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Metabolism inhibitors

CYP2C19 Polymorphisms and Proton Pump Inhibitor Metabolism... [Pg.397]

Protease inhibitors [NE] Increased protease inhibitor metabolism. [Pg.1388]

The onset of symptoms depends on the particular organophosphorus compound, but is usually relatively rapid, occurring within a few minutes to a few hours, and the symptoms may last for several days. This depends on the metabolism and distribution of the particular compound and factors such as lipophilicity. Some of the organophosphorus insecticides such as malathion, for example (chap. 5, Fig. 12), are metabolized in mammals mainly by hydrolysis to polar metabolites, which are readily excreted, whereas in the insect, oxidative metabolism occurs, which produces the cholinesterase inhibitor. Metabolic differences between the target and nontarget species are exploited to maximize the selective toxicity. Consequently, malathion has a low toxicity to mammals such as the rat in which the LD50 is about 10 g kg-1. [Pg.346]

ANTI HYPERTENSIVES AND HEART FAILURE DRUGS NS AIDs 1 hypotensive effect, especially with indometacin. The effect is variable amongst different ACE inhibitors and NSAIDs, but is most notable between captopril and indometacin NSAIDs cause sodium and water retention and raise BP by inhibiting vasodilating renal prostaglandins. ACE inhibitors metabolize tissue kinins (e.g. bradykinin) and this may be the basis for indometacin attenuating hypotensive effect of captopril Monitor BP at least weekly until stable. Avoid co administering indometacin with captopril... [Pg.35]

The CYP inhibition assay utilizes the 96-well plate format with a robotic system, where both incubation and analysis are performed in the same plates. The setup of the sample plates is shown in Figure 4.1. For each compound, both direct inhibition and metabolism/mechanism-based inhibition, which is caused by a metabolite of the NCE that is either a more potent direct reversible inhibitor (metabolism-based) or a time-dependent irreversible inhibitor (mechanism-based), are evaluated. Both direct and mechanism-based inhibitors could result in inhibitory DDIs [51,52],... [Pg.101]

There are a number of well known inhibitors of cytochromes P-450 which form stable complexes with the enzyme. Thus SKF 525A, piperonyl butoxide, triacetyloleandomycin, amphetamine, isoniazid and cimetidine are a few of those known to form complexes with cytochromes P-450. In the case of several of these inhibitors, metabolism catalysed by cytochromes P-450 takes place and the metabolite so produced inhibits the enzyme. Thus, amphetamine is believed to be metabolized to a nitroso intermediate which complexes with the enzyme. Piperonyl butoxide is a commonly used microsomal enzyme inhibitor. It is active both in vivo and in vitro,... [Pg.314]


See other pages where Metabolism inhibitors is mentioned: [Pg.46]    [Pg.29]    [Pg.74]    [Pg.1686]    [Pg.225]    [Pg.180]    [Pg.789]    [Pg.7]    [Pg.75]   
See also in sourсe #XX -- [ Pg.38 , Pg.387 ]




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2,4-Dinitrophenol metabolism inhibitor

Angiotensin-converting enzyme inhibitors metabolism

Antibiotics bacterial cell metabolism inhibitors

Bacteria cell metabolism inhibitors

Caffeine metabolism inhibitors

Ceramide metabolism, inhibitors

Cholesterol metabolic inhibitors

Cholinesterase inhibitors metabolic effects

Endocannabinoids metabolic inhibitors

Enzyme inhibitors drug metabolism

Growth metabolic inhibitors, phenolic compound

Inhibitors suicide metabolism

Lipid metabolism, protease inhibitors

Metabolic inhibitor

Metabolic inhibitor

Metabolic inhibitor selectivity

Metabolic inhibitors effect

Metabolism succinate dehydrogenase inhibitor

Metabolism/mechanism-based inhibitor

Peptide metabolism inhibitors

Pharmacological Inhibitors of Arachidonic Acid Release and Metabolism

Protease inhibitors metabolism

Selective serotonin reuptake inhibitor metabolic

Selective serotonin reuptake inhibitors metabolism

Splicing Inhibitors From Small Molecule to RNA Metabolism

Suicide inhibitors/metabolic

Xenobiotic metabolizing enzymes inhibitors

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