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Diug Metabolism

JV-Acetyltransferases (NATs) catalyze the conjugation of an acetyl group from acetyl-CoA on to an amine, hydrazine or hydroxylamine moiety of an aromatic compound. NATs are involved in a variety of phase II-diug metabolizing processes. There are two isozymes NAT I and NAT II, which possess different substrate specificity profiles. The genes encoding NAT I and NAT II are both multi-allelic. Especially for NAT II, genetic polymoiphisms have been shown to result in different phenotypes (e.g., fast and slow acetylators). [Pg.12]

Diug metabolism, to predict whether a diug candidate will cause drug-drug interactions... [Pg.528]

The identification of specific nuclear receptors as molecular targets of P450 inducers impacts diug metabolism and diug development in several important ways ... [Pg.893]

The immediate metabolic precursor to dopamine, l-DOPA (L-dihydroxphenylalanine) is converted to the active neurotransmitter dopamine by the action of the enzyme aromatic amine acid decarboxylase (AADC). l-DOPA (INN name Levodopa) is the main diug used to treat Parkinson s disease. [Pg.437]

Interactions resulting from a change in the amount of diug reaching the site of action are called pharmacokinetic interactions (Fig. 1). A co-administered diug can affect any of the processes of absorption, distribution, metabolism, and excretion of the original diug, which are determinants of its pharmacokinetic profile [1-3]. [Pg.447]

Hyperthyroidism (thyrotoxicosis), defined as excessive thyroid activity, causes a state of thyroid hormone excess (thyrotoxicosis) characterized by an increased metabolic rate, increase in body temperature, sweating, tachycardia, tremor, nervousness, increased appetite and loss of weight. Common causes of hyperthyroidism are toxic multinodular goiter, toxic adenoma or diffuse toxic goitre ( Graves disease). Antithyroid diugs (methimazol, carbimazole, propylthiouracil) block thyroid hormone production and are hence suitable for the treatment of hyperthyroidism. [Pg.608]

Lipid-lowering diugs are diugs that affect the lipoprotein metabolism and that used in therapy to lower plasma lipids (cholesterol, triglycerides). The main classes of... [Pg.690]

Lipoprotein Metabolism Antidiabetic Diugs other than Insulin Adipokines... [Pg.945]

Diugs with metabolic interactions that can enhance the half-life of active compounds. An example of this regimen is the interaction between azole- and vitamin D-deiivatives that inhibit the metabolism of retinoids in skin cells leading to increased intracellular amounts of active RA-isomers. Further study and the identification of novel interactions of this type ofdtug interaction is of great clinical interest since they may decrease the dose of retinoids required for efficacy thereby also reducing the risk of side effects of the retinoids. [Pg.1078]


See other pages where Diug Metabolism is mentioned: [Pg.893]    [Pg.893]    [Pg.893]    [Pg.893]    [Pg.103]    [Pg.893]    [Pg.893]    [Pg.893]    [Pg.893]    [Pg.103]    [Pg.139]    [Pg.158]    [Pg.184]    [Pg.253]    [Pg.257]    [Pg.374]    [Pg.586]    [Pg.699]    [Pg.699]    [Pg.789]    [Pg.926]    [Pg.926]    [Pg.926]    [Pg.949]    [Pg.139]    [Pg.158]    [Pg.184]    [Pg.253]    [Pg.257]    [Pg.374]    [Pg.586]    [Pg.699]    [Pg.699]    [Pg.789]    [Pg.926]    [Pg.926]    [Pg.926]    [Pg.949]   


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