Metabolic inactivation hydroxylic

Pharmacokinetic properties Butorphanol (Vachharajani et al., 1997) is rapidly inactivated by first pass metabolism in the gut. Intramuscular and nasal administration induces a peak effect between 0.5-1 hr and a duration of action of about 3 h, corresponding to the plasma half-life time of the compound. Butorphanol has a plasma protein binding of about 80%, metabolic inactivation includes hydroxylation,... 

Pharmacokinetic properties The compound has an acceptable oral bioavailability (Bondesson, 1980). Metabolic inactivation occurs via N-demethylation and glucuronidation at the phenolic hydroxyl. 

Pharmacokinetic properties After oral administration levorphanol has a relatively slow onset, but a long (up to 8 h) duration of action. Metabolic inactivation occurs via glucuronidation of the phenolic hydroxyl and via N-demethylation (Dixon et al., 1983). 

Monoamine oxidase (MAO) inactivates serotonergic and catecholanunergic neurotransmitters MAO (A and B) inhibitors exhibit mood elevatmg properties 5-FIuoro-OC-methyltryptamine (19) is an important MAO A-selective inhibitor In the treatment of certain depressive illnesses, 4-fluorotranylcypromine (20b) is 10 tunes more potent than the parent tranylcypromine (TCP, 20a) The enhanced in vivo activity may be due to increased lipophilicity of 20b and/or to blockade of metabolic para hydroxylation [52]... 

Nortestosterone (N-I) and 19-Nortestosterone Esters. The original results (3.33 anabolic-androgenic ratio) of Hershberger [187] were confirmed a year later [65]. In spite of the favorable ratio, nortestosterone has only short-lived activity and therefore the 17-esters are used clinically, preventing quick metabolic inactivation of the 17/8-hydroxyl group. 

Androsta-1,4-dien-17(i-ol-3-one 17-(cyclopent-l -enyl) ether. The 17-ether function instead of the 17a-methyl group in this derivative (Quin-bolin, S-147) [14] is present in order to assure protection against metabolic inactivation of the 17-hydroxyl group [12]. The compound is orally applied and shows androgenic and anabolic activities similar to those of 17o -methyl-17/3-hydroxyandrost-1,4-dien-3-one. 

Metabolic inactivation of mephenytoin and its demethyl celalxilitc is by p-hydroxylation and then conjugation of the... 

As shown in Fig. 3, 2,3-DHBA and 2,5-DHBA may derive from SA as the products of metabolic inactivation which arises from additional hydroxylation of the aromatic ring. The rapid conjugation of SA with glucose to form P-D-o-glucosylsalicylic acid is the main metabolic inactivation mechanism in tobacco [37,38]. The glucose ester of SA was detected in soybean cell cultures fed with [ C]-labelled SA [39] and a small amount of these compound is also detected in tobacco [38]. 

The steroid hormones are mainly inactivated in the liver, where they are either reduced or further hydroxylated and then conjugated with glucuronic acid or sulfate for excretion (see p. 316). The reduction reactions attack 0X0 groups and the double bond in ring A. A combination of several inactivation reactions gives rise to many different steroid metabolites that have lost most of their hormonal activity. Finally, they are excreted with the urine and also partly via the bile. Evidence of steroids and steroid metabolites in the urine is used to investigate the hormone metabolism. 

Metabolism. Eicosanoids are inactivated within a period of seconds to minutes. This takes place by enzymatic reduction of double bonds and dehydrogenation of hydroxyl groups. As a result of this rapid degradation, their range is very limited. 

Catecholamine neurotransmitters are subsequently inactivated by enzymic methylation of the 3-hydroxyl (via catechol-O-methyltransferase) or by oxidative removal of the amine group via monoamine oxidase. Monoamine oxidase inhibitors are sometimes used to treat depression, and these drugs cause an accumulation of amine neurotransmitters. Under such drug treatment, simple amines such as tyramine in cheese, beans, fish, and yeast extracts are also not metabolized and can cause dangerous potentiation of neurotransmitter activity. 

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