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Cytochrome isoenzymes

Oxcarbazepine, like its analogue carbamazepine, acts by blocking voltage-sensitive sodium channels. It is rapidly and extensively metabolised in the liver the of the parent drug is 2 h but that of its principal metabolite (which also has therapeutic activity) is 11 h. Unlike carbamazepine, it does not form an epoxide which may explain why oxcarbazepine has fewer unwanted effects. Oxcarbazepine is a selective inducer of a cytochrome isoenzyme that metabolises the oral contraceptive and a 50 microgram oestrogen preparation is necessary for... [Pg.419]

Aprepitant has the potential for numerous drug interactions because it is a substrate, moderate inhibitor, and an inducer of cytochrome isoenzyme CYP3A4 and an inducer of CYP2C9. Aprepitant... [Pg.671]

Metabolism is still a barrier to be overcome. Some QSAR, pharmacophore, protein, and rule-based models are available to predict substrates and inhibitors of a specific cytochrome P450 isoenzyme [47-55]. [Pg.608]

Imidazole antimycotics, ketoconazole, clotrimazole, and miconazole are potent inhibitors of various cytochrome P450-isoenzymes that also affect the metabolism of retinoids. They were fust shown to inhibit the metabolism of RA in F9 embryonal carcinoma cells. When tested in vitm liarazole, a potent CYP-inhibitor, suppressed neoplastic transformation and upregulated gap junctional communication in murine and human fibroblasts, which appeared to be due to the presence of retinoids in the serum component of the cell culture medium. Furthermore, liarazole magnified the cancer chemopreventive activity of RA and (3-carotene in these experiments by inhibiting RA-catabolism as demonstrated by absence of a decrease in RA-levels in the culture medium in the presence of liarazole over 48 h, whereas without liarazole 99% of RA was catabolized. In vivo, treatment with liarazole and ketoconazole reduced the accelerated catabolism of retinoids and increased the mean plasma all-irans-RA-concentration in patients with acute promyelocytic leukemia and other cancels. [Pg.1077]

FIGURE 7-8. Pharmacologic activity and metabolism of warfarin. CYP, cytochrome P-450 isoenzyme. (Reproduced from Haines ST, Zeolla M, Witt DM. Venous thromboembolism. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. [Pg.150]

Tobacco smoke contains chemicals that induce the cytochrome P-450 isoenzymes 1A1,1A2, and 2E1. Theophylline is metabolized by 1A2 and 2E1, and therefore smoking leads to increased clearance and subsequently decreased plasma levels of the drug.15 Because most patients with COPD are current or past smokers, it is important to assess current tobacco use and adjust the theophylline dose as required based on altered plasma theophylline levels if tobacco use changes. [Pg.238]

CYP450, cytochrome P-450 isoenzyme. Data from references 36, 37, 38. [Pg.458]

Codeine, hydrocodone, morphine, methadone, and oxycodone are substrates of the cytochrome P-450 isoenzyme CYP2D6.47 Inhibition of CYP2D6 results in decreased analgesia of codeine and hydrocodone due to decreased conversion to the active metabolites (e.g., morphine and hydromorphone, respectively) and increased effects of morphine, methadone, and oxycodone. Methadone is also a substrate of CYP3A4, and its metabolism is increased by phenytoin and decreased by cimetidine. CNS depressants may potentiate the sedative effects of opiates. [Pg.497]

CYP. cytochrome P450 isoenzyme HIV, human immunodeficiency vims INR, International Normalized Ratio LFTs, liver function tests MAOI, monoamine oxidase inhibitor PT, prothrombin time TCA, tricyclic antidepressant. [Pg.535]

Several antidepressants, including most of the SSRIs, nefa-zodone, and duloxetine, are known to inhibit various cytochrome P-450 isoenzymes, thereby elevating plasma levels of substrates for those isoenzymes and thus potentially leading to increased adverse effects or toxicity of those drugs. The propensity to cause these drug interactions will vary with the particular antidepressant and the precise isoenzyme9,19,30 (Table 35-6). [Pg.576]

Half-life (t1/2) 18-27 hours (adult) greater than 36 hours (elderly or patients with renal impairment) Cytochrome P-450 (CYP450) isoenzyme t1/2 decreases over time due to autoinduction 25-65 hours (initial) 12-1 7 hours (adult multiple dosing) 8-14 hours (children multiple dosing) 2 hours (parent) 9 hours (metabolite) 5-20 hours (adult) 25 hours increases to 59 hours with concomitant valproic acid therapy... [Pg.596]

Vardenafil can cause QT-interval prolongation this effect in combination with certain anti-arrhythmic agents can lead to life-threatening arrhythmias. CYP, cytochrome P-450 isoenzyme. [Pg.785]

BUN, blood urea nitrogen CBC, complete blood cell count CNS, central nervous system CYP, cytochrome P-450 isoenzyme LFT, liver function test MAO, monoamine oxidase QTc, Q-T interval corrected for heart rate SCr, serum creatinine TMP-SMX, trimethoprim-sulfamethoxazole. [Pg.1183]

Oral azoles are associated with significant interactions, particularly due to cytochrome P-450 isoenzymes. Medications that interact with azoles include warfarin, phenytoin, theophylline, rifampin, cyclosporine, and zidovudine. For patients receiving only a few doses, these interactions do not pose a significant risk. These interactions may pose a risk for patients receiving long-term suppressive therapy for recurrent infections. [Pg.1202]

Pharmacogenetics of ethnic populations Table 5.3 Major cytochrome P isoenzymes... [Pg.75]

Circulating melatonin is metabolized mainly in the liver, where it is first hydroxylated in the C6-position by cytochrome P450 monooxygenases (isoenzymes... [Pg.286]

CYP2D6 The principal isoenzyme (isoform) of cytochrome P-450 involved in the metabolism of psychotropic drugs. [Pg.240]


See other pages where Cytochrome isoenzymes is mentioned: [Pg.128]    [Pg.351]    [Pg.332]    [Pg.398]    [Pg.1199]    [Pg.128]    [Pg.351]    [Pg.332]    [Pg.398]    [Pg.1199]    [Pg.258]    [Pg.1286]    [Pg.26]    [Pg.28]    [Pg.29]    [Pg.247]    [Pg.60]    [Pg.150]    [Pg.159]    [Pg.222]    [Pg.230]    [Pg.335]    [Pg.458]    [Pg.460]    [Pg.499]    [Pg.511]    [Pg.563]    [Pg.563]    [Pg.567]    [Pg.1184]    [Pg.1229]    [Pg.1276]    [Pg.43]    [Pg.95]    [Pg.113]    [Pg.195]    [Pg.31]   
See also in sourсe #XX -- [ Pg.246 ]




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Cytochrome P-450 isoenzymes

Cytochrome P450 isoenzyme inducers

Cytochrome P450 isoenzyme inducers Tacrolimus

Cytochrome P450 isoenzyme inhibitors

Cytochrome P450 isoenzyme substrates

Cytochrome P450 isoenzyme substrates Protease inhibitors

Cytochrome P450 isoenzymes

Cytochrome P450 isoenzymes drug metabolism

Cytochrome P450 isoenzymes drugs metabolized

Cytochrome P450 isoenzymes genetic polymorphism

Cytochrome P450 isoenzymes oxidative reactions

Isoenzyme

Isoenzymes

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