeys (8.9), houbara bustard (5.7) and fingerling rainbow trout (Oncorhynchus mykiss) at 15°C (1.25). Systemic clearance of enrofloxacin represents mainly hepatic clearance composed of a variety of metabolic pathways, which include N-deethylation to ciprofloxacin. [Pg.43]

More recently it has become apparent that genetic factors also affect phase 1, oxidation pathways. Early reports of the defective metabolism of diphenylhydantoin in three families and of the defective deethylation of phenacetin in certain members of one family indicated a possible genetic component in microsomal enzyme-mediated reactions. Both these cases resulted in enhanced toxicity. Thus, diphenylhydantoin, a commonly used anticonvulsant, normally undergoes aromatic hydroxylation and the corresponding phenolic metabolite is excreted as a glucuronide (figure 7,35). Deficient... [Pg.268]

B in Fig. 13.3 represent important metabolic pathways that affect many drugs. When X = N (by far the most frequent case), the metabolic reactions are known as N-demethylations, N-dealkylations, or deaminations, depending on the moiety being cleaved. Consider for example fenfluramine (10)(Fig. 13.12), which isN-deethylated to norfenfluramine (11), an active metabolite, and deaminated to (m-trifluoro-methyDphenylacetone (12), an inactive metabolite that is further oxidized to m-trifluoro-methylbenzoic acid (13). [Pg.449]


See other pages where Deethylation pathways is mentioned: [Pg.251]    [Pg.244]    [Pg.251]    [Pg.244]    [Pg.783]    [Pg.75]    [Pg.128]    [Pg.783]    [Pg.114]    [Pg.471]    [Pg.253]    [Pg.425]    [Pg.85]    [Pg.126]    [Pg.394]    [Pg.284]    [Pg.52]    [Pg.534]    [Pg.44]    [Pg.211]   
See also in sourсe #XX -- [ Pg.244 ]




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Deethylation

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